Academic literature on the topic 'Hight fat Diet'
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Journal articles on the topic "Hight fat Diet"
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Dewi, Ervina, Fadliyani Fadliyani, and Ismiranda Ismiranda. "ANALISIS POTENSI ANTIHIPERKOLESTEROLEMIA EKSTRAK ETANOL BUAH ASAM JAWA (Tamarindus indica L) TERHADAP STRUKTUR MIKROSKOPIS HATI MENCIT (Mus musculus)." Jurnal Kedokteran Syiah Kuala 18, no. 2 (August 1, 2018): 86–92. http://dx.doi.org/10.24815/jks.v18i2.17998.
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Abstrak. Penelitian ini bertujuan untuk mengetahui potensi antihiperkolesterolemia ekstrak etanol buah asam jawa terhadap struktur mikroskopis hati mencit. Rancangan yang digunakan adalah Rancangan Acak Lengkap, terdiri atas 6 perlakuan dan 4 ulangan. Perlakuan terdiri atas Pemberian pakan standard dan akuades (P0), pakan aterogenik dan Aquades (P1), pakan aterogenik dan simvastatin 10 mg (P2), pakan aterogenik dan ekstrak asam jawa 5, 25 dan 50 mg/kg bb (P3, P4, P5). Volume simvastatin dan ekstrak etanol buah asam jawa adalah 0,5mL. Pembuatan sediaan histologis menggunakan metode parafin. Parameter yang diamati adalah kadar kolesterol total, infiltrasi lemak, degenerasi lemak dan nekrosa hepatosit. Data hasil penelitian dianalisis dengan analisis varian dan dilanjutkan dengan Uji Berjarak ganda Duncan. Hasil penelitian menunjukkan ekstrak etanol buah asam jawa berpengaruh nyata dalam menurunkan rerata infiltrasi lemak, degenerasi lemak dan nekrosa sel hati yan diindikasikan dengan penurunan kadar kolesterol secara bermakna. Kesimpulannya, ekstrak etanol buah asam jawa mampu menurunkan rerata infiltrasi lemak, degenerasi lemak dan nekrosa sel hati mencit akibat pakan aterogenikKata Kunci : Pakan Aterogenik, Hiperkolesterolemia, Hati, Ekstrak Etanol Buah Asam Jawa, SimvastatinAbstract. This research aimed to determine the potential antihypercholesterolemic of ethanol extract of tamarind at heart microscopic structure of mice induced with high cholesterol diet. A completely randomized-block design was used with 6 treatments and 4 repetitions of eachtreatment. The treatments were normal diet and aquadest (P0), hight-fat diet and aquadest (P1), hight-fat diet and Simvastatin 10 mg/Kg (P2), hight-fat diet and tamarind extract 5, 25 and 50 mg/Kg (P3, P4, P5). The volume of Simvastatin and tamarind extract given to each mice is 0,5 mL. Paraffin method was apllied of microscopic structure observation. The parameters observed were total cholesterol level, lipid infiltration, lipid degeneration and necrosis of hepatocyte of hepatocyte. A variance analysis followed by Duncan Multiple Range Test was tested to the data mice microscopic structure. The result showed that etnanol extract of tamarind could significant to decrease of lipid infiltration, lipid degeneration and necrosis of hepatocyte showed decrease total cholesterol level. Inconlusion, the that etnanol extract of tamarind could significant to decrease of lipid infiltration, lipid degeneration and necrosis of hepatocyte due to hight-fat diet.Key Word : Atherogenic Feed, Hypercholesterolemia, Liver, Ethanol Extract of Tamarind, Simvastatin
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Hadi, Novian Swasono, Arta Farmawati, and Ahmad Ghozali. "Pencegahan hipertensi dan penebalan dinding aorta dengan pemberian kecambah kacang hijau (Phaseolus radiatus (L)) pada tikus putih Sprague Dawley." Jurnal Gizi Klinik Indonesia 12, no. 3 (January 30, 2016): 116. http://dx.doi.org/10.22146/ijcn.22454.
