Tesis: "Hight fat Diet"

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Lynes, Matthew D. "Control of CD36 phosphorylation by global intestinal alkaline phosphatase mediates intestinal adaptation to high-fat diet." Thesis, Boston University, 2012. https://hdl.handle.net/2144/32031.

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Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. The mechanisms by which diets high in saturated fat (HFD) contribute to intestinal adaptation and obesity are unknown. The hypothesis that functional changes in distal portions of small intestine are induced by HFD was tested in C57B1/6 mice. Specifically, it was examined whether the putative fatty acid translocase CD36 was phosphorylated in mouse intestinal epithelial cells and whether dephosphorylation of CD36 increased long chain fatty acid (LCFA) absorption. Co-immunoprecipitation was used to investigate specific intestinal alkaline phosphatases that might interact with CD36. It was also examined whether chronic ingestion of an HFD would lead to upregulation of the CD36 and/or one or more intestinal alkaline phosphatases that may activate CD36. CD36 was found to be phosphorylated on the surface of mouse enterocytes, indicating that there may be a phosphatase-sensitive pool of phospho-CD36 (pCD36) in mouse small intestinal tissue. CD36 was dephosphorylated by alkaline phosphatase and this treatment increased long chain but not short chain fatty acid uptake. Long chain fatty acid uptake was blocked with a specific CD36 inhibitor. CD36 from mouse small intestines physically interacted specifically with global intestinal alkaline phosphatase (gIAP) but not duodenal alkaline phosphatase (dIAP). As expected, HFD increased body weight, adiposity, and plasma triglycerides compared to control mice. CD36 and gIAP but not dIAP protein levels were significantly increased in distal but not proximal regions of intestines of HFD mice. Finally, HFD increased the absorptive capacity of the distal small intestine for LCFA in a CD36-dependent manner. It is concluded that HFD specifically upregulates gIAP protein in epithelial cells of the distal regions of the small intestine of mice, and that one of its substrates is pCD36, which has been implicated in transcellular fat transport. This diet also increases the absorptive capacity of the distal small intestine for LCFAs. Taken together, these results suggest that HFD causes intestinal adaptation that results in an increased capacity to absorb dietary fat. This effect is mediated in part by increasing the expression and activity of the fatty acid transporter CD36 and its regulatory enzyme gIAP. 2031-01-02

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Reginato, Andressa 1990. "Modulação de autofagia na prole de animais submetidos à dieta hiperlipídica na vida intrauterina, lactação e vida adulta." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/244500.

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Orientador: Marciane Milanski Ferreira Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas Made available in DSpace on 2018-08-27T16:06:12Z (GMT). No. of bitstreams: 1 Reginato_Andressa_M.pdf: 3622201 bytes, checksum: 6c4d49212fa7262052afb4aec8d81f48 (MD5) Previous issue date: 2015 Resumo: O excesso na ingestão calórica e a obesidade têm afetado um número crescente de pessoas em diferentes países, sendo que a obesidade durante a gestação e lactação desempenha impacto negativo no fenótipo prole. Na vida adulta, a obesidade e a sobrecarga de lipídeos constituem fatores que resultam no comprometimento da autofagia, um processo de degradação lisossomal essencial para a manutenção da homeostase celular. A autofagia é responsável pela degradação e reciclagem de componentes citoplasmáticos como organelas senescentes, proteínas agregadas ou mal formadas, microrganismos invasores e macromoléculas. Apesar do conhecimento acerca do prejuízo na atividade autofágica no contexto da obesidade, alterações na homeostase deste processo na prole de mães obesas ainda não foram investigadas. Neste estudo, foi avaliada a hipótese de que a obesidade materna induzida por dieta hiperlipídica seria capaz de modular proteínas da via autofágica no hipotálamo e no fígado da prole de camundongos. Embora sem nenhuma alteração na atividade de autofagia no hipotálamo, a prole de mães obesas ao nascimento (d0) apresentou prejuízo nos marcadores de autofagia no fígado representado por aumento no conteúdo proteico de p62 e diminuição no conteúdo proteico de LC3-II. Ao desmame (d18), a prole de mães obesas teve comprometimento no conteúdo proteico dos marcadores de autofagia em ambos os tecidos (fígado e hipotálamo) quando comparados à prole de mães magras. Após o desmame, a prole de mãe controle e a prole de mãe obesa receberam dieta controle até a vida adulta (d82). Nessa condição não houve modulação dos marcadores de autofagia em nenhum dos tecidos avaliados, sendo que somente a reexposição à dieta hiperlipídica (dos 42 dias até 82 dias) foi responsável por alterar o conteúdo proteico dos marcadores de autofagia quando comparados aos animais com dieta hiperlipídica sem reexposição. Assim, parece que dieta hiperlipídica é essencial para a modulação negativa dos marcadores de autofagia na prole de mães obesas. Em conclusão, a prole de mãe obesa apresentou comprometimento precoce de marcadores de autofagia no fígado e no hipotálamo, o que poderia estar associado ao desenvolvimento de distúrbios metabólicos na prole na idade adulta Abstract: The nutritional excess and obesity have affected a growing number of people in different countries, being that obesity during pregnancy and lactation has negative impact on offspring phenotype. In adulthood, obesity and lipids overload constitute factors that result in impairment of autophagy, a lysosomal degradation process essential for maintaining cellular homeostasis. Thus, autophagy is responsible for degradation and recycling of cytoplasmic components as senescent organelles, aggregated proteins or proteins poorly formed, microorganisms invaders and macromolecules. It is known that obesity and the use of high fat diet have a negative impact on cellular homeostasis. However, modulation of autophagy in the offspring of obese mothers has yet to be investigated. This study tested the hypothesis that maternal obesity induced by high fat diet would be able to modulate proteins of autophagy in the hypothalamus and liver of mice offspring. At birth (d0), the offspring exhibited prejudice in autophagy markers in liver and after weaning (d18) both tissues (liver and hypothalamus) had compromised autophagy markers. The animals receiving control diet after weaning until adulthood (d82) had no impairment of autophagy proteins in both tissues examined. However, when the animals were re-exposed to high-fat diet they had alteration in protein content of autophagy, when compared to animals with high fat diet without re-exposure. Thus, high fat diet seems to be essential for negative modulation of autophagy markers. In conclusion, the offspring of obese mothers presented early impairment of autophagy proteins in the liver and hypothalamus, which may be associated with the development of metabolic disorders in the offspring in adulthood Mestrado Metabolismo e Biologia Molecular Mestra em Ciências da Nutrição e do Esporte e Metabolismo

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Carmo, Luciana Simão do. "Proliferação e diferenciação in vitro de células mononucleares medulares após estímulo com fatores de crescimento em ratos Wistar submetidos à dieta hiperlipídica." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-05062013-123012/.

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O aumento da adiposidade corpórea pode gerar diversos mediadores inflamatórios com capacidade de influenciar a proliferação e a diferenciação hematopoética e, consequentemente, a complexa regulação da hematopoese. Por isso, propusemo-nos, neste trabalho, avaliar a influência do aumento da adiposidade corpórea sobre a proliferação e a diferenciação de células hematopoéticas, bem como sua capacidade em sintetizar citocinas. Ratos Wistar, machos foram alimentados com uma dieta rica em lipídios durante 14 semanas. Após esse período foram avaliados hemograma, mielograma, perfil lipídico, concentrações séricas de leptina, insulina e adiponectina. Citômetria de fluxo foi utilizada para avaliação da porcentagem de células CD34+/CD133+, bem como o ciclo celular de células medulares. Células medulares foram utilizadas para avaliar a atividade proliferativa in vitro e a capacidade de diferenciação, in vitro, na presença de IL-3, EPO, GM-CSF e G-CSF. Animais, alimentados com dieta hiperlipídica, apresentaram maiores concentrações de leptina circulante, com aumento de gordura corporal, aumento da concetração de proteína C reativa, colesterol total, LDL, VLDL e triacilglicerol. O hemograma apresentou neutrofilia absoluta e a medula óssea apresentou-se hipercelular com aumento do número de granulócitos maduros e da população celular CD133-/CD34+. Os resultados dos testes in vitro demonstraram aumento da capacidade de síntese de IL-3 e aumento de G-CSF, com aumento do potencial proliferativo, também evidenciado pelo maior número de células medulares na fase S/G2/M, bem como o aumento da diferenciação granulocítica. Esses resultados sugerem que a leucocitose e neutrofilia observadas em situações de aumento da adiposidade corpórea são decorrentes de uma complexa modulação do sistema hematopoético. The body fat increase can generate various inflammatory mediators, that are capable to influence the proliferation and differentiation of hematopoietic cells and consequently modulate the complex regulation of the hematopoiesis. In this study we have proposed to evaluate the effect of increase body fat on the proliferation and differentiation of hematopoietic cells, as well as its ability to synthesize cytokines. Male Wistar rats were subjected to a high fat diet during a period of 14 weeks. After that period were evaluated hemogram, mielogram, lipid profile and the serum concentrations of leptin, insulin and adiponectin. Flow cytometry was used to evaluate the percentage of CD34+/CD133+, as well as the cell cycle of bone marrow cells. Bone marrow cells were used to perform the proliferation and differentiation capacity in vitro in the presence of IL-3, EPO, GM-CSF and G-CSF. Animals fed high-fat diet had higher concentrations of circulating leptin with increase body fat, and increase of C-reactive protein, total cholesterol, LDL, VLDL and triacylglycerol concentrations. The hemogram showed absolute neutrophilia and a hypercellular bone marrow with increase of granulocytic mature population and CD133-/CD34+ cells. The results in vitro, showed an increase of IL-3 and G-CSF production, and higher proliferative potential with an increase in S/G2/M bone marrow cell cycle phases, as well as an increase of the granulocytic differentiation. The results suggest that leukocytosis and neutrophilia observed in this model of body fat increase are in fact a result of a complex modulation of the hematopoietic system.

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Wüest, Stephan. "Activation of Fas (CD95) in adipocytes contributes to high fat diet-induced insulin-resistance /." [S.l.] : [s.n.], 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000282894.

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Pattison, Claire A. "Modelling perceptions of risk for food related hazards-Appendices." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270311.

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Wagner, Jana Louise. "Promoting one low-fat, high-fiber choice in a fast-food restaurant: use of point-of-purchase prompts." Thesis, Virginia Polytechnic Institute and State University, 1987. http://hdl.handle.net/10919/80169.

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This research project investigated a method to promote one low-fat, high-fiber choice in a national chain fast-food restaurant. It is an extension of efforts toward large-scale dietary change. A procedural extension of a prompting strategy was used in an attempt to influence customers to choose a salad. A simple visual and print message based on themes derived from formative and pilot research at the restaurant was presented during two intervention phases of a reversal design. The message, "Be Fit and Healthy; Eat a Low-fat SALAD as Your Meal or Add a Side Salad," was displayed in colorful posters and tent cards which were placed on all the tables. Data from a comparison base in a neighboring town were obtained. A one-month follow-up phase was included in the design. Prices and in-store advertisements were identical in both locations. The existing computerized cash register system was used to obtain accurate, objective data. Daily and weekly sales percentages of several entrees were obtained. Results of analysis using a correction procedure indicate that when graphically represented, salad sales across phases increased with the introduction of the prompts, and decreased with their removal. In addition, three entrees not represented by associated prompts remained stable across phases. For Salads-combined, results indicate that sales increased about 15% and 9%, respectively, for the first and second intervention phases. Daily temperature during this project was variable. Although a comparison site was used to control for the effects of weather, results indicate that salad prompting may have increased sales more during warmer temperature. Population demographics were recorded. Analyses of the customer population during this project indicate customers were about equal by gender, and consisted primarily of white, 18-39 years old individuals. The cost for each added salad bought during the intervention was about $.22, and the cost to raise the percent of salad sales, each percent, across the four weeks was about $16.00. Future research should attempt to foster longer term behavior change and integrate multifaceted promotions. Master of Science

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Fontelles, Camile Castilho. "Paternal pre-conceptional nutrition programs breast cancer risk in rat female offspring: opposing effects of animal- and plant- based high fat diets." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-28092016-142616/.

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Breast cancer is a persistent public health problem. Interesting hypothesis suggests that its risk can be modulated in early life periods, a phenomenon known as fetal programming. In this context, most fetal programming studies focus on maternal influence, due to the greater interaction between mother and fetus in both fetal and lactation periods. However, recent studies show that paternal preconception diet has also a major role in the offspring\'s susceptibility to metabolic chronic non-communicable diseases. Therefore, this direct doctoral project aimed to assess whether the paternal consumption of different high fat diets during the development period of the reproductive system of male rats increased the susceptibility of female offspring to mammary carcinogenesis. In addition we sought to evaluate which mechanisms could be involved in this process. We used male rats of the Sprague-Dawley strain (n = 20/group) that consumed high fat diet with 60% of calories from lipids from lard (LB group) or corn oil (CB group), or AIN-93G control diet (CO group) for nine weeks, during development and sexual maturation periods. These rats were mated with females who consumed only commercial diet in 1:1 ratio. Their 50 days old offspring were subjected to mammary carcinogenesis model using 7,12-dimethylbenz[a]anthracene (50mg/kg). Paternal consumption of high fat diet of animal or plant source had opposite effects, with the paternal consumption of diet with high content of saturated fatty acids (LB) increasing and consumption of diet with high content of n-6 polyunsaturated fatty acids (CB) reducing the risk of breast cancer development in female offspring. These effects were due to changes in the expression of 89 miRNAs in the father\'s sperm and 23 miRNAs in the offspring\'s mammary gland, with overlapping of three miRNAs (miR-1897-5p, miR- 219-1-3p and miR-376a #) that were altered in both tissues. Additionally, female offspring of males fed diets with high content of saturated fatty acids showed less differentiation of the mammary gland, higher levels of cell proliferation, lower levels of apoptosis and altered expression of keys proteins that regulate important cellular functions, such as epithelial to mesenchymal transition. Finally, these females had also altered lipid profile of the fat pad similar to their male parent as well as epigenetic changes that may be related to the etiology of breast cancer. Thus, we conclude that the high-fat preconception paternal diet programmed the susceptibility of female offspring to mammary carcinogenesis, but this effect was dependent on the type of fatty acid consumed and the observed effects possibly results from changes in miRNA expression profile. O câncer de mama é um persistente problema de saúde pública. Hipótese intrigante sugere que a suscetibilidade à doença pode ser modulada em períodos precoces da vida, fenômeno conhecido como programação fetal. Nesse sentido, a maior parte dos estudos de programação fetal refere-se à influência materna, dada a intensa interação existente entre mãe e feto tanto no período fetal, quanto na lactação. Entretanto, estudos recentes mostram que a dieta paterna pré-concepcional também tem um papel de grande importância na suscetibilidade da prole à uma série de doenças crônicas não-transmissíveis de origem metabólica. Portanto, o presente projeto de doutorado direto teve como objetivo avaliar se o consumo paterno de diferentes dietas hiperlipídicas, durante o período de desenvolvimento do sistema reprodutivo de ratos machos, aumentaria a suscetibilidade da prole feminina à carcinogênese mamária. Adicionalmente buscou-se avaliar quais mecanismos poderiam estar envolvidos nesse processo. Utilizaram-se ratos machos da linhagem Sprague-Dawley (n=20/grupo) que consumiram dieta hiperlipídica com 60% de calorias provenientes de lipídeos de banha (grupo LB) ou óleo de milho (grupo CB), ou dieta controle AIN-93G (grupo CO), por nove semanas, durante os períodos de desenvolvimento e maturação sexual. Esses ratos foram acasalados com fêmeas, que consumiram apenas dieta comercial, na proporção 1:1. Sua prole de 50 dias foi submetida ao modelo de carcinogênese mamária com o uso de 7,12-dimetil-benza[a]antraceno (50mg/kg). O consumo paterno de dietas hiperlipídicas de origem animal ou vegetal conferiram efeitos opostos, com o consumo de dieta com alto teor de ácidos graxos saturados (LB) aumentando e o consumo de dieta com alto teor de ácidos graxos poli-insaturados n-6 (CB) diminuindo o risco de desenvolvimento de câncer de mama na prole feminina. Esses efeitos foram associados à alteração da expressão de 89 miRNAS no espermatozoide dos pais e 23 miRNAs na glândula mamária da prole, com sobreposição de 3 miRNAs (miR-1897-5p, miR-219-1-3p e miR-376a#) que estavam alterados em ambos tecidos. Adicionalmente, a prole feminina de machos que consumiram dieta com alto teor de ácidos graxos saturados apresentou menor diferenciação da glândula mamária, maior nível de proliferação celular, menor nível de apoptose e alteração da expressão de proteínas chaves da regulação celular, como na transição epitélio-mesenquimal. Finalmente, essas fêmeas também apresentaram perfil lipídico alterado semelhante à do seu progenitor masculino, bem como modificações epigenéticas que podem estar relacionadas à etiologia do câncer de mama. Assim, concluímos que a dieta paterna hiperlipídica pré-concepcional programou a suscetibilidade da prole feminina à carcinogênese mamária, porém esse efeito é dependente do tipo de ácido graxo consumido e os efeitos observados possivelmente decorrem de alterações no perfil de expressão de miRNAs.

