Dissertations / Theses on the topic 'Obesity and metabolic disfunction'
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Bonacina, F. "ROLE OF THE LONG PENTRAXIN 3 (PTX3) IN CARDIOMETABOLIC DISEASES." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/353808.
Full textRahman, Olaiwola. "Metabolic studies in leanness and obesity." Thesis, University of Surrey, 1986. http://epubs.surrey.ac.uk/2728/.
Full textKempen, Kitty Petronella Gertruda. "Metabolic effects of weight cycling in obesity." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=6679.
Full textBoyle, Kristen E. Houmard Joseph A. "Metabolic inflexibility in skeletal muscle with obesity." [Greenville, N.C.] : East Carolina University, 2009. http://hdl.handle.net/10342/1904.
Full textPresented to the faculty of the Department of Exercise and Sports Science. Advisor: Joseph A. Houmard. Title from PDF t.p. (viewed Apr. 30, 2010). Includes bibliographical references.
Camerotto, C. "OBESITY AND METABOLIC SYNDROME: PLASMA LIPOPROTEINS ALTERATIONS." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/151781.
Full textPorras, Jordi Sanz. "Obesity surgery : an ethnography of metabolic im/balance." Thesis, Lancaster University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.662193.
Full textBenrick, Anna. "Cytokines in metabolic functions /." Göteborg : Section of Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 2008. http://hdl.handle.net/2077/9608.
Full textLaPensee, Christopher Ryan. "METABOLIC FUNCTIONS OF PROLACTIN IN THE MOUSE." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1172587296.
Full textBerg, Erika L. "Endocrinology of equine metabolic pathophysiology." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4472.
Full textThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 31, 2007) Includes bibliographical references.
Juanola, Falgarona Martí. "Glycemic index in the management of Obesity and Metabolic syndrome." Doctoral thesis, Universitat Rovira i Virgili, 2014. http://hdl.handle.net/10803/319948.
Full textLa obesidad y el síndrome metabólico (SMet) son una de las principales causas de la mortalidad a nivel mundial. El índice glucémico (IG) i la carga glucémica (CG) han estado asociados a un mayor riesgo de obesidad, diabetes tipo 2, SMet y enfermedades cardiovasculares. Actualmente la evidencia científica sugiere posibles beneficios del IG/CG para la prevención y tratamiento de la obesidad y SMet. Nuestro objetivo fue analizar la asociación entre el IG/CG de la dieta y el riesgo de desarrollar SMet i sus componentes, además de analizar la relación del IG/CG y marcadores de inflamación periféricos. Por otro lado, analizamos la efectividad de una dieta de alto IG/CG contra una dieta baja en IG/CG y una dieta baja en grasa sobre la pérdida de peso i la mejora del perfil metabólico, a través de la modulación de mecanismos relacionados con la saciedad, la inflamación y otros marcadores metabólicos. Esta tesis se ha realizado dentro del marco del estudio PREDIMED, una ensayo clínico nutricional, multicéntrico i aleatorizado; y el estudio GLYNDIET, un ensayo clínico en paralelo, aleatorizado y controlado de 6 meses de duración. Los resultados obtenidos muestran como las dietas de alto IG/CG podrían jugar un papel importante en el desarrollo del SMet y alguno de sus componentes. Además, el consumo de estas dietas también podría modular algunos marcadores cardiometabólicos que contribuyen a la ganancia de peso y al desarrollo de enfermedades cardiovasculares. Finalmente, observamos como el consumo de una dieta de bajo IG y una moderada cantidad de carbohidratos era más efectiva para la pérdida de peso y la mejora de la sensibilidad y la resistencia a la insulina que una dieta de alto IG y una moderada cantidad de carbohidratos o una dieta baja en grasa.