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Background: Lifestyle changes with high-fat food consumption is one of the factors the risks of cardiovascular diseases like of coronary heart disease and atherosclerosis. A healthy diet and a balanced diet and consume foods that contain lots of antioxidants is one of the effective ways to prevent hyperlipidemia. Mung bean sprouts have properties that neutralize free radicals cause Hyperlipidemia and cardiovascular diseases because it is an antioxidant compound.Objective: The aim of this study was to determinate the effect of mung bean sprouts (Phaseolus radiatus (L)) to blood pressure and histopathology aorta of Sprague-Dawley male rats.Method: The type of study was experimental research using pre-post test controlled group design for blood pressure variable and post test only controlled group design histopathology aorta. The thirty-five of Sprague-Dawley male rats was eight weeks divided into 5 groups. The first group was given standard diet, group 2 was given a hight fat diet, the third group was given a high-fat diet and mung bean sprout 0,67 gram, group 4 was given a high-fat diet and mung bean 1,34 gram, and group 5 was given a high-fat diet and vitamin E doses of 23 IU.Results: Result of this study showed that after 4 weeks of treatment, increased in blood pressure systole in the given of high fat diet higher than group who were given a high fat diet and mung bean sprout and also on group who were given high fat diet and vitamin E, but there is no difference effect a decrease in blood pressure between the provision of mung bean sprouts and vitamin E (p>0,05). Statistical analysis to thick the wall the aorta show the similarity meaningful in all the treatment group, it can be said that overall thick the wall the aorta in this research is not different.Conclusion: A dose of mung bean sprout 0,67 g is optimal doses in preventing a rise in blood pressure and prevent alterations histopathology Sprague-Dawley male rats.
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Samiilenko, Natalia, Vira Khorunzha, Hanna Bielokoz, Olga Bezugla, Karina Deineko, Marta Lisevych, Olha Aleksieieva, Diana Zubach, and Olena Alypova. "The Effect of Chronobiology and Variety of Macronutrients on BMI, Waist, Body Fat and HOMA-IR in Patients with Metabolic Syndrome." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1685. http://dx.doi.org/10.1093/cdn/nzaa063_083.
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Abstract Objectives The aim of this study was to assess the effect of both meal timing and diet composition on BMI, waist, body fat and HOMA-IR in patients with metabolic syndrome (MS). Methods We studied 77 patients with MS (32 men and 45 women). Detailed analysis of baseline food-diaries showed that 43 patients (56%) were mostly eating after 3 p.m., generally skipping breakfast, and had more frequent carbohydrate snacks. We divided patients into two groups. The first group consisted of patients with most caloric intake after 3 PM, and the second group included patients who were evenly consuming their food throughout the day. Following diet were offered: 3-fold meal (food intake was at 7–9a.m., 1–2p.m. and 6–7p.m.) with very low-carbohydrate (LC) breakfast and dinner, lunch consisted of LC, proteins (P), polyunsaturated fatty acids (PUFAs) and non-starchy vegetables(V); there were absolutely no snacks during the day. Daily calorie intake was reduced by 20% from baseline. Diet intervention lasted 12 weeks. No medication were used during this period. Results 60 patients completed the trial (32 and 28 patients in first and second groups respectively). BMI was reduced from 33,1 ± 5,0 kg/m2 to 29,8 ± 4,6 kg/m2, the effect was similar in both groups (Cohen's d = 0,7, P = 0003). Mean body fat decreased from 40,7 ± 7,0% to 35,8 ± 7,5% in 12 weeks and treatment effect was more pronounced in second group (Cohen's d = 0,76, P = 0007). The most significant changes were observed in HOMA-IR, which decreased from 4,0 ± 1,1 to 2,1 ± 1,1, treatment effect was also more pronounced in second group (Cohen's d = 1,22, P = 0001). Waist circumference statistically decreased too (from 100,9 ± 16,8сm to 92,0 ± 14,6сm), although with more modest effect - Cohen's d = 0,58, P = 0003. Maximum effect size was in HOMA-IR changes. whereas minimum in waist circumference. Conclusions Our findings demonstrate that this diet (low carb, hight fat, 3-fold meal diet with lunch before 3 p.m.) is associated with statistically different changes in BMI, waist, body fat and HOMA-IR and the intervention was more effective among patients in second group. Funding Sources Not funded.
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Baz, Lina, Salha Algarni, Mona Al-thepyani, Abdullah Aldairi, and Hana Gashlan. "Lycopene Improves Metabolic Disorders and Liver Injury Induced by a Hight-Fat Diet in Obese Rats." Molecules 27, no. 22 (November 10, 2022): 7736. http://dx.doi.org/10.3390/molecules27227736.