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Werner, Tim J. "The effect of high-carbohydrate, low-fat & low-carbohydrate, high protein diets on physiologic and performance variables on row ergometry training." Ohio : Ohio University, 2006. http://www.ohiolink.edu/etd/view.cgi?ohiou1140557597.

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Sekar, Sunderajhan. "Effects of dietary saturated fatty acids on the onset and progression of osteoarthritis in rat knee joints." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/116166/1/Sunderajhan_Sekar_Thesis.pdf.

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Chronic intake of a high-fat diet has been associated with increased incidence of osteoarthritis. However, at present, there is a lack of a clear understanding of what type of dietary fats causes major concern and how much of it alters osteoarthritis risk. Therefore, this study evaluated the specific effects of individual dietary saturated fats on both the onset and the progression of knee osteoarthritis. The study found that high susceptibility to dietary obesity was associated with increased OA like changes in the knee. Palmitic and Stearic acid supplementation exhibited increased knee cartilage degeneration and decreased bone volume, leading to a quicker onset and increased progression of OA. In contrast, Lauric and Myristic acid supplementation showed reduced degeneration of the cartilage, increased bone volume and increased pain threshold.

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Fante, Thaís de 1990. "Dieta hiperlipídica, inflamação e programação metabólica : efeitos na sinalização de insulina em camundongos recém-desmamados e adultos." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/244499.

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Orientadores: Adriana Souza Torsoni, Marciane Milanski Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas Made available in DSpace on 2018-08-27T16:45:13Z (GMT). No. of bitstreams: 1 Fante_Thaisde_M.pdf: 3029616 bytes, checksum: 5e68ab17d3076784e4f20c127d76838f (MD5) Previous issue date: 2015 Resumo: O estilo de vida moderno tem levado ao aumento na prevalência de obesidade e suas co-morbidades em gestantes e na população cada vez mais jovem. Muitos dos efeitos do consumo direto de dieta hiperlipídica (DH) no metabolismo de glicose e lipídios já são bem estabelecidos. No entanto, considera-se importante avaliar se o consumo de DH durante períodos críticos do desenvolvimento seria capaz de ativar mecanismos epigenéticos, perpetuando mudanças no metabolismo da prole e criando um ciclo vicioso que não poderia ser interrompido. O objetivo desse estudo foi avaliar o efeito potencial da programação metabólica em prejudicar a sinalização de insulina na prole recém desmamada de mães alimentadas com dieta hiperlipídica durante a gestação e lactação. Além disso, investigamos se a exposição precoce a um ambiente obesogênico seria capaz de exacerbar o prejuízo no metabolismo de glicose na vida adulta de animais reexpostos à dieta hiperlipídica. Para isso, camundongos fêmeas da linhagem Swiss foram alimentados com dieta controle ou DH durante os períodos de adaptação, gestação e lactação, e os tecidos da prole macho foram analisados nos dias 28 e 82. Os resultados mostram que a prole de mães obesas (HC-O) apresentou maior ganho de peso, adiposidade e ingestão alimentar que a prole de mães controle (CC-O). Além do mais, apresentou prejuízos na sinalização de insulina em tecidos periféricos como fígado, adiposo e músculo, e centrais, como o hipotálamo, provavelmente devido à maior ativação de vias inflamatórias. A reexposição à DH parece agir como um fator agravante para o desenvolvimento do fenótipo obeso, levando a resistência sistêmica à insulina e hiperleptinemia. É válido ressaltar que o tecido adiposo parece ser o tecido mais afetado na prole adulta após a reexposição da dieta (HH-O), o que pode contribuir para a desregulação metabólica observada. Em conjunto, nossos resultados sugerem que o consumo materno de dieta hiperlipídica durante a gestação e lactação pode ocasionar alterações no metabolismo glicídico da prole tanto em animais recém desmamados quanto adultos. Por fim, a obesidade materna leva à maior susceptibilidade ao desenvolvimento de obesidade e prejuízos na sinalização de insulina na prole que não podem ser revertidos pelo consumo de uma dieta controle, no entanto, podem ser agravados especialmente quando os animais são reexpostos à DH Abstract: Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnancy and young population. Many effects from direct consumption of a high-fat diet (HFD) on glucose and lipid metabolism are well established. However, it is important to assess whether maternal consumption of HFD during critical periods of development can trigger epigenetic mechanisms, perpetuating changes in offspring metabolism and creating a vicious circle that cannot be broken. This study evaluated the potential effect of metabolic programming in impairing the insulin signaling in recently weaned offspring of obese dams. In addition, we investigated if early exposure to obesogenic environment is able to exacerbate the impairment of glucose metabolism in adult life in response to a high-fat diet. For this, Swiss female mice were fed with Stardard chow (SC) or HFD before and during mating, gestation and lactation. Tissues from male offspring were obtained at d28 and d82 to analyze activation of key proteins of inflammatory and insulin signaling pathways by Western Blot. Offspring of obese dams (HC-O) showed greater weight gain, adiposity and food intake than offspring of control dams (CC-O). Furthermore, they showed impairment in insulin signaling in central and peripheral tissues, associated to increased activation of inflammatory pathways. The HFD re-exposure seems to be an aggravating factor in development of obese phenotype leading to systemic insulin resistance and hyperleptinaemia. Moreover, adipose tissue was ultimately the most affected tissue in adult offspring after HFD rechallenged (HH-O) which may have contributed to the metabolic deregulation observed. Together our results suggest that maternal consumption of high-fat diet during pregnancy and lactation can cause changes in glucose metabolism of offspring in both weaned and adult animals. Additionally, maternal obesity leads to increase susceptibility to the development of obesity and impairment in insulin signaling in offspring that cannot be reversed by SC consumption, but can be aggravated especially when re-exposed to HFD Mestrado Metabolismo e Biologia Molecular Mestra em Ciências da Nutrição e do Esporte e Metabolismo

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Sarmento, Isabele Bringhenti. "Efeitos precoces da dieta materna hiperlipídica sobre o crescimento e fisiopatologia do pâncreas em camundongos." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9063.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Dieta materna hiperlipídica (HF) em roedores ocasiona o desenvolvimento de resistência à insulina e o diabetes mellitus tipo 2 na prole adulta. Camundongos fêmeas foram alimentadas com dieta SC (standard chow) ou HF (hiperlipídica) durante oito semanas anteriores ao acasalamento, durante o período gestacional e metade da lactação. Os filhotes machos foram avaliados ao nascimento (0 dia) e aos 10 dias de idade. Nas progenitoras, foram avaliados o ganho de massa corporal (MC), a pressão arterial (PA), a eficiência alimentar (EA) e o teste oral de tolerância à glicose (TOTG). Na prole, foram avaliadas a evolução da massa corporal (MC), a glicemia, a estrutura da ilhota do pâncreas e a massa de célula-beta. Nas progenitoras, a ganho de massa corporal (MC) e a eficiência alimentar (EA) do grupo HF apresentaram um aumento de 50% em relação ao grupo SC durante o período pré-gestacional e um aumento de 70% do ganho de MC e 250% na EA, durante a gestação (P<0,0001). A pressão arterial e os níveis de corticosterona foram maiores no grupo HF quando comparados ao grupo SC (P=0,001). Em relação à massa corporal das proles, não houve diferença ao nascimento, contudo aos 10 dias de idade o grupo HF apresentou um aumento neste parâmetro, assim como um aumento dos níveis de glicemia e aumento do diâmetro da ilhota em relação ao grupo SC (P<0,001). Ao nascimento, a razão da massa de célula-beta/massa do pâncreas (MCB/MP), foi menor no grupo HF quando comparado ao grupo SC (-54%, P<0,0001), no entanto essa diferença não foi observada aos 10 dias de idade. A MCB/MP foi maior no grupo HF aos 10 dias de idade em relação ao grupo SC (+146%, P<0,0001). Desta forma, sugere-se que a administração de dieta materna hiperlipídica durante o período pré-gestacional, durante a gestação e metade da lactação, culmina em alterações precoces no pâncreas da prole, incluindo um remodelamento e uma hipertrofia da célula-beta, a qual apresenta uma recuperação da massa de célula-beta ao final da organogênese, podendo desta forma afetar a sua função na vida adulta.

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Vianna, André Rodrigues da Cunha Barreto. "Ativação da via central anorexigênica pela Liraglutida (análogo do hormônio GLP-1) em modelo de obesidade induzida por dieta." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9431.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior No presente estudo, foram investigados o mecanismo central e a termogênese pelo tecido adiposo marrom (BAT) envolvidos com a perda de massa corporal (MC) observada com a administração de liraglutida (análoga do hormônio GLP1). Camundongos machos C57BL/6, foram alimentados com dieta padrão e tratados com veículo (SC) ou com liraglutida (SC/Lir) ou com dieta hiperlipídica e tratados com veículo (HF) ou com liraglutida (HF/Lir) Nossos resultados demostram que a administração de liraglutida aumentou o neuropeptídeo anorexigênico pro-opiomelanocortina no hipotálamo e diminuiu a expressão do mRNA da proteína supressora da sinalização de citocinas-3. A administração de liraglutida melhorou os níveis plasmáticos de adiponectina e diminuiu tanto a intolerância à glicose, como a resistência à insulina. Além do mais, tanto o grupo SC como o grupo HF, consumiram a mesma quantidade de comida, já o grupo SC/Lir comeu 17,5 menos comida comparado com o grupo SC e, da mesma forma, o grupo HF/lir diminuiu o consumo alimentar em 22,5% comparado com o grupo HF. A massa corporal final foi 8,5% menor no grupo SC/Lir comparado com o grupo SC e 16% menor no grupo HF comparado com o grupo HF/Lir. Além do mais, a administração de liraglutida aumentou o consumo de oxigênio e a produção de dióxido de carbono, e diminuiu o quociente respiratório. A liraglutida aumentou ainda os níveis do receptor beta 3 adrenérgico, da proteína desacopladora mitocondrial-1, do TC10 e do transportador de glicose estimulado pela insulina (GLUT)-4 no BAT. Em conclusão, a administração de liraglutida em camundongos obesos induzidos por dieta ativou a via anorexigênica, diminuindo o consumo alimentar, atuando sinergicamente com o aumento do gasto energético.

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Bedê, Teresa Palmisciano. "Efeito do consumo de bebidas ricas em polifenóis sobre a função e integridade do tecido hepático de ratos alimentados com dieta hiperlipídica." Niterói, 2017. https://app.uff.br/riuff/handle/1/3165.

