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Diabetes Mellitus --- Insulin

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Non-alcoholic steatohepatitis is the hepatic complication of the metabolic syndrome. Altered nutrition, resistance to insulin and decreased adiponectine levels may be implicated in its pathogenesis. The aim of this work was to examine the consequences of adiponectine deficiency on insulin resistance and hepatic lesions induced by a diet rich in saturated fatty acids and sugar, in mice.
Methods : male and female wild type C57 mice or deficient in adiponectin (KO) have been exposed to a diet rich in glucose and in saturated fatty acids (containing 60% of pork fat (HF/HG), or 58% of coconut oil (HFcoco/HG)). Fasting glycaemia, dynamic in vivo glucose tolerance tests and liver histology were analysed after 5 or 8 weeks of exposure to diet. Phosphorylation of ERK protein after intra-portal injection of insulin or PBS was assessed by western blot as an indicator of intrehepatic insulin signalling. It induced mild hepatic lipid overload without steatohepatitis. Experiments in younger mice, in females or using a diet enriched in coconut oil, richer in saturated fatty acids, gave similar results. Serum adiponectin was slightly increased in HF/HG-fed C57 male mice, suggesting that adiponectin may protect them from hepatic complications induced by such diet.
When fed the control diet, adiponectin KO mice have decreased glucose tolerance and exhibit signs of intrahepatic insulin resistance compared to C57 mice. Male KO mice fed the HF/HG diet gained more weight than C57 mice, but this regimen did not modify glucose tolerance, nor hepatic insulin resistance. Hepatic lesions in HF/HG-fed KO mice are extremely variable ranging from the absence of lesion (50%), to moderate steatosis (31.25%) and severe steatohepatitis (18.75%). Female KO mice fed the HF/HG diet develop more severe glucose intolerance, but had no hepatic morphological abnormities. However, the exposure of both male ad female adiponectin KO mice to HFcoco/HG diet induced more severe hepatic lesions compared to those induced in C57 mice. However, this was not paralleled by further impairment of glucose tolerance.
In conclusion, a diet rich in pork fat and glucose together with the absence of adiponectin is not sufficient to induce significant lesion of steatohepatitis. The association of a diet rich in coconut oil and glucose, with glucose intolerance results in significant and consistent hepatic steatosis on the absence of adiponectin La stéatohépatie non alcoolique est la complication hépatique du syndrome métabolique. L’augmentation des apports alimentaires, l’insulino-résistance et la diminution de l’adiponectine pourraient participer à la pathogenèse de cette maladie. L’objectif de ce mémoire est d’étudier le rôle de l’adiponectine sur l’insulino-résistance et les lésions hépatiques induites par une dite enrichie en glucose et en acides gras saturés chez la souris.
Méthodes : des souris sauvages C57 ou déficientes en adiponectine (mâles et femelles) ont été soumises à une diète enrichie en glucose et en acides gras saturés (soir 60%de graisse porcine (HF/HG), soit 58% d’huile de noix de coco (HFcoco/HG)). Nous avons évalué la glycémie à jeun, la tolérance au glucose par test dynamique in vivo et analysé l’histologie hépatique après 5 à 8 semaines de ce régime. L’insulino-résistance intra-hépatique a été évaluée par analyse de la phosphorylation de la protéine ERK en réponse à un bolus d’insuline (ou de PBS).
Chez les souris C57 mâles, la diète HF/HG induit une hyperglycémie à jeun, une intolérance glucidique modérée sans insulino-résistance intra-hépatique et entraîne une légère surcharge lipidique hépatique mais sans inflammation ni signes de lésions hépatocellulaires. Des résultats similaires sont obtenus quand la diète est administrée à des animaux plus jeunes, à des femelles ou quand la graisse porcine est remplacée par de l’huile de noix de coco. La discrète augmentation de l’adiponectine sérique pourrait protéger ces souris des conséquences métaboliques et hépatiques de telles diètes.
Les souris mâles déficientes en adiponectine sont moins tolérantes au glucose que les souris sauvages et ont une insulino-résistance intra-hépatique sous régime standard. La diète HF/HG induit une prise de poids plus importante que chez les souris C57 mais n’influence pas la tolérance au glucose, ni l’activité des voies de signalisation en réponse à l’insuline. Les lésions hépatiques sont extrêmement variables : 50% des souris ont un foie normal, 31.25% une stéatose légère et 18.75% une stéatohépatite sévère. Les souris KO femelles sous la diète HF/HG ont une intolérance glucidique plus marquée mais sans répercussion significative sur la morphologie hépatique. En réponse à une diète HFcoco/HG, les souris déficientes en adiponectine développent des lésions hépatiques plus sévères que les souris C57, tant chez les mâles que chez les femelles, mais ceci ne semble pas associé à une moindre tolérance glucidique que chez les C57.
En conclusion, une diète HF/HG combinée à l’absence d’adiponectine est insuffisante pour induire de façon homogène la stéatohépatite. L’association d’une diète HFcoco/HG, d’une intolérance glucidique et de la déficience en adiponectine induit une stéatose hépatique plus sévère

Adiponectin --- Insulin Resistance --- Mice --- Diet --- Carbohydrates --- Fatty Acids --- Fatty Liver