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Epidemiological studies have shown that the consumption of a high-fat diet (HFD) is positively related to the development of obesity. Lycopene (LYC) can potentially combat HFD-induced obesity and metabolic disorders in rats. This study aimed to investigate the effect of LYC on metabolic syndrome and assess its anti-inflammatory and antioxidant effects on the liver and adipose tissue in rats fed an HFD. Thirty-six male Wistar albino rats were divided into three groups. Group Ι (the control group) was fed a normal diet, group ΙΙ (HFD) received an HFD for 16 weeks, and group ΙΙΙ (HFD + LYC) received an HFD for 12 weeks and then LYC (25 mg/kg b.wt) was administered for four weeks. Lipid peroxidation, antioxidants, lipid profile, liver function biomarkers, and inflammatory markers were determined. The results showed that long-term consumption of an HFD significantly increased weight gain, liver weight, and cholesterol and triglyceride levels. Rats on an HFD displayed higher levels of lipid peroxidation and inflammatory markers. Moreover, liver and white adipose tissue histopathological investigations showed that LYC treatment mended the damaged tissue. Overall, LYC supplementation successfully reversed HFD-induced changes and shifts through its antioxidant and anti-inflammatory activity. Therefore, LYC displayed a therapeutic potential to manage obesity and its associated pathologies.
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Sokolova, I. B. "Effects of Metabolic Disorders and Streptozotocin-Induced Diabetes on Cerebral Circulation in Rats on a Hight-Fat Diet." Journal of Evolutionary Biochemistry and Physiology 58, no. 3 (May 2022): 915–21. http://dx.doi.org/10.1134/s0022093022030255.
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Chen, D., J. Kang, L. Li, and H. Ma. "Long-term administration of DHEA prevents fat deposition in rats fed a high-fat diet." Czech Journal of Animal Science 61, No. 4 (July 15, 2016): 177–85. http://dx.doi.org/10.17221/8849-cjas.
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P. Angelova, P. Angelova, N. Boyadjiev N. Boyadjiev, and K. Georgieva K. Georgieva. "Aerobic Capacity of Rats Subjected to a Combined High-Fat-Carbohydrate Diet." Indian Journal of Applied Research 3, no. 10 (October 1, 2011): 1–3. http://dx.doi.org/10.15373/2249555x/oct2013/8.
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Leitch, Harry G., and Petra Hajkova. "Eggs sense high-fat diet." Nature Genetics 50, no. 3 (March 2018): 318–19. http://dx.doi.org/10.1038/s41588-018-0068-1.
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Mukai, Rieko. "High-fat diet and constipation." Free Radical Biology and Medicine 120 (May 2018): S134—S135. http://dx.doi.org/10.1016/j.freeradbiomed.2018.04.443.
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Hao, Yilin, Toshihiro Tsuruda, Yoko Sekita-Hatakeyama, Sumiharu Sakamoto, and Kazuo Kitamura. "A high-fat diet is deleterious to mice under glycolysis restriction." Applied Physiology, Nutrition, and Metabolism 43, no. 4 (April 2018): 419–22. http://dx.doi.org/10.1139/apnm-2017-0506.
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It is debated whether carbohydrate restriction has metabolic advantage for its variable weight loss. Five-week-old male mice fed a high-fat diet and receiving a glycolytic inhibitor, 2-deoxyglucose, died within 9 days. They exhibited greater decreases in rectal temperature, appetite, and decline in body weight accompanied by increasing total cholesterol level than the other groups. This study suggests that carbohydrate is necessary for adequate physical and metabolic performance when lipid-rich diet is loaded.
Dissertations / Theses on the topic "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 UniversityPLEASE 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 FerreiraDissertação (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 MilanskiDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas
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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
Books on the topic "Hight fat Diet"
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Jameson, Judy. Fat burning foods and other weight-loss secrets. Baltimore: Ottenheimer Publishers, 1994.
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Jameson, Judy. Fat burning foods and other weight-loss secrets. Baltimore: Ottenheimer Publishers, 1994.
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Jameson, Judy. Fat-burning foods: And other weight-loss secrets. Chicago: Contemporary Books, 1994.
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Eat fat get thin: Why the fat we eat is the key to sustained weight loss and vibrant health. London: Hodder & Stoughton, 2016.
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High flavour low fat. Paddington, N.S.W: Jane Curry Publishing, 2003.
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Steven Raichlen's high-flavor, low-fat vegetarian cooking. New York: Viking, 1995.
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Shaw, Judith B. Raising low-fat kids in a high-fat world. San Francisco: Chronicle Books, 1997.
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Steven Raichlen's high-flavor, low-fat chicken. New York: Viking, 1996.
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Fitzpatrick, Wyatt Nancy, ed. Low-fat, high-flavor cookbook. Birmingham, AL: Oxmoor House, 1995.