Obesity and Metabolic Syndrome (MetS) are one of the main causes of disability and death worldwide. It has been proposed that high glycemic index (GI) and high glycemic load (GL) diets are associated with increased risks of obesity, type 2 diabetes mellitus, MetS and cardiovascular disease. To date, evidence suggests possible benefits of the GI/GL for the prevention and management of obesity and MetS. We aimed to analyze the association between dietary GI and GL and the risk of to develop MetS and its features, as well as, the relationship between dietary GI and GL, peripheral adipokines and inflammatory markers. Also, we aimed to analyze the effectiveness of a high GI/GL diet versus a low-GI/GL and a low-fat diet in body weight loss and the improvement of metabolic profile, through the modulation of some mechanisms related to satiety, inflammation and other metabolic risk markers. This thesis has been conducted in the framework of the PREDIMED Study, multicenter randomized nutrition trial, and the GLYNDIET study, a 6-month randomized, parallel, controlled clinical trial. Our results suggest that high dietary GI and GL have a potential role in the development of MetS and some of its components. The consumption of diets with high-GI foods or high dietary GL may also modulate some cardiometabolic markers thus contributing to weight gain and cardiovascular disease. Finally, we found that a moderate-CH low-GI diet may be more effective for weight loss than a moderate-CH high-GI diet or a conventional low-fat diet. The metabolic benefits observed for insulin resistance and sensitivity in those subjects following a low-GI diet, and the tendency to improve other inflammatory and associated metabolic risk markers, also indicate that low-GI diets are better tools for managing obesity and its associated comorbidities.
Vartiainen, J. (Johanna). "Ghrelin, obesity and type 2 diabetes:genetic, metabolic and epidemiological studies." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514290657.
Full textTiivistelmä Greliini on peptidihormoni, jolla on osoitettu olevan anabolisia vaikutuksia. Se voimistaa kasvuhormonin eritystä, toimii ruokahalua ja ravinnonottoa lisäävänä signaalina, vähentää rasvahappojen käyttöä energian lähteenä ja lisää rasvakudoksen määrää. Lisäksi greliinillä on osoitettu olevan vaikutuksia sokeriaineenvaihduntaan, sydämen toimintaan ja tulehduksellisiin prosesseihin. Näiden ominaisuuksiensa ansiosta greliinistä on tullut tärkeä tutkimuskohde lihavuuteen ja sen liitännäissairauksiin, kuten verenpainetautiin, tyypin 2 diabetekseen ja ateroskleroosiin liittyvässä tutkimuksessa. Tässä väitöskirjatutkimuksessa oli tavoitteina etsiä uusia geneettisiä poikkeamia greliiniä ja greliinireseptoria koodaavista geeneistä ja tutkia löytyneiden poikkeamien kytkeytymistä lihavuuteen sekä ateroskleroosin aineenvaihdunnallisiin riskitekijöihin. Tavoitteina oli myös selvittää geneettisten- ja ympäristötekijöiden roolia greliinipitoisuuksien säätelyssä. Lisäksi greliinipitoisuuksien yhteyttä tyypin 2 diabetekseen ja sokeriaineenvaihdunnan häiriöihin tutkittiin seurantatutkimuksessa. Greliinireseptorin geenin eksoneista löytyi viisi ja greliinigeenin 5´reunustavilta alueilta yksitoista yhden nukleotidin geneettistä poikkeamaa. Löytyneillä greliinireseptorin geenin poikkeamilla ei havaittu olevan yhteyttä plasman IGF-1 pitoisuuksiin, mutta kahdella niistä oli yhteyttä insuliini- ja/tai lipidiaineenvaihduntaan liittyviin muuttujiin. Greliinigeenin 5´reunustavan alueen geneettiset poikkeamat eivät liittyneet plasman greliinipitoisuuksiin, mutta yhdellä variaatiolla oli yhteyttä kehon painoindeksiin. Kaksostutkimukimuksissa greliinipitoisuudet olivat korkeammat hoikilla kaksosilla verrattuna lihaviin kaksospareihinsa, huolimatta samasta geeniperimästä. Seurantatutkimuksen alussa mitatut seerumin greliinipitoisuudet eivät ennustaneet tyypin 2 diabeteksen tai muun sokeriaineenvaihdunnan häiriön ilmaantumista. Yhteenvetona voidaan sanoa, että tutkimuksessa löytyneet greliinireseptorin geneettiset poikkeamat saattavat liittyä sokeri- ja rasva-aineenvaihduntaan, mutta eivät niinkään muihin tunnettuihin ateroskleroosin riskitekijöihin. Yksi greliinigeenin variaatioista näyttäisi liittyvän lihavuuteen. Tutkimukset osoittavat, että geneettiset tekijät säätelisivät plasman greliinipitoisuutta vähemmän kuin hankittu lihavuus. Lisäksi serumin greliinipitoisuuksilla ei ole merkittävää ennusteellista arvoa tyypin 2 diabeteksen ilmaantuvuuden suhteen
Gemert, Wilhelmus Gerardus van. "Surgical treatment of morbid obesity technical, psychosocial and metabolic aspects /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=8566.