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Insulin --- Diabetes Mellitus --- therapeutic use --- drug therapy --- Diabetes --- Treatment --- Diabetes Mellitus. --- Diabetes. --- Insulin. --- therapeutic use. --- Brittle diabetes --- Diabetes mellitus --- IDDM (Disease) --- Insulin-dependent diabetes --- Ketosis prone diabetes --- Type 1 diabetes --- Hormones --- Hypoglycemic agents --- Pancreas --- Proinsulin --- Carbohydrate intolerance --- Endocrine glands --- Diabetic acidosis --- Glycosylated hemoglobin --- Diabetes Insipidus --- Glucose Intolerance --- Secretions --- Diseases --- Clinical Endocrinology

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This volume examines the problem of the overweight individual and the metabolic syndrome from the laboratory bench to the bedside. Clearly, translating the findings we make in the laboratory to the betterment of humankind is an important mission. Areas where basic science is making important contributions to the problems associated with metabolic syndrome are illustrated in the chapters on Neuroendocrine Control of Food Intake, Current Views of the Fat Cell as an Endocrine Cell: Lipotoxicity, and Ectopic Fat and Metabolic Syndrome. For each of these, the fast-moving basic science area is opening new vistas for translation to the bedside and clinic. The larger segment of the book deals with the clinical context for the metabolic syndrome, central adiposity and overweight. The methods for measurement are well described and the application of these methods to evaluating patients and determining the prevalence in society is indicated. Genetic components of overweight and the metabolic syndrome are reviewed. The key role of visceral fat is emphasized by giving it a chapter of its own written by one of the foremost investigators of this problem. The importance of overweight and the metabolic syndrome in children is recognized in a separate chapter. There are a number of chapters focusing on treatment including behavioral therapy, exercise, diet, medications and surgery. In summary, this book is the alpha and omega of the overweight and metabolic syndrome problem. Series editor comments: Drs. Bray and Ryan have assembled a superb panel of authors who bring their expertise to this very timely book for medical practice. The epidemic of obesity is addressed in authoritative and cutting edge chapters ranging from the fundamental genetics and physiology of appetite control through the latest pharmacologic applications and surgical interventions. This is a "must have" volume for those treating patients with appetite disorders, obesity and diabetes, as well as those studying the intrinsic cellular and whole body pathogenesis of this modern population disorder. Shlomo Melmed, M.D. Series Editor Endocrine Updates.

Obesity. --- Metabolic syndrome. --- Cardiovascular syndrome, Metabolic --- Dysmetabolic syndrome X --- Insulin resistance syndrome --- Metabolic cardiovascular syndrome --- Metabolic syndrome X --- Insulin resistance --- Metabolism --- Syndromes --- Adiposity --- Corpulence --- Fatness --- Overweight --- Body weight --- Nutrition disorders --- Disorders --- Endocrinology. --- Metabolic diseases. --- Biochemistry. --- Diabetes. --- Metabolic Diseases. --- Medical Biochemistry. --- Brittle diabetes --- Diabetes mellitus --- IDDM (Disease) --- Insulin-dependent diabetes --- Ketosis prone diabetes --- Type 1 diabetes --- Carbohydrate intolerance --- Endocrine glands --- Diabetic acidosis --- Glycosylated hemoglobin --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Biology --- Chemistry --- Medical sciences --- Disorders of metabolism --- Metabolic diseases --- Metabolic disorders --- Metabolism, Disorders of --- Diseases --- Internal medicine --- Hormones --- Composition --- Endocrinology . --- Medical biochemistry. --- Medical biochemistry --- Pathobiochemistry --- Pathological biochemistry --- Biochemistry --- Pathology

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The increasing prevalence of diabetes and obesity in western societies today makes these two diseases the leading epidemics of the 21st century. Closely linked with the development of serious complications, including cardiovascular disease and several malignancies, the morbidity and mortality associated with obesity and diabetes will continue to escalate as the population ages and becomes more sedentary. In Obesity and Diabetes, international experts from world-renowned medical schools comprehensively review for practicing clinicians and scientists alike the latest understanding of the epidemiology, causation, and consequences of diabetes and obesity. The authors discuss in detail their diagnosis, clinical manifestations, complications, and best practices for diagnosis and treatment. They also review the history and epidemiology of these conditions, explain their genetics and pathophysiology, and illuminate their known mechanisms and interactions. State-of-the-art survey-chapters critique current approaches (lifestyle and pharmacological) to the treatment of these conditions. Authoritative and up-to-date, Obesity and Diabetes offers a comprehensive review of the scientific and clinical aspects of obesity and diabetes, even while providing a powerful incentive to focus our public health efforts on prevention and our clinical efforts on treatment.

Diabetes. --- Obesity. --- Diabetes --- Obesity --- Complications. --- Medicine. --- Endocrinology. --- Medicine & Public Health. --- Internal medicine --- Hormones --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Brittle diabetes --- Diabetes mellitus --- IDDM (Disease) --- Insulin-dependent diabetes --- Ketosis prone diabetes --- Type 1 diabetes --- Carbohydrate intolerance --- Endocrine glands --- Diabetic acidosis --- Glycosylated hemoglobin --- Adiposity --- Corpulence --- Fatness --- Overweight --- Body weight --- Metabolism --- Nutrition disorders --- Diseases --- Disorders --- Complications and sequelae --- Endocrinology .