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Updike, Earl F. The miracle diet: Easy permanent weight loss cookbook : fat free, cholesterol free, high fiber. Phoenix, AZ: Best Possible Health, 1995.
Find full textBook chapters on the topic "Hight fat Diet"
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Jackson, Richard L., Mark T. Yates, Constance A. McNerney, and Moti L. Kashyap. "Diet and HDL Metabolism: High Carbohydrate vs. High Fat Diets." In Advances in Experimental Medicine and Biology, 165–72. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1268-0_24.
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Higashida, Kazuhiko, and Mitsuru Higuchi. "High Fat Diet and Endurance Exercise Performance." In Sports Performance, 151–56. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55315-1_13.
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Hawley, John A., and Wee Kian Yeo. "Metabolic Adaptations to a High-Fat Diet." In The Encyclopaedia of Sports Medicine, 166–73. Chichester, UK: John Wiley & Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118692318.ch13.
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Zhang, Jianzhong, and Vay Liang W. Go. "High Fat Diet, Lipid Peroxidation, and Pancreatic Carcinogenesis." In Dietary Fats, Lipids, Hormones, and Tumorigenesis, 165–72. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1151-5_13.
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Farooqui, Akhlaq A. "Neurochemical Effects of Long Term Consumption of High Fat Diet." In High Calorie Diet and the Human Brain, 29–76. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15254-7_2.
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Hall Burton, Denise M., Miya Asato, and Charles Boucek. "High Fat Diet (I): No Juice For The Ketotic Kid." In A Case Approach to Perioperative Drug-Drug Interactions, 833–35. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-7495-1_186.
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Sethi, Pranshul, Tanu Chaudhary, Tejesvi Mishra, Aradhana Prajapati, and Sumit Kumar. "High-Fat Diet and Psychiatric Disorders: What Is the Interplay?" In Nutritional Neurosciences, 369–83. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-5021-6_16.
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Korach-André, Marion. "In Vivo Investigation of High-Fat Diet–Induced Hepatic Lipid Dysfunctions." In Methods in Molecular Biology, 109–19. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0704-6_12.
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Hatamipour, Mahdi, Tannaz Jamialahmadi, Mahin Ramezani, Sayyed Abolghasem Sajadi Tabassi, Luis E. Simental-Mendía, Mohammad Reza Sarborji, Maciej Banach, and Amirhossein Sahebkar. "Protective Effects of Curcumin Phytosomes Against High-Fat Diet-Induced Atherosclerosis." In Pharmacological Properties of Plant-Derived Natural Products and Implications for Human Health, 37–44. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64872-5_4.
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Heber, David. "Interrelationships of High Fat Diets, Obesity, Hormones, and Cancer." In Dietary Fats, Lipids, Hormones, and Tumorigenesis, 13–25. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1151-5_2.
Full textConference papers on the topic "Hight fat Diet"
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Novita, Risqa, and Sehatman. "The study of glucose and hight-fat diet administration on male sprague Dawley rats." In INTERNATIONAL CONFERENCE ON BIOINFORMATICS AND NANO-MEDICINE FROM NATURAL RESOURCES FOR BIOMEDICAL RESEARCH: 3rd Annual Scientific Meeting for Biomedical Sciences. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5109996.
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Thomas, David, Emma Bermingham, Mark Roberts, and Wayne Young. "An investigation into the effect of high fat and carbohydrate diets on a range of biomarkers associated with pancreatitis in dogs." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/uvdt4784.
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Studies suggest that dogs preferentially choose fat as their major dietary energy source (59-63% of the total metabolisable energy (ME) content of the diet). However, high fat diets have been linked to the development of pancreatitis in dogs. This study investigated several biomarkers associated with pancreatitis in dogs fed either a high fat (HF; Protein: Fat: Carbohydrate content; 35%:63%:2% ME; n= 10 dogs) or high carbohydrate (HC; Protein: Fat: Carbohydrate content; 17%:32%:51% ME) diet.A high fat meal tolerance test (MTT) was undertaken on dogs (n=20) at baseline consuming a commercial dry food diet (Protein: Fat: Carbohydrate content; 23%:25%:52% on an ME basis) and then again after 8 weeks consuming either a HF (n=10) or HC (n=10) diet. Briefly, after an overnight fast, dogs were fed a single meal containing 100% of their daily requirements (P: F: C content; 35%:63%:2% ME). Each dog was then blood sampled 1, 2, 3, 4, 5, 6, 12, and 24 hours post-prandially. Samples were analysed for plasma triglycerides and markers of pancreatitis (i.e., pancreatic lipase, endotoxin, C-reactive protein, Interleukin 1-alpha, Interleukin 6 and Tumour necrosis factor-alpha). The postprandial peak plasma concentration of triglycerides (Cmax) were higher (p less than 0.001) at baseline, compared to after feeding of the either the HC or HF diets for 8 weeks. This suggests dietary components such as moisture level, specific ingredients, level of diet processing, and possibly apparent nutrient digestibility were potential factors driving this response. There was no effect of feeding either HF or HC diets on Cmax values (P >0.05) during the final MTT. This study suggests that feeding a HF diet for 8 weeks does not elevate blood markers associated with pancreatitis, with the serum biochemistry and complete blood count indicating the dogs remained clinically healthy.