Full textScott, William Robert. "Investigation of molecular mechanisms underlying obesity and related metabolic disturbances." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/54837.
Full textPetry, Clive John. "Metabolic consequences of intrauterine growth retardation combined with adult obesity." Thesis, University of Cambridge, 1998. https://www.repository.cam.ac.uk/handle/1810/270434.
Full textRetallick, Christopher. "Arterial stiffness, obesity and metabolic syndrome in children and adolescents." Thesis, University of South Wales, 2012. https://pure.southwales.ac.uk/en/studentthesis/arterial-stiffness-obesity-and-metabolic-syndrome-in-children-and-adolescents(cd768264-d8af-45ba-b858-285979d05ba2).html.
Full textGriesemer, Rebecca. "Index of central obesity as a parameter to evaluate metabolic syndrome for white, black, and hispanic adults in the United States." unrestricted, 2008. http://etd.gsu.edu/theses/available/etd-07232008-232710/.
Full textTitle from file title page. Ike Okosun, committee chair; Richard Rothenberg, Rodney Lyn, committee members. Electronic text (73 p.) : digital, PDF file. Description based on contents viewed November 25, 2008. Includes bibliographical references (p. 69-73).
Chen, Pin-Yen. "Identification of biomarkers for obesity with metabolic syndrome using machine learning models." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/401351.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Liddell, Mary Katherine. "Nrf2 in metabolic related inflammation in the brain." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/071665a4-1d42-450c-ad49-854ead5d6814.
Full textLuo, Jing. "Exploring the metabolic role of GPR30 in mice." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/101091.
Full textDoctor of Philosophy
Azmi, Shazli. "Longitudinal studies in metabolic neuropathies : development of imaging biomarkers." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html.
Full textOates, Christie S. "Psychological and metabolic correlates of obesity in african-americans and caucasions /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Oates2006.pdf.
Full textMacLaren, Robin. "Metabolic hormones and their receptors in obesity: Insulin, Visfatin, and ASP." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32282.
Full textLe taux d'obésité et des maladies liées à celle-ci augmentent à une vitesse inquiétante. Aussi, la connaissance du mécanisme de régulation de certaines hormones anaboliques et de leurs récepteurs dans le tissu adipeux constitue une étape importante dans la compréhension du métabolisme lipidique. Cette thèse a pour but (i) d'étudier l'impact du traitement hormonal associé à la résistance à l'insuline et au métabolisme sur la régulation directe, in vitro, de la visfatine et du C5L2 en utilisant des modèles de 3T3-L1 préadipocytes et des adipocytes, et (ii) d'explorer, en utilisant des techniques de micro puces à ARN, la régulation de plusieurs gènes impliqués dans la résistance à l'insuline et dans la fonction de l'ASP, ex vivo, dans des tissus adipeux humains provenant de dépôts sous-cutanés (SC) versus omental (OM) extraits de sujets minces et de sujets atteints d'obésité morbide. Nos travaux ont démontré que le traitement à l'insuline, le TNFa, la progestérone, l'oléate, le palmitate et le traitement au TZD rosiglitizone régulent directement l'expression des ARNm de la visfatine dans les 3T3-L1 préadipocytes et/ou adipocytes. De plus, dans les tissus adipeux humains ex vivo, nous avons noté une régulation préférentielle des gènes impliqués dans la signalisation par l'insuline, surtout dans le tissu adipeu omental de sujets atteints d'obésité morbide et ayant des taux d'insuline et de glucose relativement plus élevés. Par contre, les changements touchant la signalisation ASP-C5L2 se trouvent dans le tissu adipeux sous-cutané. Cette étude nous a permis de déterminer la présence du C5L2 dans les tissus adipeux humains
Kyrou, Ioannis. "Impact of obesity and metabolic syndrome on morbidity, inflammation and adipokines." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/55046/.