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Submitted by Biblioteca da Faculdade de Farmácia (bff@ndc.uff.br) on 2017-03-28T17:01:20Z No. of bitstreams: 1 Bedê, Teresa Palmisciano [Dissertação, 2015].pdf: 1365884 bytes, checksum: 2fb9e05630c2ebc5ce56e4099bbd7366 (MD5) Made available in DSpace on 2017-03-28T17:01:20Z (GMT). No. of bitstreams: 1 Bedê, Teresa Palmisciano [Dissertação, 2015].pdf: 1365884 bytes, checksum: 2fb9e05630c2ebc5ce56e4099bbd7366 (MD5) Introdução: A busca da população por melhor qualidade de vida contribui para os estudos acerca de alimentos com propriedades funcionais e de prevenção de doenças. Destacam-se o suco de uva tinto integral (SUTI) e o vinho tinto (VT) que, ricos em polifenóis, vem demonstrando potente ação antioxidante e antinflamatória. Objetivo: Avaliar os efeitos do consumo de SUTI, de VT e de solução de resveratrol (SR) sobre a função e integridade hepática de ratos alimentados com dieta hiperlipídica. Materiais e Métodos: Foi realizado ensaio biológico com 50 Rattus Novergicus Wistar Albino, fêmeas adultas, divididas em 5 grupos: controle (GC)- ração caseína + água; hiperlipídico (GH)- ração hiperlipídica + água; vinho tinto (GV)- ração hiperlipídica + 10mL/dia de VT; suco de uva (GS)- ração hiperlipídica + 15mL/dia de SUTI e, resveratrol (GR)- ração hiperlipidica + 15mL/dia de SR. Durante 60 dias, ração e água foram ofertados em livre demanda e o peso corporal, o consumo alimentar e a pressão arterial foram verificados e registrados. Ao final do estudo, os animais foram sacrificados, amostras de sangue foram coletadas para análises bioquímicas e o fígado foi retirado para avaliações histológicas. Para comparação das médias entre grupos foi utilizado Anova one-way e Tukey como pós-teste, considerando um nível de significância de 5%. Resultados: A concentração de polifenóis totais (mg EAG -1) e de trans-resveratrol (mg/L) foi menor (p<0,05) no SUTI do que nas demais bebidas, mas a capacidade antioxidante não diferiu entre elas. Não houve diferença no peso corporal e no consumo alimentar dos grupos. A pressão arterial sistólica (mmHg) foi menor (p<0,05) no GS e GC. O GH apresentou maior (p<0,05) variação de glicemia (mg/dL) e o GR foi o único que apresentou diminuição de glicemia ao longo do estudo. A concentração (mg/dL) de colesterol total foi menor (p<0,05) no GS do que no GC, mas não houve diferença na concentração (mg/dL) de lipoproteína de alta densidade – HDL e, a concentração (mg/dL) de triglicerídeos foi maior (p<0,05) no GC. Não houve diferença na concentração (U/L) de aspartatotransaminase, mas o GS foi o único que apresentou-se dentro do intervalo de normalidade. Todos tiveram concentração (U/L) de alaninatransaminase acima do recomendado, mas o GS apresentou concentração numericamente menor e, a concentração de fosfatase alcalina (U/L) do GR foi menor (p<0,05) do que o GH e GV. A concentração de interleucina 6 (pg/mL) foi menor (p<0,05) no GS do que no GV. O peso do fígado (g/100gPC) foi semelhante entre os grupos, mas a concentração de gordura hepática (g%) foi menor (p<0,05) no GS e GC, e o teor de proteínas no fígado (g%) do GS foi menor (p<0,05) do que no GV e GR. A área dos núcleos dos hepatócitos (μm²) foi menor (p<0,05) no GC do que no GH, GV e GS, mas o IOD mostrou-se menor (p<0,05) no grupo GC, seguido pelo GS e maior no GH e GV. Conclusões: O consumo de SUTI parece ser capaz de minimizar os efeitos da dieta hiperlipídica sobre o tecido hepático. Mesmo diante do menor teor de polifenóis, o SUTI pode ter conferido proteção sobre certos parâmetros bioquímicos avaliados, assim como sobre o desenvolvimento de hipertensão arterial e da doença hepática gordurosa não alcoólica, o que não foi observado com o VT e a SR Introduction: The search for people for better quality of life contributes to the studies of food with properties functional and disease prevention. Stand out from the full red grape juice (JG) and red wine (RW) that are rich in polyphenols, has demonstrated potent antioxidant action and antinflammatory. Objective: To evaluate the effects of consumption of JG, RW and resveratrol solution (SR) on liver function and integrity of mice fed high-fat diet. Materials and Methods: This was a biological assay with 50 Rattus Novergicus Wistar Albino adult females divided into 5 groups: control (GC) - casein diet + water; hyperlipidic (GH) - fat diet + water; red wine (GW) - fat diet + 10 mL of RW / day; juice (GJ) - fat diet + 15mL of JG / day and resveratrol (GR) - fat diet + 15 mL of SR / day. During 60 days, feed and water were offered on free demand and, body weight, food intake and blood pressure were checked and recorded. At the end of the study, the animals were sacrificed, blood samples were collected for biochemical analysis and the liver was removed for histological evaluation. To compare the means between groups we used one-way ANOVA and Tukey as post-test, considering a 5% significance level. Results: The concentration of total polyphenols (mg EAG -1) and trans-resveratrol (mg/ L) was lower (p<0.05) in JG than the other drinks, but the antioxidant capacity did not differ between them. There was no difference in body weight and food consumption groups. Systolic blood pressure (mmHg) was lower (p<0.05) in the GJ and GC. GH had higher (p<0.05) blood glucose change (mg/ dL), and GR is the only one that decreases in blood glucose throughout the study. Concentration (mg / dL) of total cholesterol was lower (p<0.05) in GJ than in the GC, but there was no difference in the concentration (mg/ dL) of high-density lipoprotein - HDL and the concentration (mg/ dL) triglyceride was higher (p<0.05) in GC. There was no difference in the concentration (U/L) aspartatotransaminase, but the GJ was the one who introduced himself within normal range. All had concentration (U/L) alaninatransaminase above recommended, but the GJ presented numerically lowest concentration, and the concentration of alkaline phosphatase (U/L) of GR was smaller (p<0.05) than GH and GW. The concentration of interleukin-6 (pg/mL) was lower (p<0.05) in GJ than in the GW. Liver weight (g /100g body weight) was similar between the groups, but the concentration of liver fat (g%) was lower (p<0.05) in the GJ and GC, and the protein content in the liver (g%) GJ was lower (p <0.05) than the GW and GR. The area of the nuclei of hepatocytes (μm²) was lower (p<0.05) in the GC than in the GH, GW and GJ, but the IOD was lower (p <0.05) in the GC, followed by GJ and higher in GH and GW. Conclusions: Consumption of JG seems to be able to minimize the effects of high fat diet on liver tissue. Even with the lower polyphenol content, the JG may have conferred protection on certain biochemical parameters, as well as on the development of hypertension and non-alcoholic fatty liver disease, which was not observed with RW and SR

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Gilmer, Cori, and Allan Forsman. "The Effects of a High Fat/High Sugar Diet on the Myometrium." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/1.

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This study comprises the ramifications of a diet high in fat and sugar contents that manifest in the uterus. What a clinical setting deems excessive is unfortunately a societal norm in terms of diet. For this reason, it is of a critical nature to investigate the consequences of diets high in sugar and fat contents for the sake of women’s health. Our hypothesis is that consumption of excessive amounts of fat and sugar will have detrimental effects on the muscle layers of the uterus, the myometrium. Since much of the research concerning uterine tissue behavior involves aspects such as pregnancy and fertility assays, this study does not include such facets. The uterine horns of nine high sugar/high fat diet fed mice were collected and transversely sectioned in order to measure the thickness of each uterine layer. At the time of this submission measurements were still being taken and statistical analyses has not yet been completed.

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Riggs, Amy Jo Gropper Sareen Annora Stepnick. "Changes in energy expenditure associated with injestion of high protein, high fat versus high protein, low fat meals among underweight, normal weight, and overweight females." Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Spring/doctoral/RIGGS_AMY_28.pdf.

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Koutsari, Christina. "High-carbohydrate diets, exercise and postprandial lipaemia." Thesis, Loughborough University, 2000. https://dspace.lboro.ac.uk/2134/35001.

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Low-fat, high-carbohydrate diets are recommended by various scientific bodies for the prevention of coronary heart disease. However, these diets increase postprandial lipaemia and so their net benefit for coronary heart disease risk has been the subject of vigorous debate. Exaggerated postprandial lipaemia has been implicated in the development of atherosclerosis. Previous research suggests that physical exercise improves triacylglycerol metabolic capacity. The present thesis investigated whether exercise, when simultaneously adopted with a high-carbohydrate diet, could prevent the augmentation of postprandial lipaemia observed with this dietary change.

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Oliveira, Liliane Soares Corrêa de. "Dieta rica em sacarose: perfil inflamatório e danos hepáticos em camundongos." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6922.

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Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro Ainda não está bem definido na literatura se uma dieta rica em sacarose, mesmo sendo isoenergética, provoca danos à saúde. Camundongos C57BL/6 foram alimentados com uma dieta controle (10% da energia proveniente de gordura, 8% da energia proveniente da sacarose - SC), uma dieta rica em sacarose (10% de energia proveniente da gordura, 32% da energia proveniente da sacarose - HSu), uma dieta hiperlipídica (42% da energia proveniente de gordura, 8% da energia proveniente da sacarose - HF) ou uma dieta combinada HF/HSu (42% da energia proveniente de gordura, 32% da energia proveniente da sacarose), durante oito semanas. Apesar da massa corporal e do índice de adiposidade não terem sofrido alteração, o grupo HSu apresentou hipertrofia dos adipócitos, o que também foi observado nos grupos HF e HF/HSu. Os grupos HF, HSu e HF/HSu foram intolerantes à glicose e apresentaram níveis séricos de insulina elevados. Os níveis séricos de leptina, resistina e proteína quimiotática de monócitos-1 (MCP-1) aumentaram, enquanto adiponectina sérica reduziu nos grupos HF, HSu e HF/HSu. No tecido adiposo, os animais HF, HSu e HF/HSu apresentaram maiores níveis de expressão protéica de leptina e níveis mais baixos de expressão protéica de adiponectina, em comparação ao grupo SC. Colesterol hepático foi maior nos grupos HF e HF/HSu, enquanto TG hepático foi maior nos grupos HSu e HF/HSu. Os animais dos grupos HF, HSu e HF/HSu apresentaram esteatose hepática, aumento da expressão protéica hepática de elemento regulador de esterol ligante da proteína 1 (SREBP-1c) e diminuição da expressão protéica do receptor ativador de proliferação peroxissomal alfa (PPAR-α). Em conclusão, a dieta rica em sacarose não provoca obesidade nos animais, mas provoca alterações nos adipócitos (hipertrofia), intolerância à glicose, hiperinsulinemia, hiperlipidemia, esteatose hepática e aumento de citocinas inflamatórias. Os efeitos prejudiciais da dieta rica em sacarose, mesmo quando a sacarose substitui isocaloricamente o amido na alimentação, pode ter consequências para a saúde. It is still unclear if an isoenergetic, sucrose-rich diet leads to health conse-quences. Mice were fed a control diet (10% energy from fat, 8% energy from sucrose - SC), a high-sucrose diet (10% energy from fat, 32% energy from sucrose - HSu), a high-fat diet (42% energy from fat, 8% energy from sucrose - HF) or a HF/HSu diet (42% energy from fat, 32% energy from sucrose) for eight weeks. Despite the un-changed body mass and adiposity indices, HSu presented adipocyte hypertrophy, which was also observed in the HF and HF/HSu. The HF, HSu and HF/HSu were glucose intolerant and had elevated serum insulin levels. The levels of leptin, resistin and Monocyte Chemotactic Protein-1 (MCP-1) increased, while the serum adiponectin decreased in the HF, HSu and HF/HSu. In the adipose tissue, the HF, HSu and HF/HSu showed higher levels of leptin protein expression and lower levels of adiponectin protein expression in comparison with the SC. Hepatic cholesterol was higher in the HF and HF/HSu, while hepatic TG was higher in the HSu and HF/HSu. Liver steatosis was higher, sterol regulatory element-binding protein-1c (SREBP-1c) hepatic expression was increased, and peroxisome proliferator-activated receptor-alpha (PPAR-α) hepatic protein expression was decreased in the HF, HSu and HF/HSu in comparison with the SC. In conclusion, a sucrose-rich diet does not lead to a state of obesity but has the potential to cause changes in the adipocytes (hypertrophy) as well as glucose intolerance, hyperinsulinemia, hyperlipidemia, hepatic steatosis, and increases in the number of inflammatory cytokines. The deleterious effects of a sucrose-rich diet in an animal model, even when the sucrose replaces starch isocalorically in the feed, can have far-reaching consequences for health.

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Toma, Kumika. "Effects of High-Carbohydrate and Low-Fat Versus High-Protein and Low-Carbohydrate Diets on High-Intensity Aerobic Exercise." View abstract, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3372362.

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Hayes, Jasmine Marie. "Skeletal Muscle Adaption to 5 days of High-Fat Feeding in Humans." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/85059.

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Skeletal muscle is highly involved in macronutrient metabolism. To maintain proper energy metabolism and physiology, skeletal muscle must adapt to nutrient supply. Thus, diet macronutrient composition is an important modulator of skeletal muscle metabolism. Evidence from rodent and human models show high-fat diets contribute to impaired insulin signaling, as well as decreased fatty acid and glucose oxidation. Utilizing proteomic analysis of metabolic proteins in humans may lead to the mechanism behind skeletal muscle adaption to macronutrient composition, potentially providing the groundwork for characterizing the etiology of high-fat feeding induced metabolic disease. The objective of this study was to compare the substrate oxidation patterns and the levels of metabolic proteins in the fasted skeletal muscle of lean, healthy males that either increased fatty acid oxidation in response to the high-fat diet, termed responders, or males that decreased fatty acid oxidation, termed non-responders. We employed a controlled feeding study design, where the participants served as their own controls. Following a 2-week control diet (30% fat, 55% carbohydrate and 15% protein), participants came to the lab fasted overnight and a muscle biopsy was taken from their vastus lateralis muscle. Participants were then placed on a 5-day high-fat diet (50% fat [45% saturated fat], 35% carbohydrate, and 15% protein). Following this diet, participants again came to the lab fasted overnight and another muscle biopsy was taken from their vastus lateralis muscle. Both the control and the high-fat diets were isocaloric to habitual diets. Muscle from the biopsies were utilized for substrate metabolism measures and mass spectrometry. We did not observe any significant differences in glucose oxidation between responders and non-responders, prior to or following the high-fat diet. Our proteomic analysis identified 81 proteins and protein subunits involved in substrate metabolism but only 6 were differentially regulated by the high-fat diet. Independent of the high-fat diet, compared to non-responders, responders contained an overall higher content of protein subunits belonging to Complex I and ATP synthase. The findings from this study suggest that adaption to high-fat feeding is individual specific and proteomic changes alone cannot explain high-fat feeding induced metabolic changes. Ph. D.

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Oliveira, Rafaela Benatti 1989. "Avaliação da expressão hepática de microRNAs relacionados ao metabolismo lipídico na prole de camundongos com obesidade induzida por dieta." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/244470.

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Orientador: Adriana Souza Torsoni Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas Made available in DSpace on 2018-08-24T18:35:57Z (GMT). No. of bitstreams: 1 Oliveira_RafaelaBenatti_M.pdf: 1191668 bytes, checksum: 30188f35804e6016d9ee2cffa54ee9d5 (MD5) Previous issue date: 2013 Resumo: O consumo materno de uma dieta rica em gordura (HFD) durante a gestação e lactação está intimamente relacionada ao acúmulo de lipídios no fígado, a resistência à insulina e ao aumento de citocinas no soro, na prole jovem e na idade adulta. MicroRNAs (miRNAs) têm sido relacionados com a biossíntese do colesterol e no metabolismo dos ácidos graxos. Nós avaliamos a modulação da síntese hepática de ácidos graxos (de novo), as vias da beta-oxidação e a expressão dos microRNAs miR-122 e miR -370 em prole recém desmamados (d28) de mães alimentadas com HFD (grupo HFD-O) ou ração padrão (grupo SC-O) durante a gestação e lactação. Comparado com os camundongos SC-O, os camundongos HFD-O apresentaram um maior peso corpóreo, maior massa de tecido adiposo e eram intolerantes à glicose e insulina. HFD-O camundongos também apresentaram níveis séricos elevados de colesterol, triglicérides, ácidos graxos não esterificados e maior fosforilação hepática de IKK e JNK em comparação com camundongos SC-O. Os níveis das proteínas FAS, ACC e HMGCR foram semelhantes entre os camundongos HFD-O e SC-O, enquanto os níveis de RNAm e proteína da SCD1 foram mais abundantes nos camundongos HFD-O comparados com camundongos SC-O. Curiosamente, a expressão de RNAm de genes relacionados com a ?-oxidação, como a ACADVL CPT1 estavam diminuídos em camundongos HFD-O. Embora não observamos uma diferença nos níveis de HNF4? hepáticas, a expressão de miR -122 estava diminuída, e a expressão de miR-370 estava aumentada em HFD-O em comparação com camundongos SC-O. Alterações no metabolismo lipídico hepático foram acompanhados pelo aumento da deposição de triglicerídes em camundongos HFD-O. Em conjunto, os nossos resultados sugerem fortemente que o consumo materno de HFD afeta precocemente o metabolismo lipídico da prole de camundongos através da modulação da expressão de genes e miRNAs relacionados com a ?-oxidação hepática e que podem contribuir para as alterações metabólicas na vida adulta Abstract: Maternal consumption of high-fat diet (HFD) during pregnancy and lactation is closely related to liver lipid accumulation, insulin resistance, and increased serum cytokines in offspring and into adulthood. MicroRNAs (miRNAs) have been implicated in cholesterol biosynthesis and fatty acid metabolism. We evaluated the modulation of hepatic fatty acid synthesis (de novo), beta-oxidation pathways and miR-122 and miR-370 expression in recently weaned offspring (d28) of mice dams fed HFD (group HFD-O) or standard chow (group SC-O) during pregnancy and lactation. Compared with SC-O mice, HFD-O mice weighed more, had a larger adipose tissue mass and were more intolerant to glucose and insulin. HFD-O mice also presented more serum cholesterol, triglycerides, non-esterified fatty acids and hepatic IKK and JNK phosphorylation compared with SC-O mice. Protein levels of FAS, ACC and HMGCR were similar in HFD-O and SC-O mice, whereas SCD1 mRNA and protein were more abundant in HFD-O mice compared with SC-O mice. Interestingly, mRNA expression of ?-oxidation-related genes ACADVL and CPT1 was decreased in HFD-O mice. Although we did not observe a difference in hepatic HNF4? levels, the expression of miR-122 was reduced but that of miR-370 was increased in HFD-O mice compared with that in SC-O mice. Changes in hepatic lipid metabolism were accompanied by increased triglyceride deposition in HFD-O mice. Taken together, our results strongly suggest that maternal consumption of HFD affects the early lipid metabolism of offspring by modulating the expression of hepatic ?-oxidation-related genes and miRNAs that can contribute to metabolic disturbances in adult life Mestrado Metabolismo e Biologia Molecular Mestra em Ciências da Nutrição e do Esporte e Metabolismo

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Freitas, Marcelo Conrado [UNESP]. "Efeitos do treinamento resistido e do destreinamento na inflamação e expressão de genes do metabolismo muscular e tecido adiposo de ratos alimentados por dieta hiperlipídica." Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/136325.