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Bukowski, Michael, Brij Singh, James Roemmich, and Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.
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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.
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Angelotti, Austin, Rachel Cole, Amy Webb, Maciej Pietrzak, and Martha Belury. "Diet-induced Gene Expression Changes of Cachectic Muscle, Adipose, and Liver." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/gvbe2596.
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Cancer cachexia is a systemic disease characterized by muscle and adipose loss that cannot be reversed by increasing caloric intake. Our previous research has shown insulin resistance precedes cancer cachexia in the C26 mouse model of cachexia, and a diet high in linoleic acid, the essential omega-6 polyunsaturated fatty acid, attenuates the C26-induced insulin resistance. Therefore, to better understand how dietary linoleic acid is improving insulin sensitivity, we characterized gene expression changes in three major tissues responsible for controlling insulin sensitivity: skeletal muscle, adipose, and liver. To do this male CD2F1 (Charles River, MA) were randomized to semi-purified diet (24% fat by weight) containing fat prominently from lard, or containing fat prominently from safflower oil (a linoleic acid-rich oil). One week after diet randomization, mice were inoculated with colon-26 (C26) adenocarcinoma cells (1.0E6 cells). 13 days after inoculation mice were euthanized and gastrocnemius skeletal muscle, epididymal white adipose tissue, and liver tissue were collected for total transcriptome analysis using poly-A enriched next generation RNA-sequencing. Differentially expressed genes were selected based on p-values < 0.05. There were no detectable differences in body weight or food intake between the two diets in mice with C26 tumors. Between the two diets 12 genes were differentially expressed in the muscle, while 57 genes were differentially expressed in the liver, and 314 genes were differentially expressed in adipose. A linoleic acid enriched diet had little effect on the skeletal muscle transcriptome but induced larger transcriptome changes in liver and adipose. This could suggest dietary linoleic acid increases insulin sensitivity through affecting metabolism in adipose and liver, rather than skeletal muscle. Determining these diet-induced transcriptome changes allows us to better target tissue-specific molecular mechanisms of linoleic acid in future research.
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Agouni, Abdelali, Duck Y. Lee, Assaad A. Eid, Yves Gorin, and Kumar Sharma. "The Protective Role of Sestrin2 in High Fat Diet-Induced Nephropathy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0134.
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Introduction: Obesity is a major risk factor for type-2 diabetes predisposing patients to diabetic nephropathy (DN), the leading cause of end-stage renal failure. Glomerular injury is a prominent pathological feature of DN. Sestrin2 (Sesn2) is a stress-induced protein, but its role in DN has not been investigated. Therefore, we have determined the impact of Sesn2 deletion in a mouse model of obesityinduced nephropathy. Materials and methods: We examined the effects of Sesn2-deficiency in a longterm (22 weeks) mouse model of high fat diet (HFD)-induced obesity on glomerular structure. The severity of renal injury and fibrosis in wild type (Sesn2+/+) mice (fed HFD or chow diets) was compared to that in Sesn2-deficient mice (Sesn2-/- ) fed HFD or chow diets. Animal work was carried out under an IACUC-approved protocol. Results: Data showed that Sesn2 ablation exacerbated HFD-induced glomerular fibrotic injury as evidenced by mesangial matrix hypertrophy and accumulation of both fibronectin and collagen IV. Western blot analysis revealed that HFD- or chow-fed Sesn2-/- mice exhibited higher protein expression of key lipogenic enzymes, fatty acid translocase CD36 (an indicator of lipid uptake), fatty acid synthase and ATP citrate lyase. Sesn2-deficiency in obese mice resulted in podocyte loss as indicated by reduced expression of synaptopodin. Glomerular lesions like those observed in HFD-fed wild-type mice were detected in Sesn2-/-mice fed a chow diet, indicating that the basal deletion of Sesn2 is deleterious by itself. Conclusions: We provide the first evidence that Sesn2 is renoprotective in obesity-induced nephropathy by diminishing lipid accumulation and blocking excessive lipid uptake and de novo lipid synthesis. Understanding the protective of Sesn2 should yield novel therapeutic interventions to effectively preserve glomerular function in obesity and diabetes.
