Animal obesities.
Genetically or experimentally-produced (e.g. via lesions of the hypothalamus) obese animals have several common features such as increased hepatic lipogenesis (resulting in fat infiltration) and increased hepatic lipoprotein secretion, together, with increased adipose tissue lipogenesis. These abnormalities appear to be related primarily to hyperinsulinemia as they are reversed to or toward normal when hyperinsulinemia is corrected or, conversely, as they develop concomitantly with hyperinsulinemia. In the liver (ob/ob mice), another defect can be demonstrated, i.e. a decreased hepatic insulin clearance. This defect is also related to hyperinsulinemia and is markedly reduced upon normalizing hyperinsulinemia of obese mice. Hyperinsulinemia may thus be a key feature of the obesity syndromes, and bring about most of the abnormalities noted, including the subsequent state of insulin resistance known to exist in obese animals. The etiology of hyperinsulinemia of genetically obese animals is still unknown. Among the possible mechanisms one should cite possible primary dysfunction of the pancreas, possible primary dysregulation, by the hypothalamus, of overall endocrine pancreas activity.
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism; D007031:Hypothalamus / Q000293:injuries; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000503:physiopathology; D008099:Liver / Q000378:metabolism; D051379:Mice; D008820:Mice, Obese; D009765:Obesity / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D051381:Rats
D007328:Insulin; D005947:Glucose