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Submitted by MARCELO CONRADO DE FREITAS null (marceloconrado013@gmail.com) on 2016-03-18T12:57:04Z No. of bitstreams: 1 Tese final MCF.pdf: 1468918 bytes, checksum: 06f97c742fe0f27fb15e0ed7d61c7c09 (MD5) Approved for entry into archive by Ana Paula Grisoto (grisotoana@reitoria.unesp.br) on 2016-03-21T19:12:17Z (GMT) No. of bitstreams: 1 freitas_mc_me_prud.pdf: 1468918 bytes, checksum: 06f97c742fe0f27fb15e0ed7d61c7c09 (MD5) Made available in DSpace on 2016-03-21T19:12:17Z (GMT). No. of bitstreams: 1 freitas_mc_me_prud.pdf: 1468918 bytes, checksum: 06f97c742fe0f27fb15e0ed7d61c7c09 (MD5) Previous issue date: 2016-02-16 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) A ingestão de dieta hiperlipídica pode afetar negativamente o metabolismo celular de diversos tecidos podendo desencadear aumento da inflamação e resistência à insulina no tecido adiposo (TA) e músculo esquelético (ME). A realização do treinamento resistido (TR) pode resultar em adaptações importantes para indivíduos com alterações metabólicas. No entanto, ainda há poucos relatos na literatura sobre os efeitos crônicos do TR na inflamação e expressão de genes envolvidos no metabolismo do TA e ME. Também é pouco conhecido se a cessação do TR poderia causar reversão ou piora dos prováveis beneficios dos efeitos do TR sobre estes parâmetros. Objetivos: Analisar o efeito do TR e do destreinamento de 4 semanas sobre a inflamação e padrão de expressão de genes do metabolismo muscular e do tecido adiposo de ratos alimentados por dieta hiperlipídica. Métodos: Trinta ratos machos Wistar com idade de 2 meses foram subdivididos em três grupos, Dieta Hiperlipídica (DH), Dieta Hiperlipídica Treinado (DHT) e Dieta Hiperlipídica Destreinado (DHD). O treinamento resistido durou 12 semanas, sendo realizado numa plataforma de salto, 3x na semana, cada sessão com 3 séries de 12 repetições, com incremento de carga a cada duas semanas. O grupo DHD interrompeu o treinamento a partir da oitava até a décima segunda semana. Foi analisada a expressão da proteína TNFα, a expressão gênica de AMPK, GLUT-4 e MEF2A no músculo sóleo. Já no TA periepididimal foi analisada a expressão proteica de TNFα e PPARγ, e expressão gênica de TNFα, PPARγ, ACC e HIF-1α, utilizando as técnicas de RT-PCR e Western blotting. Resultados: o TR aumentou a expressão dos genes AMPK em 23%, GLUT-4 em 24% e MEF2A em 20% (p<0,05) e ainda reduziu a expressão proteica em 51% e gênica em 28% de TNFα no ME (p<0,05). Já no TA o grupo DHT apresentou menor expressão gênica de TNFα (40%), ACC (32%) e HIF-1α (31%) (p<0,05) comparado ao grupo DH. O grupo DHT também apresentou expressão proteica de TNFα 40% menor e apresentou aumento de 49% na expressão proteica de PPARγ (p<0,05) comparado ao grupo DH. Com o destreinamento a expressão de TNFα permaneceu reduzida tanto no músculo esquelético como no TA (p<0,05). Além disso, a expressão proteica de PPARγ no TA também permaneceu aumentada (p<0,05). Conclusão: O TR exerce efeitos positivos na redução da inflamação e melhora na expressão de genes relacionados ao metabolismo celular do ME e TA, com manutenção , destas adaptações mesmo após quatro semanas de destreinamento. High fat diet can adversely affect cellular metabolism of various tissues and trigger increased inflammation and insulin resistance in adipose tissue (AT) and skeletal muscle (SM). The resistive training (RT) may result in positive adaptations for individuals with metabolic disorders. However, there are few reports in the literature showing chronic effects of TR on the inflammation and expression of genes involved in the metabolism of the AT and SM. It is also unknown if the cessation of the resistive training could reverse or could impair the likely benefits of the RT on these gene expression. Objectives: To analyze the effect of TR and 4-week detraining on the inflammation and metabolism gene expression of the SM and AT from rats fed with high fat diet. Methods: Thirty male Wistar rats aged 2 months were divided into three groups, high fat diet (HD), High Fat Diet Trained (DHT) and Detrained High Fat Diet (DHD). Resistive training was performed during 12 weeks, in a jump platform, 3x a week, each session with 3 sets of 12 reps, with load increasing every two weeks. The DHD group interrupted the training from the eighth week until the twelfth week. TNFα protein expression and AMPK, GLUT4 and MEF2A gene expression was evaluated in the soleus muscle. In the periepididymal adipose tissue, PPARγ and TNFα protein expression was evaluated of, as well as TNFα, PPARγ,HIF-1α and ACC gene expression by RT-PCR and Western blotting. of. Results: RT increased the expression of AMPK gene in 23%, GLUT-4 in 24% and MEF2A by 20% (p<0.05), and reduced TNFα protein expression in 51% and 28% in the SM (p<0.05). In the AT, DHT group presented lower (p <0.05) TNFα of (40%), ACC (32%) and HIF-1α (31%) gene expression compared to DH group. DHT group also showed 40% less TNFα protein expression and presented an increase of 49% in the PPARγ protein expression (p<0.05) compared to DH group. With the detraining TNFα expression remained reduced in both SM and AT (p<0.05). Furthermore, the expression of PPARγ protein also remained increased in AT (p<0.05). Conclusion: RT has positive effects in reducing inflammation and improvement in the expression of genes related to cellular metabolism in the SM and AT, which can be maintained even after 4 weeks of the cessation.

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22

Silva, Cynthia Carneiro Soares da. "Dieta hiperlipídica compromete a morfologia e alguns parâmetros funcionais de testículo e tireóide de ratos jovens." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=8299.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Estudos demonstram que o sobrepeso e a obesidade podem afetar a fertilidade masculina. Além disso, a função tireóidea também esta associada à alteração da função testicular, entretanto, o papel fisiológico dos hormônios tireoideanos na regulação do sistema reprodutor masculino ainda não esta claro. Aos 21 dias de idade, ratos machos receberam uma dieta manipulada contendo diferentes concentrações de óleo de soja até a idade de 30 e 60 dias, os grupos controle (C30, n=6 e C60, n=6), receberam dieta contendo 7% e os grupos hiperlipídicos (HL30, n=6 e HL60, n=6), receberam dieta contendo 19% deste óleo. Ao final de cada período, os animais foram avaliados por DXA (Absorciometria de Raios-x em Duas Energias) e sacrificados por exsanguinação. Para avaliar alterações na estrutura dos tecidos testicular e tireóideo, foram realizados a morfologia e a estereologia. No plasma, para determinar os perfis bioquímico e hormonal, foram avaliados, triglicerídeos, colesterol total, HDL-colesterol, VLDL, glicose e albumina, por métodos colorimétricos e leptina, insulina, T4, T3, TSH e testosterona por radioimunoensaio (RIE). Para evidenciar a expressão de receptor androgênico (AR) em testículos, foi realizado imunomarcação, com anti-AR. Durante todo o período experimental, foram analisados a massa corporal, a ingestão alimentar e o comprimento corporal, os quais permaneceram inalterados. No grupo HL, a massa magra foi menor aos 30 dias, já a gordura corporal total foi maior no mesmo grupo, aos 60 dias nenhuma diferença foi notada entre os grupos. No grupo HL30 não houve diferença quanto à massa dos tecidos, já no grupo HL60, o peso do epidídimo, fígado e gordura visceral mantiveram-se aumentados. No grupo HL30 não houve diferença em relação ao perfil bioquímico, já no grupo HL60, os níveis de glicose, mantiveram-se altos. Quanto às dosagens hormonais no grupo HL30, TSH e leptina estiveram aumentados e T3 reduzido, e no grupo HL60, T3 e leptina estiveram aumentados. Os dados morfométricos e estereológicos de testículo no grupo HL30 mostram aumento no número de túbulos seminíferos e da densidade de comprimento (Lv), já no grupo HL60, há redução no número de túbulos seminíferos e no diâmetro do mesmo. Quanto à expressão de receptor androgênico nas células testiculares, não parece haver diferença entre os grupos independente da idade de consumo da dieta. A dieta hiperlipídica promoveu alterações metabólicas aos 30 dias e modificações na morfologia do tecido tireoidiano e testicular em ambas as idades, o que indica reflexos na função reprodutora. Studies show that overweight and obesity can affect male fertility. In addition, thyroid function also is associated with the alteration of testicular function, however, the physiological role of thyroid hormones in the regulation of male reproductive system is not yet clear. At 21 days of age, male rats were handled diet containing different concentrations of soy oil until the age of 30 and 60 days, the control group (C30 n=6 , C60 n=6), received a diet containing 7% and the high fat groups (HL30 n=6 , HL60n=6), received diet containing 19 % of this oil. At the end of each period, the animals were assessed by DXA (Absorptiometry X - ray Dual energy) and sacrificed by exsanguination. To assess changes in the structure of the testis and thyroid tissue morphology and stereological were performed. In plasma for determine the hormonal e biochemist profile were evaluated, triglycerides, total cholesterol, HDL cholesterol, VLDL, glucose and albumin by colorimetric assay and leptin, insulin, T4 , T3 , TSH and testosterone by radioimunoassay (RIA) . To demonstrate the expression of androgen receptor (AR) in testis, imunohistochemistry was performed with anti-AR. During the experimental period, body weight, food intake and body length were analyzed, and remained unchanged. Lean mass was lower at 30 days in the HL group, since the body fat total was higher in the same group, after 60 days, no difference was noted between the groups. In HL group at 30 days no difference was noted, and in same group at 60 days, the weight of the epididymis, liver and visceral fat remained higher. The biochemist profile in HL group at 30 days, there are no differences and at the 60 days in same group the level of glucose remained high. For hormonal dosages at 30 days in HL group, TSH and leptin were increased and T3 reduced, at 60 days in the same group, T3 and leptin were increased. Stereological and morphometric in the group Hl at 30 days, data show increases of number of seminiferous tubule and length density (Lv). At 60 days in the same group there are decreased of number of seminiferous tubule and diameter. The expression of androgen receptor (AR), in testis no differences are seems between the groups independent of the ages of consumption of diet. The fat diet promoted metabolic changes at 30 days and changes in the morphology of thyroid and testicular tissue at both ages, indicating an influence on reproductive function.

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23

Chandrruangphen, Pornpat. "The effects of high-fat diet & exercise on vascularendothelial function." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506769.

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Atherosclerotic cardiovascular diseases remain the most common causes of death in the developed world. Vascular endothelial dysfunction is considered to be central to, and the precursor of, atherosclerosis and subsequent clinical syndromes. Brachial artery reactivity using high-resolution ultrasound is the most commonly used method for non-invasive endothelial function assessment. With this method, endothelial function has been shown to be impaired by postprandial lipaemia (PPL) and improved by exercise. This thesis comprises of three studies that examined the relationship between EDV and PPL, as well as exercise, in a variety of subjects. FMD as measured during BAR testing was used to represent EDV in all studies. The first study examined the EDV response to PPL in 20 male CHD patients. There was no overall change in FMD following both meal challenge and no significant difference in the postprandial FMD between the two meals. The second study examined the effect of very short-term prior moderate-intensity exercise on EDV response to PPL in healthy male subjects. The study demonstrated a highly significant improvement in FMD during PPL in sedentary subjects when they had undertaken prior exercise. The third study examined the effect of six weeks of moderate-intensity exercise on EDV response to PPL in he'althy postmenopausal women. The study showed that FMD during PPL was significantly better when the subjects had been exercising. In these two studies, the protective effect of exercise on endothelial function appeared to be an independent and direct one. These studies add to the accumulating body of evidence that postprandial lipid metabolism is relevant to the development of atherosclerosis through its potentially adverse influence on endothelial function. They also contribute novel insights into the potential protective effect of exercise in this pro-atherogenic setting - an area that clearly deserves further research.

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24

McLean, Fiona Hamilton. "The impact of a high-fat diet on memory in mice." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=231763.

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Obesity and type II diabetes are associated with dementia and Alzheimer's disease. A high-fat diet induces memory deficits in rodents, however, complex episodic-like memory, has not been tested. Episodic memory is the recollection of events using a “what-where-when/which” experience and is the first memory to be compromised in Alzheimer's disease. To identify a link between a high-fat diet and episodic memory, 12 week old, male, C57Bl/6 mice, were fed a semi purified high-fat or low-fat diet ad libitum and tested with object-place-context (episodic-like), novel object recognition, object-place (spatial) and object-context (contextual) memory tasks for up to 2 weeks. A separate group of animals were fed a high-fat diet for 1 week followed by a low-fat diet for 1 week. Animals were killed after 3 days, 1 week or 2 weeks on diet. Brains were kept frozen until the hippocampus was dissected and proteomics performed. Further studies were carried out in rat primary hippocampal cell cultures to investigate the impact of different fatty acids on neuronal dendritic morphology. We found that episodic-like memory is compromised after only one day of a high fat diet together with spatial and contextual tasks. The ability to carry out the novel object recognition test remained intact. Proteomic analysis of hippocampal tissue revealed changes in a number of proteins associated with metabolism, cell stress, cell signalling, inflammation and the cytoskeleton. High-fat diet induced changes were reversed by a low-fat diet. Hippocampal neuron cultures showed that long chain saturated fatty acid palmitic acid, a component of the high-fat diet used in the behavioural and proteomic studies, caused reduced dendritic arborisation whist n-3 polyunsaturated fat docosahexaenoic acid negated these effects. These data link high-fat diet to indices of hippocampal neuronal damage and memory deficits and have implications for the link between diet, obesity and cognitive decline.