Full textAnhê, Fernando Forato. "The effects of polyphenol-rich extracts on obesity-linked metabolic diseases." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/32471.
Full textL'obésité et son large spectre de maladies associées ont atteint des proportions pandémiques inquiétantes, soulignant la nécessité d’identifier des stratégies alternatives afin de lutter contre ce problème. À ce titre, les régimes riches en fruits et légumes représentent des déterminants bien établis d'une incidence plus faible de ces désordres métabolique. Grandement soutenus par des évidences épidémiologiques reliant les régimes riches en polyphénols et un meilleur état de santé, des efforts considérables ont été déployés afin d’étudier les bienfaits de ces métabolites secondaires des plantes. Malgré tout, les mécanismes par lesquels ces phytoéléments améliorent la santé métabolique demeurent encore mal compris, ce qui en justifie une étude plus approfondie. D’autre part, de plus en plus d’évidences indiquent que les bactéries intestinales exercent un important contrôle sur des aspects clés du métabolisme, et on comprend aujourd’hui que plusieurs phytoéléments de baies ont une biodisponibilité limitée, atteignant ainsi le colon qui abrite la plus vaste part du microbiote intestinal. Le travail présenté dans cette thèse vise donc à étudier l’impact de phytoéléments de baies sur le syndrome métabolique de souris soumises à une diète obèsogène et d’en comprendre le rôle du microbiote intestinal dans ces effets. En traitant quotidiennement ces animaux avec des extraits riches en polyphénols d'une gamme de baies aux compositions polyphénoliques variées, nous avons montré que les extraits les plus bioactifs (c.- à-d., canneberge, cloudberry, alpine bearberry, lingonberry et camu camu) partagent la capacité de diminuer l'inflammation intestinale, l’entotoxémie métabolique, la stéatose hépatique et la résistance à l'insuline. L'analyse des populations microbiennes fécales par séquençage du gène 16S ARNr a révélé que l'état métabolique amélioré lié à l'administration de ces extraits était associé à un remodelage draconien du microbiote intestinal, marqué par une expansion d'Akkermansia muciniphila. Cette bactérie intestinale est fortement associée à un faible niveau d’adiposité chez l’humain et son administration à des souris obèses a été montrée suffisante pour renverser le syndrome métabolique. Par ailleurs, les résultats présentés dans cette thèse suggèrent que les polymères de polyphénols, à savoir les proanthocyanidines et les ellagitannins, pourraient bien être des iv molécules clés dans les effets bénéfiques observés, ouvrant la voie à plus de recherche en ce sens. L’ingestion régulière de ces polyphénols par la consommation de canneberges, de cloudberry, d'alpine bearberry, de lingonberry et de camu camu représentent donc une stratégie efficace pour la prévention de désordres métaboliques associés à l’obésité. Cet ouvrage ouvre ainsi à de nouveaux concepts mécanistiques, ciblant l’axe intestin-foie et le microbiote intestinal pour expliquer les effets bénéfiques des polyphénols sur la santé métabolique.