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Sherrod, Brandon, Shawn Gilbert, Krista Casazza, and Alan Eberhardt. "Design of a Torsion Tester for Measuring Murine Bone Properties for Studies on the Effects of Diabetes and Obesity." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14412.
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Conditions such as diabetes and obesity have been found to affect the mechanical integrity of bone. Studies have shown that diabetic rodent models exhibit lower levels of new bone formation during fracture healing 1, lower bone mineral density (BMD) 2, and increased risk of fracture 3. There are differences, however, in the bone integrity of bone samples from type I and type II diabetics, which is most likely due to obesity 2. Findings from research on obesity’s effects on bone integrity have been controversial; although there is an increase in bone mineral density (BMD) with increasing body mass index (BMI) and a decrease in fracture incidence in the central body regions in obese women compared to healthy weight women due to soft tissue padding, there is an increase in fracture incidence at extremeties 4. Other studies have shown that while cortical bone strength may not be adversely affected by high-fat diets, cancellous bone BMD and mechanical strength was significantly lower in high-fat diet mice than low-fat diet mice 5. In addition, extreme obesity has been associated with lower BMD despite the general trend of increased BMD with higher BMI 6.
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Aluko, Rotimi. "Protein gelation enhances resistance to proteolysis and in vivo cholesterol-lowering ability of the indigestible proteins." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/ztlc7556.
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Cardiovascular diseases are leading causes of death globally with excessive levels of blood cholesterol being a major risk factor. A dietary approach towards reducing this health risk is the intake of foods enriched with indigestible proteins that bind cholesterol to minimize reabsorption from the gastrointestinal tract. However, the level of indigestible proteins in regular foods is low and normal dietary intake may not provide sufficient cholesterol-lowering effect. Therefore, the aim of this work was to utilize various processing techniques to enhance resistance of food proteins to proteolysis and facilitate recovery of large amounts of indigestible proteins, which was then incorporated into the diet of Sprague-Dawley rats. Various legume seed protein isolates were subjected to the following pretreatments: dry heat, wet heat, autoclave, gelation, and freeze-thaw (3 cycles). The pretreated isolates were digested with pepsin followed by pancreatin to obtain insoluble residue as the indigestible product, which was tested for in vitro bile acid-binding ability. Results showed that the indigestible proteins from gelled cowpea protein isolate (ICP) was most abundant (68% yield) and had strong bile acid-binding ability. The rats were fed high fat diets and divided into 4 groups of 6 each (3 males + 3 females): group 1 was 20% casein diet while groups 2, 3 and 4 consumed same diets but casein was partially substituted with 1% ICP, 5% ICP, and 5% undigested cowpea protein isolate (CPI), respectively. After feeding for 6 weeks, rats that consumed the diet containing 5% ICP had the lowest increase in plasma total cholesterol of 1.8 mmol/L when compared to increases of 9.34 and 4.15 mmol/L for CPI and casein only diets, respectively. Analysis of the fecal matter by gel electrophoresis confirmed the presence of a high molecular proteins in the ICP-containing diets but absent in the casein only and CPI diets.
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Russo Heinrichsen, Erilynn, and Gabriel G. Haddad. "Fat Flies: Interaction Between High Fat Diet And Hypoxia In Drosophila." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2471.
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TSUJI, TAKAO, Ashley M. Houghton, Adriana S. Leme, Atsushi Nagai, and Steven D. Shapiro. "High Fat Diet Ameliorates Cigarette Smoke-induced Weight Loss." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5436.
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Widhiyanti, Fitria, Yulia Lanti Retno Dewi, and Isna Qodrijati. "Fad Diets and Other Factors Affecting the Risk of Chronic Energy Deficiency among Adolescent Females at The Boarding School." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.03.102.