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25

Masaki, Megumi. "Role of meltrin α (ADAM12) in high-fat diet induced obesity". Kyoto University, 2006. http://hdl.handle.net/2433/143843.

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26

Alemany, Adair Aparecida Santos. "Influência da dieta hipercolesterolêmica em camundongos knock-out LDLr -/- expostos as partículas ambientais concentradas sobre o sistema pulmonar." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-25092013-151131/.

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Introdução: Os dados epidemiológicos e experimentais têm mostrado efeitos adversos da exposição pré e pós natal ao material particulado (MP2,5) sobre a saúde fetal e adulto. Entretanto, poucos estudos abordaram a toxicidade fetal da exposição gestacional à poluição do ar ambiental, bem como efeitos a longo prazo de adversos da exposição pré-natal sobre o desenvolvimento pós-natal e maturação de vários sistemas de órgãos. Objetivos: O objetivo deste estudo foi determinar se a exposição pré-natal e / ou pós-natal ao material particulado, influencia o desenvolvimento pulmonar e resposta vascular pulmonar em um modelo de camundongo suscetível a aterosclerose (LDLr-/- camundongos knockout). Métodos: Camundongos LDLr-/- foram expostos durante a gestação ao ar filtrado (AF) ou ar poluído (AC). Após o período de desmame, os filhotes foram subdivididos e novos quatro grupos foram formados de acordo com a exposição gestacional ou a exposição pós natal contínua no ar poluído. Atingindo a idade de 3 meses, esses grupos foram novamente subdivididos, formando um total de 8 grupos e uma dieta hipercolesterolêmica foi introduzida. Os seguintes parâmetros foram analisados: desfechos gestacionais, dosagem de colesterol total (CT) e triglicerídeos (TG) do fígado, avaliação de citocinas no LBA, e avaliação imunohistoquímica da resposta vascular pulmonar . Resultados: Nos grupos que receberam dieta hipercolesterolêmica (DH) os níveis de colesterol apresentaram-se aumentados (p=0,002); A expressão da IL6 no LBA mostrou-se elevada (p=0,01) somente no grupo que não foi exposto a poluição em nunhum período da vida e recebeu dieta postnatalmente. Diferenças significativas também foram observadas na expressão pulmonar vascular dos seguintes imunomarcadores: endotelina (p=0,05); ENOS (p=0,04); IL1? (p=0,005); INOS (p=0,002); ISOP (p=0,001); NOX2 (0,01) e ICAM (0,04) quando comparados ao grupo controle. O volume pulmonar total também se mostra alterado em decorrência do tratamento. Assim, conclui-se que a resposta do desenvolvimento pulmonar à exposição gestacional à poluição particulada do ar pode ser evidenciada mais tarde durante a vida adulta e agir como um fator modulador de insultos pós-natal devido à exposição a poluição do ar e a uma dieta hipercolesterolemica em individuos predispostos aterosclerose Epidemiological and experimental data have shown adverse effects of gestational and post natal exposure to ambient particulate matter (PM) on the fetal and adult health. However, few studies addressed the fetal toxicity of gestational exposure to environmental air pollution as well as long-term adverse consequences of prenatal exposure on postnatal development and maturation of several organ systems. The aim of this study was to determine if prenatal and/or postnatal exposure to concentrated ambient particles influences lung development and pulmonary vascular response in an atherosclerosis susceptible mouse model (LDLr-/- knockout mice). LDLr-/- mice were exposed during the pregnancy to either filter (AF) or polluted air (CAP). After weaning period, pups were subdivided and new 4 groups formed according to gestational and continuous or not post natal exposure to air pollution. Reaching the age of 3 months these groups were again subdivided and a hypercholesterolemic (HC) diet introduced and a total of 8 groups were formed. Then the following parameters were analyzed: evaluation of the offspring outcomes, assessment of airway responsiveness, evaluation of cytokines in BALF, dosage of total cholesterol (TC) and triglycerides (TG) in the liver and pulmonary vascular response by immunohistochemistry. Results: Animals that received HC diet presented higher levels of cholesterol (p=0.002) when compared to those animals that received normal diet. Expression of IL-6 was only increased in the groups of mice exposed not exposed to particulate air pollution and that received the HC diet (p=0.01). Significant differences were also observed in vascular expression of immunomarkers in the lung endothelin (p=0.05); ENOS (p=0.04); IL1? (p=0.005); INOS (p=0.002); ISOP (p=0.001); NOX2 (0.01) e ICAM (0.04). Total lung volume was also different, there was an increase in those animals receiving a HC diet. In conclusion, the response of the lung development to gestational exposure to particulate air pollution can be evidenced later in life and act as a modulator factor for postnatal insults due to exposures to particulate air pollution and hypercholesterolemic diet in individual predisposed to atherosclerosis

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27

Maesako, Masato. "Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice". 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188709.

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Fundaro, Gabrielle F. "Do Probiotics Protect Against the Deleterious Effects of a High-Fat Diet?" Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/64333.

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High-fat diets and obesity have been linked to unfavorable changes in gut bacteria and increased leakage of bacterially-derived lipopolysaccharide (endotoxin) from the intestinal tract into circulation, which is associated with low-grade inflammation, metabolic dysregulation and degradation of tight-junction proteins between intestinal cells. Probiotic supplementation is the practice of ingesting live strains of bacteria that are proposed to have a beneficial effect on the host by enriching the intestine with healthy bacteria. The purpose of this project was to determine if probiotic supplementation would prevent increased inflammatory tone, decreased oxidative capacity, and decreased tight-junction protein expression associated with high-fat feeding and elevated endogenous endotoxin. Male C57BL/6J mice were fed either a control (CD, 10% fat) or high-fat (HFD, 60% fat) diet for 4 weeks while receiving a daily oral gavage of water (C-VSL#3, HF-VSL#3) or probiotics (C+VSL#3, HF+VSL#3) equivalent to 1.2 billion live cultures. Changes in body weight, body composition, respiratory exchange ratio, energy expenditure, and glucose and insulin tolerance were measured in live mice. Markers of metabolic function were measured in whole muscle homgenates and mitochondria isolated from red and white skeletal muscle. Plasma endotoxin was measured in blood collected from fasted mice at the time of euthanization. The large and small intestines were collected and mRNA levels of tight-junction proteins and markers of nutrient sensing were measured. To determine a possible protective effect against endogenous LPS, a second cohort of mice were given an intraperitoneal injection of 0.1µg/kg LPS or saline to induce endotoxemia after four weeks of the aforementioned feeding protocol. Markers of metabolic function and inflammation were measured in mitochondria, skeletal muscle and liver. VSL#3 supplementation improved glucose homeostasis and markers of inflammation while enhancing nutrient sensing in the gut. Ph. D.

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29

Habas, Elmukhtar M. A. "Antecedent diet effect on thermogenic and cardiovascular responses to different meals." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360545.

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30

von, Essen Gabriella. "Energy flow and metabolic efficiency attributed to brown adipose tissue." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-140190.

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The large capacity of brown adipose tissue (BAT) to expend energy as heat makes it an interesting potential player in weight regulation and other metabolic conditions. This is of particular interest as it has been recognized that adult humans possess BAT. The protein responsible for the heat production is uncoupling protein 1 (UCP1), which, as the name implies, uncouples the respiratory chain from ATP production; instead heat is produced. Cold is the strongest recruiter and activator of BAT. However, also obesogenic food has a low but nonetheless significant effect on the recruitment and activation of UCP1, although the significance of this has been discussed. In the present thesis, I have studied the effect of diet on BAT and the possibilities for it to be obesity-protective. This can be done by comparing responses in wild-type mice and in UCP1-ablated mice. Since the effect of diet on BAT is low, it is of importance to control the temperature and maintain thermoneutrality. Other confounding factors to keep in mind are differences in actual energy and composition of food and also cohort differences. When controlling all the parameters mentioned and giving the mice the same obesogenic diet, the mice possessing UCP1 compared to UCP1-ablated mice had higher energy expenditure, and lower weight gain, despite eating more. This confirms the presence of a UCP1-dependent diet-induced thermogenesis. Thus, the conclusion must be that possessing UCP1 does result in obesity protection at thermoneutrality. However, the relevance for human energy balance is still not established. At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 2: Manuscript. Paper 3: Manuscript.

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31

Maharjan, Babu Raja. "An Investigation of the Effect of Diet and Exercise on Adipose Tissue Function in Different Fat Depots." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17320.

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Obesity is a leading public health challenge worldwide. Personal interventions such as diet and/or exercise management are considered effective in terms of cost and feasibility to prevent/treat obesity. To effectively implement a diet or exercise intervention, it is necessary to understand the response of different adipose tissue depots to diet and exercise. In this thesis, we investigated the effect of high fat diet (HFD) and exercise on adipose tissue function compared to chow fed mice in the different fat depots. In the chow fed controls, with aging, there was a progressive increase in systemic insulin resistance which was more pronounced with the duration of HFD (45% fats). The metabolic deterioration with HFD was accompanied by the decrease in fat cell functions (adipogenesis, mitochondrial thermogenesis, extracellular matrix (ECM) remodeling and inflammation) in different fat depots of C57BL/6 mice. In the early stages of HFD, the increased adipogenesis, ECM remodeling in subcutaneous (SAT) and epididymal (EPI) fat coupled with the maintenance of thermogenic ability in SAT (beiging of white adipocytes) and brown fat enabled them to accommodate the excess fat. However, on prolonged HFD there was a decline in metabolic function which was accompanied by infiltration of macrophages and ECM accumulation that could restrict adipose tissue expansion and led to ectopic fat deposition. Both exercise programs Endurance exercise (END) and High Intensity Interval Training (HIIT) prevented the HFD induced deterioration in metabolic health by preventing body weight gain, reducing total body fat and liver weight, and increasing lean mass. Exercise also decreased adipogenesis, inflammation, ECM accumulation and preserved thermogenesis in SAT and EPI. Investigating the effect of TGFβ1 on 3T3L1 cells showed that different responses were seen depending on the stage of adipocyte maturation. Throughout adipocyte development, TGFβ1 consistently upregulated the markers for ECM remodeling. In both early and fully differentiated adipocytes, TGFβ1 inhibited adipogenic markers and upregulated the inflammatory marker genes. There was also a difference in the thermogenic marker genes with TGFβ1 increasing them in fully differentiated adipocyte and decreasing them early in the differentiation process of adipocytes.

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32

Misner, Scottie, Carol Curtis, and Evelyn Whitmer. "Fat and Cholesterol Update." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2006. http://hdl.handle.net/10150/146439.

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2 pp. Of all the nutrients in the food supply, fat and cholesterol probably receive the most attention from health professionals and the public alike. The scientific evidence is clear that a high-fat diet relates to chronic health problems such as heart disease, some types of cancer, diabetes, and obesity. But both fat and cholesterol are natural components of the body that are vital to good health, and too little fat in your diet is just as unhealthy as too much. This article reviews dietary fats and provides guidelines for choosing foods to balance the type and amount of fat in your diet.

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33

Senthil, Kumar Shiva Priya Dharshan. "Metabolic Effects of Short-Term High-Fat Diet Feeding in Male and Female Mice." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1389198918.

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34

Kavanaugh, John Wesley. "Skeletal Muscle Acetylation in Response to an Acute and Chronic High-Fat Diet." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/81138.

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The past thirty years have seen a dramatic rise in obesity worldwide owing to a change in dietary composition, quantity of food consumed- positive energy balance, and a more sedentary life style. Accompanied with obesity is a chronic low grade inflammatory state defined by increased circulating cytokines and an increase in gene expression promoting inflammation. Multiple health risks are associated with obesity such as cardiovascular disease, insulin resistance, and type II diabetes. Advances in mass spectrometry have made wide scale proteomic studies possible and are redefining cell and molecular biology. One such area of that has become of considerable interest is protein acetylation which is observed in most cellular processes such as cell cycle regulation, gene expression, subcellular localization, metabolism, muscle contraction, protein stability, apoptosis, and more. Metabolic proteins are highly susceptible to acetylation with almost all showing the capacity to be acetylated. Our research, using an obese mouse model fed a chronic high fat diet and a lean control mouse model fed a standard chow diet, showed numerous differences in the acetylome between obese and lean animals in a fasted state. As well as, differences in the acetylome's of both animal models upon receiving a high fat meal. We showed that almost every mitochondrially located metabolic protein in obese animals is hyper-acetylated in a fasted state compared to lean animals and that upon feeding lean animals have a greater response in the change to their metabolic acetylome. We show that in the fed state lean and obese mice have almost completely different acetylomic profiles of mitochondrial and glycolytic metabolic proteins. Furthermore, we have observed possible new regulatory mechanisms utilizing acetylation to 1) determine the fate of the co-factor NADH in glycolysis and 2) control an ATP producing reaction in glycolysis. Ph. D.

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35

Gaievski, Eduardo Henrique Szpak. "Avaliação do status de ferro em ratos alimentados com rações hiperlipídicas." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-01042014-151930/.