Obesity and its wide spectrum of associated diseases have reached worrisome pandemic proportions, underscoring the need for alternative strategies to fight this problem. Plant-rich diets are well-established determinants of a lower incidence of obesity-related diseases, and fruits are important components of these diets. Supported by strong epidemiological evidence linking polyphenol-rich diets and better health status, research has been focused on the potential health effects of these plant secondary metabolites, albeit the mechanisms by which these poorly bioavailable phytonutrients improve metabolic health remains are not yet fully understood. Since there is compelling evidence for a relationship between host metabolic control and the gut microbiota, the work presented in this thesis aimed to investigate the impact of polyphenol-rich berry extracts on features of the metabolic syndrome in diet-induced obese mice. The work presented in this thesis also focuses on the relationship between putative gut microbial alterations driven by dietary polyphenols and its relevance to host metabolism. By daily treating dietinduced obese mice with polyphenol-rich extracts of a wide range of berries (with varied polyphenolic concentration and composition) we demonstrated that the most bioactive extracts (i.e., cranberry, cloudberry, alpine bearberry, lingonberry and camu camu) shared in common the ability to dampen intestinal inflammation and bacterial lipopolysaccharide leakage to systemic circulation, findings associated with reduced hepatic steatosis and improved insulin resistance. 16S rRNA genebased analysis of fecal DNA revealed that the improved metabolic status linked to the administration of these polyphenolic extracts was associated with a drastic gut microbial remodeling, marked by a consistent bloom of Akkermansia muciniphila. This gut bacterium is strongly associated with leanness in humans and its administration to obese mice reversed features of the metabolic syndrome. The findings presented in this thesis suggest that polymers of polyphenols, namely proanthocyanidins and ellagitannins, may have a superior impact on the gut-liver homeostasis, supporting further research on these particular classes of phenolic phytonutrients. While bringing evidence that substantiate the regular consumption of sources of proanthocyanidins and ellagitannins as a strategy to prevent prevalent chronic diseases associated with obesity, this work provides novel mechanistic insights pointing to the gut-liver axis and the gut microbiota as primary targets of dietary polyphenols in order to improve metabolic health.
Fealy, Ciaran E. "Insulin resistance in Obesity: Targeting the Molecular Mechanisms of Metabolic Disease." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1460740841.
Full textWamil, Małgorzata. "Protective role of 11β-HSD1 inhibition in the metabolic syndrome and atherosclerosis." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3891.
Full textKarlsson, Berndt. "Metabolic disturbances in shift workers." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-242.
Full textBarr, Sarah Marie. "Origins and consequences of altered metabolic processes in obese pregnant women." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8827.
Full textFisher, Kimberly Denise. "Dietary manipulation causes childhood obesity-like characteristics in pigs." Thesis, Virginia Tech, 2011. http://hdl.handle.net/10919/36176.
Full textMaster of Science
Patel, Kishor Kantilal. "Physiological aspects of weight loss in obesity." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12052/.
Full textWOO, JESSICA GRAUS. "THE EPIDEMIOLOGY OF ADIPONECTIN DURING ADOLESCENCE: DEMOGRAPHIC, DEVELOPMENTAL, METABOLIC AND GENETIC ASSOCIATIONS." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1100808827.
Full textBailey, Swneke. "Genetic insights into obesity and its associated metabolic complications: a multiethnic perspective." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104623.
Full textL'obésité est devenue une des plus grandes menaces dans la santé publique, étant donné qu'elle est fréquemment co-reliée avec des facteurs de risque du diabète de type 2 (T2D) et de la maladie cardiovasculaire (CVD), et est donc associée à une mortalité accrue. Les facteurs génétiques représentent une partie substantielle de la variation phénotypique de l'obésité, ainsi que des facteurs de risque des maladies vasculaires qui y sont associés. Dans cette thèse, je décris l'identification de plusieurs variants génétiques communs qui prédisposent les porteurs aux complications associées à l'obésité. D'abord, je décris l'identification d'une variation commune dans le gène d'une protéine sécrétée par le tissu adipeux viscéral, visfatin, et démontre l'influence de ces variants sur la variation interindividuelle d'une insulinémie à jeun. Deuxièmement, je décris l'identification d'une interaction entre l'utilisation des thiazolidinediones une classe de médicaments anti-hyperglycémiques, et une variation génétique dans le gène nuclear factor of activated T-cells cytoplasmic component 2 (NFATC2) qui aboutit à l'œdème et potentiellement à l'insuffisance cardiaque congestive. Ensuite, en utilisant un échantillon de la population asiatique du Sud dans la découverte de gènes, j'identifie une nouvelle association entre la variation du gène dipeptidyl peptidase 4 (DPP4), une cible de la médication anti-hyperglycémique basée sur l'incretin, et les niveaux de l'apolipoprotéine B (apoB), un facteur de risque du CVD et un marqueur de la dyslipidémie associée à l'obésité. De plus, en utilisant des différences observées entre les Européens et les Asiatiques du Sud, j'ai pu identifier l'hétérogénéité dans l'association entre DPP4 et apoB causé par l'adiposité. Finalement, je décris une association entre la variation du gène sterol regulatory element binding protein 1 (SREBF1) et l'indice de masse corporelle (BMI) et démontre sa contribution potentielle aux différences de BMI observées parmi différentes ethnicités dans le monde entier. Je présente aussi des données qui suggèrent fortement que ces différences peuvent être dues à une récente sélection positive à ce locus dans des populations humaines. Les découvertes de cette thèse illustrent l'importance des variants génétiques communs dans la pathogenèse de l'obésité, ainsi que les complications qui s'y rattachent et mettent en évidence la régulation de glucose par le tissu adipeux comme étant une caractéristique sous-jacente importante.
