Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Defective BAT thermogenesis is associated with obesity in all the different types of obese animal so far studied. The deficit in normal energy expenditure may be presumed to contribute to the high metabolic efficiency and, together with the hyperphagia, to the obesity of these animals. In two types of obese animal (the ob/ob mouse, the db/db mouse) an increased propensity to become torpid provides an additional energy conserving mechanism that contributes to the high metabolic efficiency. In all these animals an abnormality of hypothalamic function appears likely. Obviously animals with induced hypothalamic lesions (the VMH-lesioned rat, the GTG-obese mouse) have an interruption in the normal pathway that links diet and the sympathetic innervation of BAT. The fa/fa rat resembles these animals in failing to activate BAT thermogenesis in response to diet: the lesion may lie in the hypothalamus itself or elsewhere in the food-intestine-hypothalamus-BAT axis, for example in intestinal peptide hormones. The ob/ob mouse has a peculiar hypothalamic defect that interferes with control of thermogenesis in BAT as well as impairing or exaggerating some aspects of thermoregulation. The db/db mouse resembles the ob/ob mouse but, since the defect is genetically distinct, presumably has a different lesion at the molecular level.
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PMID:Defective brown adipose tissue thermogenesis in obese mice. 406 36

Neuropeptide Y (NPY) is a neurotransmitter associated with feeding and obesity. We have constructed an NPY transgenic mouse model (OE-NPY(DBH) mouse), where targeted overexpression leads to increased levels of NPY in noradrenergic and adrenergic neurons. We previously showed that these mice become obese on a normal chow. Now we aimed to study the effect of a Western-type diet in OE-NPY(DBH) and wildtype (WT) mice, and to compare the genotype differences in the development of obesity, insulin resistance, and diabetes. Weight gain, glucose, and insulin tolerance tests, fasted plasma insulin, and cholesterol levels were assayed. We found that female OE-NPY(DBH) mice gained significantly more weight without hyperphagia or decreased activity, and showed larger white and brown fat depots with no difference in UCP-1 levels. They also displayed impaired glucose tolerance and decreased insulin sensitivity. OE-NPY(DBH) and WT males gained weight robustly, but no difference in the degree of adiposity was observed. However, 40% of OE-NPY(DBH) but none of the WT males developed hyperglycaemia while on the diet. The present study shows that female OE-NPY(DBH) mice were not protected from the obesogenic effect of the diet suggesting that increased NPY release may predispose females to a greater risk of weight gain under high caloric conditions.
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PMID:Diet-induced obesity in mice overexpressing neuropeptide y in noradrenergic neurons. 2311 73