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A discussão sobre a efetividade da fortificação dos alimentos com ferro como estratégia para o controle e a redução do risco da anemia vem ganhando novo enfoque, a partir da associação, em estudos epidemiológicos, entre excesso de peso e deficiência de ferro. O conhecimento dos mecanismos de regulação da homeostase de Fe pode contribuir para o entendimento das alterações no status de ferro e sua relação com a adiposidade em indivíduos obesos e com sobrepeso. Neste trabalho, o status de ferro de ratos Wistar, machos e recém-desmamados, alimentados com rações hiperlipídicas foi estudado ao longo de 60 dias. Os animais receberam, ad libitum, rações normo e hiperlipídicas. Um grupo pair-feeding foi usado, que consumiu a mesma quantidade de ferro que o grupo hiperlipídico. Foi observada maior excreção de Iipídeos nas fezes dos animais do grupo HL, em todos os períodos avaliados. Observou-se associação positiva da adiposidade com o conteúdo de Fe no baço, após 15 dias, e com o conteúdo de Fe no fígado após 30 dias, demonstrando que esses tecidos são afetados de maneira diferente pelo consumo da ração hiperlipídica, ao longo do tempo. Após 60 dias, o consumo da ração hiperlipídica resultou em diminuição da sensibilidade à insulina e em aumento da gordura corporal. Nesse período, esses animais apresentaram maior excreção de ferro nas fezes do que os controles. Além disso, houve associação negativa e significativa do ferro sérico com a adiposidade, apesar de não terem sido observadas diferenças na concentração de hemoglobina entre os grupos. Como conclusão, o consumo das rações hiperlipídicas resultou em alterações na digestibilidade do Fe na ração e em redistribuição compartimental do mineral, o que sugere interações entre o ferro e os lipídeos no lúmen intestinal ou, ainda, um processo adaptativo à condição de estresse gerada pelo excesso de lipídeos da dieta. The discussion on the effectiveness of food fortification with iron as a strategy to control and reduce the risk of anemia is gaining new focus, from the association in epidemiological studies between overweight and iron deficiency. Knowledge on mechanisms of regulation of Fe homeostasis may contribute to the understanding of changes in iron status and its relationship with adiposity in obesity and overweight. In this study, the iron status of weanling male Wistar rats fed with high-fat diets was studied during 60 days. The animals received ad libitum normo-and high-fat diets. A pair-feeding group was used, which consumed the same amount of iron as the HF group. Lipid excretion was higher in feces of the HF group, in ali periods. A positive association between fat and spleen Fe content after 15 days, and the liver Fe content only after 30 days, demonstrate that these tissues are affected differently by the high-fat diet consumption over time. After 60 days, the consumption of high-fat diet resulted in decreased insulin sensitivity and increased fat mass. During this period, these animals had higher iron excretion in feces than controls. In addition, there was a significant negative association between serum iron and adiposity, although no differences were observed in hemoglobin concentration between groups. In conclusion, consumption of high-fat diets resulted in changes in the Fe digestibility and compartmental mineral redistribution, suggesting interactions between iron and lipids in the intestinal lumen, or even an adaptive process to the condition of stress generated by excess of dietary Iipids.

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36

Yamanaka, Jéssica Suzuki. "Efeitos da dieta hiperlipídica na estrutura e consolidação de tíbias de ratas em crescimento." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17142/tde-07062017-165223/.

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O acúmulo de gordura corporal é considerado um problema de saúde pública com diversas consequências negativas, inclusive relacionado à redução da qualidade do osso, que afeta cada vez mais indivíduos jovens. São crescentes as investigações que buscam esclarecer a relação entre massa gorda e massa óssea. Portanto, o objetivo deste estudo foi investigar o efeito do consumo excessivo de lipídios na estrutura e no processo de consolidação óssea em tíbias de ratas em crescimento. Foram utilizadas cinquenta e duas ratas Wistar com 21 dias de vida, distribuídas em quatro grupos (n=13), sendo: animais submetidos à dieta padrão (DP), animais submetidos à dieta hiperlipídica (DH), animais submetidos à dieta padrão e osteotomia (DPO) e animais submetidos à dieta hiperlipídica e osteotomia (DHO). Cada um deles com período experimental de 5 semanas. Os animais dos grupos DP e DH foram mantidos sem intervenção, enquanto os animais dos grupos DPO e DHO foram submetidos à osteotomia da tíbia esquerda na terceira semana experimental. Durante o experimento a massa corporal e o consumo de ração dos animais foram avaliados. Um dia precedente à eutanásia foi realizado o teste de tolerância à insulina em 5 animais de cada grupo. Após a eutanásia a tíbia esquerda de cada rata foi dissecada, limpa das partes moles e submetidas a análises macroscópica, densitometria, ensaio mecânico, histomorfometria, estereologia do osso neoformado e imunohistoquímica. Os dados foram analisados por teste estatístico em modelo linear geral com ajuste para múltiplas comparações de Bonferroni para comparação entre as variáveis, e teste T-Student e Mann-Whitney para comparação entre dois grupos. Ao final do experimento os animais alimentados com dieta hiperlipídica apresentaram massa corporal similar aos animais alimentados com dieta padrão (p=0,115), no entanto tiveram consumo reduzido de ração (p<0,001) e menor sensibilidade à insulina (p=0,018). A variável cirurgia afetou o consumo de ração sendo que animais operados consumiram menos ração do que animais não operados (p=0,017). Os animais alimentados com dieta hiperlipídica tiveram tíbias mais compridas (p=0,041), menor força máxima (p<0,001) e rigidez relativa (p=0,003) quando comparados aos animais alimentados com dieta padrão, embora a densidade mineral óssea (DMO) tenha sido similar (p=0,958). Os animais operados tiveram menor força máxima (p<0,001), rigidez (p=0,020) e menor quantidade de colágeno proximal (p=0,029) quando comparados aos não operados. O volume de osso neoformado das tíbias submetidas à osteotomia tendeu a ser menor no grupo DHO ao grupo DPO (p=0,054). A avaliação imunohistoquímica não revelou diferença entre os grupos DHO e DPO (p<0,05). Concluímos que a dieta hiperlipídica prejudicou a resistência mecânica das tíbias e causou uma redução do volume de osso neoformado, prejudicando dessa forma a estrutura e consolidação óssea das tíbias de ratas em crescimento The body fat accumulation have been considered a public health issue with several negative consequences, including reduction of bone quality, that affects young people increasingly. The studies that seek to clarify the relationship between fat mass and bone mass have been increasing. Therefore the aim of this study was to investigate the effect of high consumption of lipids on bone structure and bone healing in growing rats. Fifty-two female Wistar rats 21 days old were used, divided into four groups (n=13), as follows: animals treated with standard diet (SD), animals treated with high-fat diet (HFD), animals treated with standard diet and osteotomy (SDO) and animals treated with high-fat diet and osteotomy (HFDO). Experimental period was of 5 weeks for every groups. The SD and HFD animals were maintained without intervention, while SDO and HFDO groups were submitted to osteotomy in left tibia at third experimental week. Animal body mass and feed intake were assessed during experimental period. One day before euthanasia insulin tolerance test was performed in 5 animal of each group. After euthanasia, the left tibia of each rat was dissected and cleaned of soft tissues and submitted to macroscopy analysis, densitometry, mechanical analysis, histomorphometry, stereology of newly formed bone and immunohistochemistry. Data were analyzed by general linear model with adjustment to multiple comparisons of Bonferroni for comparisons between variables and TStudent e Mann-Whitney test for comparisons between two groups. At end of the experiment the high-fat diet fed animals had body mass similar to standard diet fed animals (p=0.115), however they had lower feed intake (p<0.001) and lower insulin sensibility (p=0.018). Surgery affected feed intake, operated animals had lower feed intake than non-operated animals (p=0.017). High-fat diet fed animals had longer tibias (p=0,041), lower maximal load (p<0.001) and lower stiffness (p=0,003) than standard diet fed animals, although bone mineral density (BMD) had been similar (p=0,958). Operated animals had lower maximal load (p<0.001), stiffness (p=0.020) and lower collagen quantity (p=0.029) than non-operated animals. Newly formed bone of tibias submitted to osteotomy trended to be lower in HFDO group than SDO group (p=0.054). Immunohistochemistry presented no difference between HFDO e SDO group (p<0.05). We concluded high-fat diet affected bone in order to harm tibia strength and caused a decrease in the newly formed bone volume, impairing structure and bone healing

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Júnior, António Ludgero Correia. "Efeitos da associação da ovariectomia com uma dieta hiperlipídica sobre alterações no metabolismo lipídico, remodelamento e redistribuição do tecido adiposo e sobre os marcadores inflamatórios em camundongas C57BL/6." Universidade do Estado do Rio de Janeiro, 2011. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2711.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico A menopausa está associada a algumas alterações metabólicas como a obesidade, dislipidemia e inflamação, entre outras anomalias presentes na síndrome metabólica humana. Uma dieta hiperlipídica ou high-fat (HF) associada à menopausa piora tais alterações, aumentando ainda mais o risco de doença cardiovascular. A hipótese de que uma dieta HF agrava as complicações relacionadas à ovariectomia foi testada. Foram avaliadas fêmeas C57BL/6 ovariectomizadas (OVX) ou com operação SHAM e alimentados com ração padrão ou Standard Chow (SC, 10% de gordura) ou uma dieta HF (60% de gordura) por 18 semanas. A eficiência alimentar (EA), massa corporal (MC), distribuição regional das massas de gordura e a morfometria dos adipócitos foram estudados. As análises de sangue (colesterol total, CT, triglicerídeos, TG, citocinas e adipocinas) foram realizadas. Camundongas OVX-HF apresentaram maior EA e maior MC do que os demais grupos (P<0,05). A gordura visceral (ovariana e retroperitoneal) e a gordura subcutânea (gordura inguinal) tiveram o mesmo padrão de distribuição entre os grupos SHAM-SC, SHAM-HF e OVX-SC, mas o grupo OVX-HF apresentou um padrão diferente de acúmulo de gordura - muito maior do que no rupo SHAM-SC. A associação da ovariectomia com a dieta HF aumentou significativamente o diâmetro dos adipócitos dos animais OVX-HF em comparação aos SHAM-HF (P<0,0001) e também agravou a elevação dos níveis de CT, TG e de leptina nas camundongas OVX-HF, em relação aos OVX-SC (P<0,0001). Os níveis de adiponectina foram maiores nas camundongas OVX-SC comparados com as das camundongas SHAM-SC e OVX-HF (P<0,001). A associação da ovariectomia com a dieta HF agravou o aumento dos níveis séricos de leptina em camundongas OVX-HF, em relação aos OVX-SC (P<0,005). TNF-alfa não foi diferente entre os grupos, mas a IL-6 foi significativamente maior nas camundongas OVX-HF comparados a ambos os grupos SHAM-HF e OVX-SC (P<0,0001). Concluindo, a ingestão de uma dieta hiperlipídica por camundongas ovariectomizadas, leva ao aumento do acúmulo e redistribuição inadequada de gordura, à piora dos níveis de citocinas e adipocinas, assim como à desordem metabólica, o que aumenta os fatores de risco para doenças cardiovasculares. Menopause is associated with some metabolic disorders as dyslipidemia, obesity and inflammation among others abnormalities present in the human metabolic syndrome. High-fat diet (HFD) is associated with menopause enhanced menopause alterations, increasing the risk of cardiovascular disease. The hypothesis that a high-fat (HF) diet aggravates ovariectomy-related complications was tested. SHAM and ovariectomized (OVX) C57BL/6 mice fed standard chow (SC, 10% fat) or a HF diet (60% fat) for 18 weeks were studied. Feed efficiency (FE), body mass (BM), regional fat pad masses distribution and adipocyte morphometry were studied. Blood analyses (total cholesterol, TC, triglycerides, TG, cytokines and adipokines) were performed. OVX-HF mice had greater FE and BM than all other groups (P<0.05). Visceral fat (ovarian and retroperitoneal fat pads) and the subcutaneous fat (inguinal fat pad) varied with a parallel pattern of fat accumulation in SHAM-SC, SHAM-HF and OVX-SC, but OVX-HF had different pattern of fat accumulation much greater than in SHAM-SC. The association of ovariectomy with HF diet increased significantly the adipocyte diameter in OVX-HF in comparison with SHAM-HF mice (P<0.0001) and also aggravated the increment of TC, TG and leptin levels in OVX-HF mice in comparison to OVX-SC mice (P<0.0001). Adiponectin levels were higher in OVX-SC mice compared to both SHAM-SC and OVX-HF mice (P<0.001). The association of ovariectomy with HF diet aggravated the increase of serum leptin levels in OVX-HF mice in relation to OVX-SC mice (P<0.005). TNF-alpha was not different among the groups, but IL-6 was markedly higher in OVX-HF mice than in both SHAM-HF and OVX-SC mice (P<0.0001). In conclusion, high-fat diet intake worsens, in ovariectomized mice, the fat accumulation and redistribution as well as the cytokines and adipokines levels, and metabolic disorder, which increases risk factors for cardiovascular diseases.

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Marchesin, Juliana de Carvalho. "Influência de um produto probiótico à base de soja sobre a composição da microbiota intestinal de camundongos submetidos à dieta hiperlipídica /." Araraquara, 2017. http://hdl.handle.net/11449/152611.

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Orientador: Daniela Cardoso Umbelino Cavallini Banca: Vivian Marques Miguel Suen Banca: Amanda Martins Baviera Resumo: Objetivo: analisar o efeito de um produto à base de extrato aquoso de soja, fermentado com Enterococcus faecium CRL 183 e Lactobacillus helveticus 416 e com adição de Bifidobacterium longum ATCC 15707, sobre a composição da microbiota fecal, variação de peso corporal e parâmetros inflamatórios de camundongos submetidos à dieta hiperlipídica. Métodos: O protocolo experimental teve duração de 10 semanas sendo utilizados camundongos machos Swiss (Unib: SW) com oito semanas de idade. Os animais foram divididos em quatro grupos (n=10): C (controle negativo) - animais alimentados com dieta padrão para roedores (DP); OB (controle positivo) - animais induzidos à obesidade por dieta hiperlipídica (DHL - 61,01% do valor energético total de lipídios); OBF (fermentado probiótico) - animais induzidos à obesidade por DHL e que receberam o produto fermentado probiótico; OBP (placebo) - animais induzidos à obesidade por DHL e que receberam o produto placebo (sem os cultivos microbianos). A bebida probiótica e o produto placebo foram produzidos semanalmente e a viabilidade das cepas E. faecium CRL 183, L. helveticus 416 e B. longum ATCC 15707 foi determinada imediatamente após o preparo do produto probiótico (T0) e com sete dias de armazenamento à temperatura de refrigeração (5 ºC). Ao longo do protocolo experimental foram monitorados os seguintes parâmetros: ingestão hídrica e de ração (diariamente), variação do peso corporal (semanalmente) e verificação da glicemia de jejum (final do protoc... (Resumo completo, clicar acesso eletrônico abaixo) Abstract: Aim: to investigate the effect of an aqueous soy extract beverage, fermented with Enterococcus faecium CRL 183 and Lactobacillus helveticus 416, supplemented with Bifidobacterium longum ATCC 15707, on the composition of fecal microbiota, change in body weight and inflammatory parameters of mice submitted to a hyperlipidic diet. Methods: The length of the experimental protocol was 10 weeks, and it was performed using Swiss type male mice (Unib: SW) at eight weeks of age. The animals were divided into four groups (n = 10): C (negative control) - animals fed with a standard diet for rodents; OB (positive control) - animals induced to obesity by a high-fat diet (HFD - 61.01% of the total energetic value of lipids); OBF (beverage fermented with probiotics) - animals induced to obesity by HFD, that also was fed with the probiotic fermented product; OBP (placebo) - animals induced to obesity by HFD, that also was fed with the placebo product (the same product without microbial cultures). The beverage fermented with probiotics and the placebo product were produced weekly and the viability of its microbial strains (E. faecium CRL 183, L. helveticus 416 and B. longum ATCC 15707) was determined immediately after its preparation (T0) and after seven days of storage at controlled temperature (5 °C). During the experimental protocol, the following parameters were monitored: water and food intake (daily), body weight variation (weekly) and fasting glycemia (at the end of the protocol). The composition of the intestinal microbiota was evaluated by Real-Time Polymerase Chain Reaction (qPCR) at the beginning, middle and at the end of the protoc... (Complete abstract click electronic access below) Mestre

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Arcego, Danusa Mar. "Isolamento social precoce e consumo de uma dieta hiperlipídica : implicações no comportamento do tipo depressivo e em aspectos cognitivos em ratos adultos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/157485.