Stewart, Frances Maria. "The impact of maternal obesity on vascular and metabolic function throughout pregnancy." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/426/.
Full textBell, J. A. "Metabolically healthy obesity : associations with physical activity, sedentary behaviour, and metabolic decline." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1472874/.
Full textYoung, Theron Kue Hing. "Human obesity and Arctic adaptation : epidemiological patterns, metabolic effects and evolutionary implications." Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:3eb31016-a6b9-49e8-a18e-04ad7fdfdff6.
Full textSharma, Vishakha. "Aging and Gender Effects in Diet-Induced Obesity and its Metabolic Sequelae." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1522320845867142.
Full textVirtue, Anthony Thomas. "The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/276607.
Full textPh.D.
The global incidence of overweight and obese individuals has skyrocketed in the past few decades resulting in a new health epidemic. In 1980, 5% of males and 8% of females were categorized as obese; by 2008 these values doubled equating to half a billion adults worldwide. This surge of overweight and obese individuals has driven a dramatic increase in people afflicted with metabolic disorders. As such, the term "metabolic syndrome" (MetS) has been coined to describe several interrelated metabolic risk factors which often present in concert. Specifically, metabolic syndrome refers to the presence of at least three of the following five conditions: central obesity, elevated triglycerides, diminished high density lipoprotein (HDL) cholesterol, hypertension, and insulin resistance (IR). MetS is a major health concern due to its ability to increase the likelihood of cardiovascular disease (CVD), diabetes, and other life-threatening ailments. In light of this growing medical epidemic, we have concentrated our efforts in evaluating the role of microRNA-155 (miR-155) in MetS development. MicroRNAs are a newly defined class of small, non-coding RNA which contain the unique ability to regulate gene expression through RNA interference. As a result of this ability, microRNAs can mediate a wide variety of cellular processes. In order to evaluate the function of miR-155 in MetS, we established a novel miR-155-/-/ApoE-/- (DKO) mouse model. Coupling this model with the use of normal rodent or high fat diets allowed us to investigate how states of caloric balance and surplus affected the manifestation of the individual MetS components. We found that male and female DKO mice fed a high fat diet had significantly augmented body masses of 18% and 10% respectively, when compared to ApoE-/- counterparts on the same diet. Evaluation of this phenotype with body composition analysis revealed an 18% and 46% increase in body fat percentage among the male DKO mice on normal and high fat diets, respectively. This trend was also observed in female DKO mice, albeit to a lesser extent. This phenotype was further substantiated by the observation of augmented gonadal white adipose tissue pad mass within male and female DKO mice fed either chow. This equated to a 43% and 112% increase in male mice and a 45% and 57% augmentation in female mice for normal and high fat chow diets, respectively. In light of our findings, we also evaluated how miR-155 impacted glucose and insulin sensitivity. We found levels of insulin to be augmented by 181% and 148% in male DKO mice on normal and high fat diets, respectively. Furthermore, we found these mice to be euglycemic. These observations suggest that DKO mice are IR but capable of compensating for their insensitivity with elevated insulin production. Due to the tight association between MetS and the development of non-alcoholic fatty liver disease (NAFLD) as well as CVD, we felt it prudent to investigate the manifestation of these conditions. We found elevated hepatic mass of 40% and 13% in male and female DKO mice on high fat chow. Furthermore, hepatic discoloration was seen in these mice prompting us to perform in-depth histological evaluation which revealed widespread steatosis, a hallmark of NAFLD. Meanwhile, investigation of atherosclerosis, the key underlying cause of most CVDs, unexpectantly revealed diminished