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ABSTRACT Background: Women of reproductive need higher nutrition intake to obtain adequate levels of nutrition prepare for pregnancy and during their pregnancy. Inadequate nutrition intakes in pregnant women have been reported to lead to poor maternal and infant outcomes. This study aimed to investigate the effects of fad diets and other factors on the risk of chronic energy deficiency among adolescent females at the boarding school. Subjects and Method: A cross-sectional study was conducted at Islamic boarding school in Yogyakarta, Indonesia. A sample of 200 female adolescents aged 19-24 years was selected by simple random sampling. The dependent variable was CED. The independent variables were perception toward body image, calorie intake, protein intake, fad diet, stress, and knowledge toward nutrition. The data were collected by digital weight scale, microtoise, mid-upper arm circumference tape, and questionnaire. The data were analyzed by a multiple logistic regression run on Stata 13. Results: The risk of CED in female adolescents increased with negative body image (OR= 2.30; 95% CI= 1.02 to 5.18; p= 0.044), fad diet (OR= 3.94; 95% CI= 1.71 to 9.08; p= 0.001), and high stress (OR= 7.02; 95% CI= 2.93 to 16.83; p<0.001). The risk of CED decreased with high calorie intake (OR= 0.31; 95% CI= 0.14 to 0.69; p= 0.005), high protein intake (OR= 0.30; 95% CI= 0.11 to 0.83; p= 0.020), and high knowledge toward nutrition (OR= 0.43; 95% CI= 0.20 to 0.96; p= 0.038). Conclusion: The risk of CED in female adolescents increases with negative body image, fad diet, and high stress. The risk of CED decreases with high calorie intake, high protein intake, and high knowledge toward nutrition. Keywords: chronic energy deficiency, body image, fad diet Correspondence: Fitria Widhiyanti. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java, Indonesia. Email: fwidhiyanti@gmail.com. Mobile: +6282135793992. DOI: https://doi.org/10.26911/the7thicph.03.102
Reports on the topic "Hight fat Diet"
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Deng, Yingjun, ShengJing Liu, Ming Zhao, Feng Zhao, Jun Guo, and Bin Yan. Diet-induced male infertility in mice models: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0116.
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Review question / Objective: In order to compare the different high energy diet such as high-fat diet and high sugar diet how to damage the male mice model in metabolize and fertility,and explore a reliable mice model method in the study of obesity with male infertility. P：obesity mice model with male infertility. I: High energy diet such as High-fat or High-sugar diet. C:High-fat diet,High-sugar diet, compared with normal diet in mice model. O:High energy diet induce male mice obesity model and damage their fertility. S: Use network meta-analysis. Condition being studied: The relationship between obesity and male infertility attacth more and more attention at present.So many animal expriments are carried out on this problem,there are enough exprimental article to support this meta analysis.
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Ma, Jianming. Effect Evaluation of Transfat Decoction on Obesity Mice Induced by High-Fat Diet. Science Repository, April 2019. http://dx.doi.org/10.31487/j.jfnm.2019.01.01.
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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587723.bard.
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Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.
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Harn, Gam Lay. Urinary Protein Profile Changes in Diabetic Rats and Pre-diabetic Rats Fed with High Fat Diets. Biomedpress, 2019. http://dx.doi.org/10.15419/arr.2019.2.
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Jefcoate, Colin. Regulation of Tumor Cell Growth by the Mesenchymal Environment of the Bone Marrow is Enhanced by a High-Fat Diet. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470870.
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Kanner, Joseph, Mark Richards, Ron Kohen, and Reed Jess. Improvement of quality and nutritional value of muscle foods. United States Department of Agriculture, December 2008. http://dx.doi.org/10.32747/2008.7591735.bard.
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Food is an essential to our existence but under certain conditions it could become the origin to the accumulative health damages. Technological processes as heating, chopping, mincing, grounding, promote the lipid oxidation process in muscle tissues and meat foodstuffs. Lipid oxidation occurred rapidly in turkey muscle, intermediate in duck, and slowest in chicken during frozen storage. Depletion of tocopherol during frozen storage was more rapid in turkey and duck compared to chicken. These processes developed from lipid peroxides produce many cytotoxic compounds including malondialdehyde (MDA). The muscle tissue is further oxidized in stomach conditions producing additional cytotoxic compounds. Oxidized lipids that are formed during digestion of a meal possess the potential to promote reactions that incur vascular diseases. A grape seed extract (1% of the meat weight) and butylated hydroxytoluene (0.2% of the lipid weight) were each effective at preventing formation of lipid oxidation products for 3 hours during co-incubation with cooked turkey meat in simulated gastric fluid (SGF). Polyphenols in the human diet, as an integral part of the meal prevent the generation and absorption of cytotoxic compounds and the destruction of essential nutrients, eg. antioxidants vitamins during the meal. Polyphenols act as antioxidants in the gastrointestinal tract; they scavenge free radicals and may interact with reactive carbonyls, enzymes and proteins. These all reactions results in decreasing the absorption of reactive carbonyls and possible other cytotoxic compounds into the plasma. Consumptions of diet high in fat and red meat are contributory risk factors partly due to an increase production of cytotoxic oxidized lipid products eg. MDA. However, the simultaneously consumption of polyphenols rich foods reduce these factors. Locating the biological site of action of polyphenols in the in the gastrointestinal tract may explain the paradox between the protective effect of a highly polyphenols rich diet and the low bioavailability of these molecules in human plasma. It may also explain the "French paradox" and the beneficial effect of Mediterranean and Japanese diets, in which food products with high antioxidants content such as polyphenols are consumed during the meal.