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Intervenções ambientais, como a exposição precoce a estressores ou a dietas ricas em calorias, podem alterar a trajetória da maturação neural e influenciar na susceptibilidade a certas patologias a longo-prazo. Neste contexto, o objetivo do presente estudo foi investigar os efeitos de uma exposição ao isolamento social durante o período pré-pubere associado ou não ao consumo precoce e crônico de uma dieta hiperlipídica (HFD) sobre aspectos cognitivos e emocionais, e possíveis mecanismos neuroquímicos associados a essas alterações, no hipocampo, no córtex pré-frontal e no núcleo accumbens de ratos machos na idade adulta. Os resultados mostraram que os dois fatores, estresse e dieta (separadamente), induziram um comportamento do tipo depressivo nos animais na idade adulta. Além disso, os animais isolados apresentaram um déficit cognitivo associado à memória de curta-duração e de trabalho, enquanto que animais com acesso à HFD demonstraram prejuízo somente na memória de curta-duração. Curiosamente, a interação entre os fatores (estresse e dieta) causou uma reversão dos déficits na memória de curta-duração. Em relação às avaliações do comportamento alimentar hedônico, observamos que o grupo com consumo crônico de HFD apresentou uma menor motivação para obter diferentes tipos de alimentos palatáveis doces. Essa redução motivacional não parece ser associada a uma menor palatabilidade e/ou a uma maior saciedade induzida pela HFD. Em relação aos marcadores de plasticidade analisados no córtex pré-frontal, observamos interações entre os fatores estresse e dieta na atividade da enzima Na+K+-ATPase, nos níveis de BNDF e no imunoconteúdo das proteínas AKT e MAPK/ERK, sendo que os fatores quando aplicados isolados diminuem os níveis dos parâmetros analisados, porém quando associados, os níveis retornam ou aumentam em relação aos valores do grupo controle. O hipocampo foi a estrutura mais afetada pelas intervenções ambientais neste trabalho. Observamos que tanto o estresse, como a dieta hiperlipídica (separadamente) causaram uma redução da plasticidade sináptica hipocampal, por meio de diferentes mecanismos: o acesso crônico à HFD afeta proteínas relacionadas ao funcionamento das sinapses, enquanto o isolamento social parece afetar mais particularmente a via de sinalização do BDNF. Com relação aos achados neuroquímicos no núcleo accumbens, observamos uma redução dos receptores dopaminérgico-1 (D1) e canabinóide-1 (CB1) com o consumo de HFD, enquanto que os animais isolados na pré-puberdade apresentaram uma redução do metabolismo dopaminérgico nesta estrutura. Em suma, esta tese demonstra que tanto o isolamento social e como o consumo contínuo de HFD causam comportamento do tipo depressivo e outras alterações comportamentais, e reduzem marcadores de plasticidade importantes no córtex prefrontal e hipocampo. O acesso à HFD também causa uma menor motivação para o comportamento alimentar hedônico. Assim, tais eventos precoces podem afetar a plasticidade neural levando a importantes alterações comportamentais, e assim predispor a diferentes patologias durante a vida. Environmental interventions, such as early exposure to stressors or high calorie-diets, can alter the trajectory of neural maturation and influence the susceptibility to some pathologies throughout life. In this context, the aim of the present study was to investigate the effects of exposure to social isolation, during the pre-pubertal period, associated or not with early and chronic consumption of a hyperlipid diet (HFD) on cognitive and emotional aspects, and possible mechanisms associated with these changes, in the hippocampus, the prefrontal cortex and the nucleus accumbens of male rats in adulthood. The results showed that both pre-pubertal social isolation and chronic access to a hyperlipidic diet induced a depressive-like behavior in animals during adulthood. In addition, isolated animals had a cognitive deficit associated with short-term and working memory, whereas animals with access to HFD demonstrated impairment only in short-term memory. Interestingly, the interaction between the factors (stress and diet) caused a reversal in relation to short-term memory, remaining similar to the control group. Regarding the evaluations of the hedonic eating behavior, we observed that HFD group presented a lower motivation to obtain different sweet palatable foods. This impaired motivation does not appear to be associated with less palatability and/or satiety induced by the high-fat diet. Concerning plasticity markers in the prefrontal cortex, we observed interactions between stress and diet on Na+ K+-ATPase activity, BNDF levels and AKT and MAPK/ERK immunocontents. These interactions follow a similar profile: when applied alone, the levels of the analyzed parameters decrease, but when associated, the levels return or increase in relation to the values of the control group. The hippocampus was the structure most affected by the environmental interventions. Both stress and HFD caused a reduction of hippocampal synaptic plasticity through different mechanisms: chronic access to HFD affects proteins related to synaptic function, while social isolation affects the BDNF signaling pathway more significantly. Regarding the neurochemical findings in the nucleus accumbens, we observed a reduction in dopaminergic-1 (D1) and cannabinoid-1 (CB1) receptors with chronic HFD intake, whereas isolated animals had a reduction of dopaminergic metabolism in this same structure. In summary, this thesis shows that both social isolation and chronic consumption of HFD lead to depressive-like behavior and to other behavioral changes; they reduce plasticity markers in prefrontal cortex and hippocampus. HFD access also induced a lower motivation for hedonic feeding. Therefore, these early interventions may affect neural plasticity, leading to important behavioral changes, and thus, predispose to different pathologies later in life.

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Coyle, Danielle R. "High Fat Diet Effects on Erythrophagocytosis and MCP-1 Levels in Mice." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353342118.

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Chen, Guangliang [Verfasser], and Georg [Gutachter] Schett. "High fat diet increases melanoma cell growth / Guangliang Chen ; Gutachter: Georg Schett." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2017. http://d-nb.info/1137703199/34.

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Bowser, Suzanne Mae. "Skeletal muscle metabolic adaptations in response to an acute high fat diet." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82030.

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Macronutrient metabolism plays an essential role in the overall health of an individual. Depending on a number of variables, for example, diet, fitness level, or metabolic disease state, protein, carbohydrate and fat have varying capacities to be oxidized and balanced. Further, when analyzing the oxidation of carbohydrate and fat in the skeletal muscle specifically, carbohydrate balance happens quite rapidly, while fat balance does not. The ability of skeletal muscle to adapt and respond to various nutrient states is critical to maintaining healthy metabolic function. Habitual high fat intake has been associated with reduced oxidative capacity, insulin resistance, increased gut permeability, inflammation, and other risk factors often preceding metabolic disease states. The disruption of gut function leads to gut permeability and increases endotoxins released into circulation. Endotoxins have been shown to play an important role in obesity-related whole body and tissue specific metabolic perturbations. Each of these disrupted metabolic processes is known to associate with obesity, metabolic syndrome and diabetes. To date, limited research has investigated the role of high fat diet on skeletal muscle substrate oxidation and its relationship to gut permeability and endotoxins. The purpose of this study was to determine the effects of an acute, five-day, isocaloric high fat diet (HFD) on skeletal muscle substrate metabolism in healthy non-obese humans. An additional purpose was to determine the effects of a HFD on gut permeability and blood endotoxins on healthy, non-obese, sedentary humans. Thirteen college age males were fed a control diet for two weeks, followed by five days of an isocaloric HFD. To assess the effects of a HFD on skeletal muscle metabolic adaptability and postprandial endotoxin levels, subjects underwent a high fat meal challenge before and after a HFD. Muscle biopsies were obtained; blood was collected; insulin sensitivity was assessed via intravenous glucose tolerance test; and intestinal permeability was assessed via the four-sugar probe test before and after the HFD. Postprandial glucose oxidation and fatty acid oxidation in skeletal muscle increased before the HFD intervention but was decreased after. Skeletal muscle in vitro assay of metabolic flexibility was significantly blunted following the HFD. Insulin sensitivity and intestinal permeability were not affected by HFD, but fasting endotoxin was significantly higher following the HFD. These findings demonstrate that in young, healthy males, following five days of an isocaloric high fat diet, skeletal muscle metabolic adaptation is robust. Additionally, increased fasting endotoxin independent of gut permeability changes are potentially a contributor to the inflammatory state that disrupts substrate oxidation. These findings suggest that even short-term changes in dietary fat consumption have profound effects on skeletal muscle substrate metabolism and fasting endotoxin levels, independent of positive energy balance and whole-body insulin sensitivity. Ph. D.

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43

Orabi, Danny Ahmad. "The Effects of High Fat Diet on Liver Disease and Hepatocellular Carcinoma." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1619778405639812.

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Umbaugh, David S. "Neuronal Inflammation| A Potential Contributing Mechanism to High Fat Diet-Induced Neuropathy." Thesis, Southern Illinois University at Edwardsville, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10276211.

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Neuropathy, a debilitating complication of diabetes, has primarily been attributed to poor glycemic control, but has recently been associated with obesity and the metabolic syndrome in nondiabetic individuals. A robust body of evidence indicates that a high-fat diet can induce signs of neuropathy in mice but the pathogenesis of high fat diet-induced neuropathy remains unknown. PURPOSE: To determine if neuronal inflammation is a potential initiating mechanism for the development of mechanical hypersensitivity and nerve fiber changes (signs of neuropathy) in high fat fed mice. METHODS: Male C57Bl/6 mice were randomized to a standard (Std, 15% kcal from fat) or high fat diet (HF, 54% kcal from fat) for 2, 4, or 8 wks (n = 11-12 per group). Lumbar dorsal root ganglia were harvested and inflammatory mediators (IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-17, MCP-1, IFN-γ, TNF-α, MIP-1α, GMCSF, RANTES) were quantified using a Multiplex ELISA and normalized to total protein. Neuropathy was characterized by the von Frey test for mechanical sensitivity at wk 0 and every other week thereafter. Hindpaw foot pad skin was harvested at end study and used to quantify intraepidermal nerve fiber density (IENFD) and pain-sensing (TrkA) nerve fibers via immunohistochemistry. RESULTS: After 8 wks, HF had greater bodyweight (33.3 ± 1.0 vs. 26.7 ± 0.5 g, p < 0.001), fasting blood glucose (160.3 ± 9.4 vs. 138.5 ± 3.4 mg/dl, p < 0.05) and insulin (3.58 ± 0.46 vs. 0.82 ± 0.14 ng/ml, p < 0.001) compared to Std. IL-1α, RANTES and IL-5 were higher in HF compared to Std after 2 wks and 4 wks, respectively (IL-1α: 4.8 ± 1.3 vs. 2.9 ± 0.6 pg/mg, p < 0.05; RANTES: 19.6 ± 2.2 vs. 13.3 ± 1.2 pg/mg p < 0.05; IL-5: 5.8 ± 0.7 vs. 3.1 ± 0.5 pg/mg, p < 0.05 ). IENFD and TrkA fiber density were also higher in HF vs. Std after 4 wks (IENFD: 39.4 ± 1.2 vs. 32.2 ± 1.3 fibers/mm, p < 0.001; TrkA: 30.4 ± 1.8 vs. 22.4 ± 1.3 fibers/mm). There were no significant differences in hindpaw sensitivity for Std vs. HF at any time point. CONCLUSION: Increased inflammatory mediators preceded and accompanied an increase in a specific population of pain sensing nerve fibers (TrkA) in the hindpaw footpad of high fat fed mice. Diets high in fat may increase neuronal inflammation and initiate nerve fiber changes responsible for painful neuropathy in nondiabetic and diabetic individuals.

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Chen, Ting. "LKB1 Regulation of High-Fat Diet-induced Adaptation in Mouse Skeletal Muscle." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6682.

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Ad libitum high-fat diet (HFD)-induced obesity leads to insulin resistance in skeletal muscle, altered gene expression, and altered growth signaling, all of which contributes to pathological changes in metabolism. Liver kinase B1 (LKB1) is an important metabolism regulator. The purpose of this dissertation was to understand how knocking out LKB1 influences HFD induced adaptations in mouse skeletal muscle. To do so, control and skeletal muscle LKB1 knock-out (LKB1-KO) mice were put on either standard diet (STD) or HFD for 1 week or 14 weeks, or put on the HFD for 14 weeks and then switched to STD for 1 week (switched diet). The major differences in adaptation in the LKB1-KO mice include: 1) lower fasting blood glucose levels but impaired glucose tolerance compared to WT mice (although conflicting results are generated if the data is not normalized to fasting blood glucose levels), 2) altered expression of 16 HFD-induced genes, and 3) decreased muscle weight. The lower fasting blood glucose in LKB1-KO mice was likely due to elevated serum insulin levels, and the impaired glucose tolerance was associated with decreased phosphorylation of TBC1D1, an important regulator of insulin stimulated glucose uptake. 16 potential important target genes (metabolism, mitochondrial, cytoskeleton, cell cycle, cell-cell interactions, enzyme, ion channel) were identified in the context of HFD feeding and LKB1-KO. These genes were quantified by RT-PCR and grouped according to changes in their patterns of expression among the different groups. Among several other interesting changes in gene expression, the muscle growth-related protein, Ky was not affected by short-term HFD, but increased after long-term HFD, and did not decrease after switched diet, showing that its expression may be an important long-term adaptation to HFD. LKB1-KO promoted anabolic signaling through increasing t-eIF2α and eIF4E expression, and promoted protein degradation through increasing protein ubiquitination. Because the degradation is the main effect and lead to muscle weight decrease. The effect of HFD and/or LKB1-KO on the LKB1-AMPK system was also determined. The results showed that knocking-out LKB1 decreased AMPK activity, decreased nuclear distribution for AMPK α2 and increased AMPK α1 expression. Long-term HFD increased t-AMPK expression in LKB1-KO mice, decreased the cytoplasm p-AMPK and nuclear p/t-AMPK ratio in CON mice. Together the findings of this dissertation demonstrated HFD induced glucose/insulin tolerance, while LKB1-KO had a controversial effect on glucose/insulin sensitivity. Both HFD and LKB1-KO affect AMPK expression and cellular location, while LKB1-KO also affects AMPK activity. LKB1-KO promoted protein degradation through ubiquitination in skeletal muscle.

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Angiletta, Chris. "The Role of Fasting Acylcarnitines in Metabolic Flexibility from Short Term High Fat Feeding." Thesis, Virginia Tech, 2018. http://hdl.handle.net/10919/82401.

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Metabolic flexibility plays a significant role in energy homeostasis by regulating fuel selection in correspondence to energy demand. Obese and type II diabetic populations have displayed a hindered ability to properly transition from fat oxidation while in a fasted state to carbohydrate oxidation once fed, leading to a buildup of mitochondrial metabolites such as acylcarnitines. Carnitine, essential for fatty acyl-CoA transport through the inner and outer mitochondrial membranes, can be an indicator of mitochondrial distress as elevated levels tend to spill over into plasma suggesting a disruption in oxidation. The current study was designed to examine the effect of short term, high fat feeding on plasma acylcarnitine species diversity and levels and if acylcarnitines are associated with metabolic flexibility. 13 healthy, non-obese, sedentary males, aged 18-40 years participated in this study. Following a 12-hour overnight fast a biopsy was taken from the quadricep before and 4 hours after a high fat meal. Blood draws were obtained pre-biopsy while fasted and every hour for 4 hours post high fat meal consumption. Acylcarnitines from plasma were converted to their butyl esters and analyzed by electrospray ionization tandem mass spectrometry (MS/MS). Changes were observed in acetylcarntine (P=0.0125), glucose oxidation (P=0.0295), C16:1/C16:0 desaturation index (P= 0.0397), and C18:1/C18:0 desaturation index (P=0.0012). We did not find that individual changes in flexibility correlated with circulating acylcarnitine measurements in a fasted state Master of Science

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47

Ndlovu, Zibele. "The effects of maternal diets, varying in fat content, on proximal hepatic and skeletal muscle insulin signalling in neonatal wistar rat offspring." Thesis, University of the Western Cape, 2013. http://hdl.handle.net/11394/4311.