development. Due to the complex nature of atherosclerosis it is tough to explain the exact reason for this observation. Independent reports have shown that miR-155 plays a critical role in the development, maturation, or activation of B-cell, T-cells, macrophages, and dendritic cells. As a result, decreased immune cell infiltration may be the root cause for the observed decline in atherosclerosis. Taking into account our observations of obesity, IR, and NAFLD in conjunction with independent findings of blood pressure mitigation by miR-155, we feel confident in reporting that miR-155 is a vital factor in preventing MetS and NAFLD development. Despite this, we surprisingly found atherosclerosis development to be diminished in these mice suggesting a pro-inflammatory role in atherogenesis. This duality highlights the complex and ambiguous nature of miRNAs. In light of this, further evaluations should be conducted to gain additional insight into these pathologies and hopefully the development of novel therapeutics.
Temple University--Theses
Nguyen, Long The. "The roles of SIRT1 in maternal obesity-induced metabolic disorders in offspring." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/18964.
Full textPreston, Kyle J. "Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/361365.
Full textPh.D.
Obesity and insulin resistance are characterized by elevated pro-inflammatory proteins in the blood and immune cell accumulation in the visceral adipose tissue. Resident leukocytes release tumor necrosis factor α (TNFα) and other inflammatory cytokines which stimulate adipocyte lipolysis, recruit leukocytes to adipose tissue, promote pro-inflammatory immune cell polarization, facilitate oxidative stress, and activate intracellular kinases which dull insulin signaling cascades in metabolic tissues. Immune cell mediated dysregulation of stromal and parenchymal cells has raised suspicion that insulin resistance is an immune disorder initiated by activated white blood cells with over-nutrition. Efforts to improve pathological metabolism by reducing inflammation have yielded mixed results in humans and animal models. The role of inflammation and immune cell accumulation in the visceral fat (VF) in the progression of insulin resistance remains presently debated. There is, however, a consensus that identifying the triggers for obesity and impaired insulin signaling is of the utmost importance. The goal of this report is to identify dietary fat absorption as a key initiator of inflammatory action and insulin desensitization which may be dampened by reducing immune cell accumulation in adipose tissue. To explore how lean, healthy organisms become obese and insulin resistant, we examined the inflammatory consequences of isocaloric but variable macronutrient loads in the VF of lean mice. Mice were administered single liquid meals composed of low-fat (10% fat) or high-fat (60% fat) diet and observed by intravital microscopy to quantify leukocyte-endothelium interactions in mesenteric postcapillary venules (MPCV) 1, 2, 3, and 4 hours after oral gavage. Leukocyte rolling and leukocyte adhesion were transiently elevated within 1 hour after feeding and returned to baseline levels 4 hours later. Endothelial cell surface expression of P-selectin (Psel), a rapidly activated cell adhesion molecule (CAM), confirmed that high-fat feeding induced Psel dependent leukocyte rolling through the VF microcirculation. Furthermore, leukocyte accumulation in the VF was modestly increased by a single high-fat meal (HFM). Repetitive high-fat diet (HFD) consumption for 24 hours prolonged elevated leukocyte-endothelium interactions and promoted neutrophil accumulation in the VF. The neutrophilic enzyme myeloperoxidase (MPO), a producer of the chlorinating agent hypochlorous acid, increased in abundance and activity in the VF of HFM fed mice. Elevated leukocyte-endothelium interactions, leukocyte infiltration, and MPO activity in VF were not observed in Psel deficient (Psel-/-) mice following lipid overload. To ascertain if MPO is required for sustained endothelial activation, leukocyte-endothelium interactions and leukocyte infiltration were monitored in high-fat fed MPO deficient (MPO-/-) mice. Similar to the Psel-/- mice, MPO-/- mice were protected from