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Comstock, Sarah. Examining the Effect of Maternal High-Fat Diet Consumption on the Physiology and Pancreas Development of Fetal and Juvenile Nonhuman Primate Offspring. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.551.
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Wang, Jiajie, Wei Huang, Yanji Zhang, Zhengrong Zhao, and Zhongyu Zhou. Acupuncture and related interventions for the treatment of obesity: protocol for a scoping review of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0099.
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Review question / Objective: The purpose of this study is to summarize the characteristics of RCT in the treatment of obesity by acupuncture and other related intervention measures, so as to enhance evidence-based clinical practice about acupuncture for obesity. Condition being studied: Obesity is a chronic metabolic disease that is defined as a body's excessive accumulation or abnormal distribution of total or local fat content. Their complications such as Type II diabetes mellitus, hyperlipidemia, and cardiovascular diseases are strongly related to higher risks of mortality. In recent years, with the changes in diet structure and living habits, 1.9 billion adults were overweight and over 650 million were obese according to the report by the WHO in 2016. Acupuncture is a characteristic therapy of traditional Chinese medicine, which is effective and safe for the treatment of simple obesity. In recent years, many RCTs using acupuncture in simple obesity were carried out within and outside of China. But currently, acupuncture treatment has no uniform standard, and there are a number of problems with this current clinical application of modern Chinese Medicine. Unfortunately, there is an absence of high-quality data supporting their use. This scoping review aims to summarize the characteristics of RCT in the treatment of obesity by acupuncture and other related intervention measures, so as to enhance evidence-based clinical practice about acupuncture and moxibustion for obesity.
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Mitchell, Brian G., Amir Neori, Charles Yarish, D. Allen Davis, Tzachi Samocha, and Lior Guttman. The use of aquaculture effluents in spray culture for the production of high protein macroalgae for shrimp aqua-feeds. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597934.bard.
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The FAO has projected a doubling in world demand for seafood during the 21 ed from aquaculture of marine fish and shrimps fed primarily on fishmeal-based aquafeeds. However, current practices of high intensity monoculture of shrimp in coastal ponds and fish in offshore pens have been strongly criticized as being ecologically and socially unsustainable. This view derives from un- checked eutrophication of coastal marine ecosystems from fish farm effluents, and the destruction of coastal estuarine ecosystems by shrimp farm constructions, plus aquaculture’s reliance on wild-caught small fish - which are excellent food for humans, but instead are rendered into fishmeal and fish oil for formulating aquafeeds. Fishmeal-sparing and waste- reduction aquafeeds can only delay the time when fed aquaculture product are priced out of affordability for most consumers. Additionally, replacement of fishmeal protein and fish oil by terrestrial plant sources such as soybean meal and oil directly raises food costs for human communities in developing nations. New formulations incorporating sustainably-produced marine algal proteins and oils are growing in acceptance as viable and practical alternatives. This BARD collaborative research project investigated a sustainable water-sparing spray/drip culture method for producing high-protein marine macrophyte meals for incorporation into marine shrimp and fish diets. The spray culture work was conducted at laboratory-scale in the USA (UCSD-SIO) using selected Gracilariaand Ulvastrains isolated and supplied by UCONN, and outdoors at pilot-scale in Israel (IOLR-NCM) using local strains of Ulvasp., and nitrogen/phosphorus-enriched fish farm effluent to fertilize the spray cultures and produce seaweed biomass and meals containing up to 27% raw protein (dry weight content). Auburn University (USA) in consultation with TAMUS (USA) used the IOLR meals to formulate diets and conduct marine shrimp feeding trials, which resulted in mixed outcomes, indicating further work was needed to chemically identify and remove anti-nutritional elements present in the IOLR-produced seaweed meals.
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Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.
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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.