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>Magister Scientiae - MSc The incidence of type 2 diabetes (T2D) is persistently increasing globally. T2D is associated with pancreatic β cell dysfunction and insulin resistance in peripheral tissues such as the liver and skeletal muscle. Skeletal muscle is the major site for insulin stimulated glucose uptake. Maintenance on a gestational high fat diet may programme insulin resistance. Programming is induced by the exposure of organisms to either a stimulus or insult during foetal and/or early neonatal life and alters offspring physiology and metabolism. The aim of the present study was therefore to investigate the effects of maternal diets, varying in fat content, on neonatal hepatic and skeletal muscle gene (mRNA) and protein (immunoreactivity) expression of proximal insulin signalling factors: insulin receptor alpha (IRα), insulin receptor substrate 2 (IRS2) and phosphoinositide 3-kinase-p110 alpha (PI3K-p110α), and to assess the therapeutic potential of Aspalathus linearis extract after high fat programming. Pregnant rats were randomised into groups maintained on diets with varying fat proportions: 10% (control), 20% (20F), 30% (30F) and 40% (40F) fat as energy throughout gestation. Neonatal liver and skeletal muscle were collected to determine the proximal insulin signalling expression profiles of the target factors: IRα, IRS2 and PI3K-p110α. Quantitative polymerase chain reaction (qPCR) was applied to determine mRNA expression of these target insulin signalling factors. Immunostaining of the target proteins in the liver and skeletal muscle was performed followed by relative quantification with image analysis software. Further, Aspalathus linearis (Al) extract was orally administered to mothers during gestation in the 10% (Control-Al) and 40% (HFD-Al) diets at a dose of 150 mg/kg. Body weight, food intake and blood glucose concentrations were monitored throughout gestation in mothers. Maternal diets, varying in the percentage of fat content, showed no significant effect on neonatal hepatic IR and IRS2 mRNA expression. However, hepatic PI3K mRNA expression was elevated in 30F neonates compared to 20F neonates. Skeletal muscle IR and PI3K mRNA expression were reduced in the 30F and 40F neonates compared to 20F neonates. There was reduced hepatic IRα immunoreactivity in 40F neonates compared to control and 20F neonates. Further, skeletal muscle IRα immunoreactivity was significantly reduced in 30F and 40F neonates compared to control neonates. Therefore foetal high fat programming reduced IRα in both the liver and skeletal muscle which may impair proximal insulin signalling in these glucose recipient organs. Aspalathus linearis had no effect on maternal serum insulin and glucagon concentrations. In addition, maternal caloric intake, body weight and organ weights (liver, brain and pancreas) were not altered amongst the groups. Further, HFD-Al neonates were heavier than control neonates. In conclusion, Aspalathus linearis, at a dose of 150 mg/kg, had neither harmful nor ameliorative effects in pregnant mothers fed high fat diet during gestation. In addition, Aspalathus linearis treatment had no ameliorative effects on neonates from mothers fed high fat diet throughout gestation.

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48

Werner, Tim. "The Effect of High-Carbohydrate, Low-Fat & Low-Carbohydrate, High Protein Diets on Physiologic and Performance Variables on Row Ergometry Training." Ohio University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1140557597.

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49

Rodrigues, Manuela Ortega Marques. "Efeitos da perda de peso corporal induzida por dieta hipolip?dica ad libitum e pela restri??o cal?rica com dieta hiperlip?dica na inflama??o do tecido adiposo de camundongos obesos." UFVJM, 2017. http://acervo.ufvjm.edu.br/jspui/handle/1/1614.

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Submitted by Jos? Henrique Henrique (jose.neves@ufvjm.edu.br) on 2018-03-26T12:48:59Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) manuela_ortega_marques_rodrigues.pdf: 2356674 bytes, checksum: e576d7cb84dd67e4068acfffffe22e9f (MD5) Approved for entry into archive by Rodrigo Martins Cruz (rodrigo.cruz@ufvjm.edu.br) on 2018-03-29T12:57:38Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) manuela_ortega_marques_rodrigues.pdf: 2356674 bytes, checksum: e576d7cb84dd67e4068acfffffe22e9f (MD5) Made available in DSpace on 2018-03-29T12:57:38Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) manuela_ortega_marques_rodrigues.pdf: 2356674 bytes, checksum: e576d7cb84dd67e4068acfffffe22e9f (MD5) Previous issue date: 2017 Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico (CNPq) Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior (CAPES) Funda??o de Amparo ? Pesquisa do Estado de Minas Gerais (FAPEMIG) A expans?o do tecido adiposo branco na obesidade leva ? express?o alterada de prote?nas em seus adip?citos, bem como a infiltra??o de c?lulas do sistema imune, especialmente macr?fagos, cujas secre??es levam ao desenvolvimento da inflama??o cr?nica de baixo grau, a qual ? considerada subjacente ao desenvolvimento de in?meras comorbidades. Dentre as formas de tratamento da obesidade, dietas de restri??o cal?rica (RC) nutricionalmente balanceadas induzem a perda de peso e melhorias em marcadores sist?micos da inflama??o, mas os efeitos diretos no tecido adiposo visceral ainda s?o controversos. No entanto, existe uma lacuna sobre qual o impacto dessas dietas na inflama??o local, mesmo em condi??es de sobrecarga lip?dica. Assim, o objetivo deste estudo foi avaliar os efeitos da perda de peso corporal induzida por dieta hipolip?dica ad libitum e pela restri??o cal?rica com dieta hiperlip?dica na inflama??o do tecido adiposo visceral de camundongos obesos. Para tal, inicialmente, camundongos C57BL/6 com 12 semanas de idade, machos, foram divididos em dois grupos: LF ? alimentados com dieta controle hipolip?dica ? do ingl?s low fat (10% das calorias, fonte ?leo de soja, rica em ?cidos graxos poli-insaturados); e HF ? alimentados com dieta controle hiperlip?dica ? do ingl?s high fat (60% calorias, fonte banha de porco, rica em ?cidos graxos saturados) para indu??o da obesidade. Ap?s oito semanas, seis animais de cada grupo foram eutanasiados para verifica??o da adiposidade visceral e estado inflamat?rio (dosagens de prote?na C reativa ? PCR s?rica e hep?tica). Em seguida, os animais HF foram aleatoriamente divididos em tr?s grupos HF ? continuaram recebendo dieta HF; LFAL ? submetidos ao emagrecimento pela substitui??o da dieta HF pela LF e acesso livre (ad libitum) e RHF ? submetidos ao emagrecimento por receberem quantidades restritas em calorias da dieta HF para atingir o mesmo peso corporal dos animais LFAL. A partir deste momento, esses grupos foram alimentados, juntamente com os animais LF, por mais sete semanas. Ao final, foram avaliados o ganho/perda de peso corporal, a adiposidade, as concentra??es s?ricas e hep?ticas de PCR, e as concentra??es de leptina, adiponectina, e das citocinas IL-6, TNF e MCP-1 no tecido adiposo retroperitoneal, al?m da morfologia dos adip?citos e a presen?a de infiltrados inflamat?rios no tecido adiposo retroperitoneal. Ao final da fase de indu??o da obesidade, os animais HF estavam obesos e inflamados. Ao final da fase de indu??o da perda de peso, os grupos LFAL e RHF tiveram pesos corporais semelhantes, menores que o HF e se igualaram ao LF. No entanto, houve maior dificuldade em perder peso pelo grupo RHF em compara??o ao LFAL, dado pelas diferen?as significativas entre os deltas de perda de peso, que foram menores para RHF e pelos coeficientes de efici?ncia energ?tica, que foram maiores para o grupo RHF. Os animais LFAL retornaram a adiposidade e a hipertrofia dos adip?citos viscerais a valores semelhantes ao grupo LF. Isto provavelmente foi o que levou ? menor concentra??o de leptina com concomitante aumento da adiponectina e menor infiltra??o de c?lulas inflamat?rias neste tecido, igualando-se tamb?m ao LF. Em consequ?ncia, houve menor concentra??o tecidual de citocinas pr?-inflamat?rias, al?m de menor concentra??o hep?tica e circulante de PCR. J? para os animais RHF, houve apenas atenua??o da adiposidade e da hipertrofia dos adip?citos retroperitoneais. Isso foi suficiente para restabelecer a concentra??o local de leptina a n?veis semelhantes ao grupo LF, embora n?o tenha elevado a concentra??o de adiponectina. Al?m disso, a infiltra??o de c?lulas inflamat?rias menteve-se tamb?m elevada. N?o houve redu??o da concentra??o de citocinas pr?-inflamat?rias, ? exce??o da IL-6, que reduziu levemente. A concentra??o hep?tica de PCR foi atenuada, o que n?o refletiu na concentra??o s?rica dessa prote?na. Concluiu-se que a restri??o cal?rica com dieta hiperlip?dica foi menos eficiente em promover a perda de peso e de adiposidade e n?o melhorou a inflama??o do tecido adiposo visceral, comparada com a dieta hipolip?dica ad libitum. Inferiuse que a ingest?o de dieta com sobrecarga de lip?deos (60% das calorias) e de ?cidos graxos saturados foi mais determinante da inflama??o local do que a restri??o cal?rica per se. Disserta??o (Mestrado) ? Programa Multic?ntrico de P?s-gradua??o em Ci?ncias Fisiol?gicas, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2017. The expansion of white adipose tissue in obesity leads to altered protein expression in its adipocytes, as well as the infiltration of immune cells, especially macrophages, whose secretions lead to the development of chronic low-grade inflammation, which underlies the development of several comorbidities. Among treatments, caloric restriction (CR) nutritionally balanced diets induce weight loss and ameliorates inflammation systemic markers, but adipose tissue effects are still controversial. Moreover, there is a gap on the impact of these diets on local inflammation, even under lipid overload. Thus, the aim of this study was to evaluate effects of body weight loss induced by a low fat ad libitum diet and a CR in a high fat diet in the visceral adipose tissue inflammation of obese mice. Firstly, 12 weeks of age male C57BL/6 mice were divided into two groups: LF - fed a control low fat diet (10% calories, source soybean oil, high in polyunsaturated fatty acids); and HF - fed a control high fat diet (60% calories, source lard, high in saturated fatty acids) for obesity induction. After eight weeks, six animals from each group were euthanized to verify visceral adiposity and inflammatory status (serum and hepatic C-reactive protein-CRP). Then, HF animals were randomly divided into three groups: HF ? keept at HF diet; LFAL - a weight loss group that was switched from HF to LF and maintained on it ad libitum; RHF - a weight loss group that received restricted amounts of HF to maintain the same body weight as LFAL. Thereafter, these groups were fed, along with the LF animals, for another seven weeks. At end, body weight gain / loss, adiposity, serum and hepatic CRP concentrations, and adipose retroperitoneal tissue concentrations of leptin, adiponectin, IL-6, TNF and MCP-1 were evaluated, as well as adypocite morphology and the presence of inflammatory infiltrates in the retroperitoneal adipose tissue. Obesity was induced, since HF animals had higher weights, adiposity and were inflamed. At the end of the weight loss period, both LFAL and RHF had similar body weight, lower than HF and equal to LF. However, it was more dificcult to loose wheight by the RHF group compared to LFAL, since weight loss deltas were lower for RHF and energy efficiency ratios were higher for RHF group. LFAL animals returned visceral adiposity and retroperitoneal adipocyte hypertrophy similarly to the LF group. Also, there was a lower leptin level with concomitant increase of adiponectin and less infiltration of inflammatory cells in this tissue, also matching to LF. Still, there was a lower tissue concentration of proinflammatory cytokines, and a lower hepatic and serum CRP. For RHF animals, there was only an attenuation in adiposity and visceral adipocyte hypertrophy, although it was sufficient to restore local leptin concentration similarly to LF. However, this regimen was not able to elevate the adiponectin concentration. In addition, the inflammatory cells infiltration was highly elevated. There was no reduction in proinflammatory cytokines concentration, despite IL-6, which was reduced slightly. Hepatic CRP concentration was attenuated, which did not reflect in its serum concentrations. In mice with diet-induced obesity, the weight loss by means a CR in a high fat diet was less effective in promoting wheight and adiposity losses and it did not improve visceral adipose tissue inflammation. It can be inferred that a lipid overload (60% from calories) as well as a saturated fatty acid surplus from the high fat diet were more determinant of local inflammation than caloric restriction per se.

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50

Ho, Dao Hong. "Cocaine hypophagia and hyperlocomotion in rats before and after exposure to a high-fat diet." Thesis, Texas A&M University, 2003. http://hdl.handle.net/1969.1/1641.

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Relatively few studies have examined the effects of psychostimulants in obese subjects. Using the dietary obese rat model, the present experiments determined the reductions in food intake (hypophagia) and increases in locomotion (hyperlocomotion) induced by cocaine in diet-induced obese prone (DIO-prone) rats and diet resistant prone (DR-prone) rats as well as diet-induced obese (DIO) rats and diet resistant (DR) rats. In Experiment 1, thirty-six male Sprague-Dawley rats were given intra-peritoneal (i.p.) injections of cocaine (0, 10, 20, and 30 mg/kg) immediately prior to placement into locomotor chambers outfitted with a food source and a water source for a 60-minute test period. In Experiment 2, the same rats were exposed to a high-fat diet, and were subsequently divided into groups according to the extent of the weight gain (high weight gainers DIO group, low weight gainers DR group, and residual weight gainers MIX group). The rats were retested for reactivity to cocaine using conditions similar to those in Experiment 1. Rats injected with cocaine prior to high-fat exposure (Experiment 1) showed a dose dependent suppression of food intake, as well as a dose dependent increase in locomotor activity, with DR-prone rats exhibiting an enhanced degree of cocaine-induced hypophagia, as well as cocaine-induced hyperlocomotion as compared to the other groups. In Experiment 2, DIO rats exhibited a suppression of food intake after injection of 10 mg/kg cocaine, as well as an increase in locomotor activity that was significantly greater than noted in the other groups. When the results of Experiment 1 were analyzed as a function of prospective body weight gain (as opposed to placement into distinct groups), reactivity to cocaine decreased as body weight gain increased. In contrast, after high-fat exposure and weight gain, increased body weight gain was associated with an increased magnitude of suppression in food intake after cocaine administration. Similar patterns of differential cocaine sensitivity were observed for cocaine hyperlocomotion in Experiment 2. These studies indicate that although the propensity to develop obesity is associated with a diminished cocaine response, cocaine reactivity is enhanced after the induction of obesity.

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