the inflammatory effects of high-fat feeding. Our data supports postprandial hyperlipemia as an inducer of transient and Psel dependent inflammatory reactions that are sustained by prolonged HFD consumption. To study whether early phase inflammatory interventions granted late phase metabolic improvements, wild-type (WT), Psel deficient (Psel-/-), and MPO deficient (MPO-/-) C57BL/6 mice were given ad libitum access to LFD (10% fat) or HFD (60% fat) for 12-16 weeks. All mouse groups given HFD became obese. Prolonged HFD consumption sustained elevated leukocyte-endothelium interactions in MPCVs and was accompanied by increased local and systemic TNFα in WT mice. High-fat fed WT mice were hyperglycemic, hyperinsulinemic, glucose intolerant, and insulin resistant compared to LFD fed controls. Psel-/- mice were protected from leukocyte-endothelium interactions as well as local and systemic TNFα accumulation despite extended HFD consumption. Surprisingly, high-fat fed Psel-/- mice were equally hyperglycemic, hyperinsulinemic, glucose intolerant, and insulin resistant as the inflamed, high-fat fed WT mice. MPO-/- mice were also protected from elevated systemic TNFα and gained slightly less weight than the other high-fat fed groups. While MPO-/- mice were hyperglycemic and glucose intolerant, they did have improved insulin stimulated glucose clearance. The data presented in this report demonstrates the pro-inflammatory nature of postprandial hyperlipemia and the insulin desensitizing nature of prolonged HFD consumption. Ablation of VF immune cell accumulation by Psel deletion is not sufficient for improving insulin signaling or glycemic control, which is consistent with prior reports. Deletion of MPO, however, did result in slightly less obesity and marginally improved insulin signaling. We conclude that while immune cell accumulation in the VF contributes to the progression of insulin resistance, it is not a prerequisite for metabolic pathology development.
Temple University--Theses
Ma, Man Chun John. "Genetic determinants of Metabolic Syndrome in Lyon Hypertensive rats." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/1987.
Full textKohlhaas, Kaylee Shevon. "Resveratrol: therapeutic role in metabolic and reproductive function in obese broodmares." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/23155.
Full textMaster of Science
Bell, Balyssa Bridget. "Hypothalamic mechanisms underlying the cardiovascular and metabolic actions of leptin." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6054.
Full textPrasai, Madhu Janina. "The effect of obesity on diurnal variation in cardiovascular and metabolic processes in a mouse model of diet-induced obesity." Thesis, University of Leeds, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.582132.
Full textCalay, Ediz Suha. "Cellular and Systemic Metabolic Adaptations to Energy Status." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11547.
Full textFava, Francesca. "Measurement of diet : microbiota intermetabolic syndromeactions relevant to obesity and the metabolic syndrome." Thesis, University of Reading, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486348.
Full textFalconer, Catherine. "The metabolic and environmental determinants of obesity in childhood : observational and interventional studies." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/945/.
Full textBloor, Ian David. "Inflammation and end-organ damage with obesity and gender." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12592/.
Full textFrappier, Alexandrine. "The Metabolic Syndrome and the Effects of Different Types of Exercise Modalities in Adolescents with Obesity: a HEARTY Study." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/31970.
Full textLean, M. E. J. "Brown adipose tissue in humans." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333609.
Full textMarini, Lisa Elizabeth. "Maternal Consumption of Sweeteners: A Possible Contribution to the Development of the Metabolic Syndrome in Offspring." Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1674100881&sid=3&Fmt=2&clientId=1509&RQT=309&VName=PQD.
Full text"Department of Physiology." Keywords: Maternal, Metabolic, Obesity, Sweeteners. Includes bibliographical references (p. 103-111). Also available online.