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)

Bilateral basomedial hypothalamic (BMH) electrolytic lesions in White Leghorn cockerels produced six main physiological categories characterized by typical sets of symptoms: 1) functional castration (FC); hyperphagia, obesity, occasional diabetes insipidus, involuted adenohypophysis, dwarfism, atrophied comb and testes, reduced hematocrit, reduced plasma testosterone and thyroid activity, involuted thymus and adrenal cortex and elevated liver fat and plasma triglycerides and free fatty acids. The FC birds demonstrated defective immune response for the first 12 to 16 wk post-surgery. 2) functional castration with large comb (FCLC); hyperphagia, obesity, transient diabetes insipidus, slight diminution of adenohypophy-seal weight with marked reduction in basophilic cell population, fully atrophied testes but only slight reduction in comb size and hematocrit, plasma testosterone levels between those found in the first category and the control. 3) obese with normal testes (ONT); hyperphagia, obesity, high level of plasma lipids, normal histological organization of the adenohypophysis, normal testes, semen production and comb size. The next three categories exhibited physiological syndromes identical to the former three categories except for food intake, which operationally could be defined as normal. A marked difference among the BMH-lesioned birds was found in sexual behavior when the FC birds completely lost their libido. None of the replacement therapy regimens caused complete rehabilitation from adiposity or restoration of reproductive traits. Lipoprotein lipase activity increased at an early stage postlesioning and preceeded the development of hyperphagia. Placement of BMH lesions in newly hatched chicks resulted in marked dwarfism and obesity without hyperphagia. The BMH-lesioned heavy breed White Rock cockerels exhibited a lesser degree of adiposity than the light White Leghorn birds. Removal of the olfactory bulbs and destruction of the septal area resulted in increased thyroid activity, with secondary hyperphagia without obesity. In a short-term study, administration of sodium pentobarbital to the BMH area resulted in increased feeding. Conversely, glucose administration to the same area suppressed feeding in satiated but not in food-deprived chickens.
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PMID:Role of the basomedial hypothalamus in regulation of adiposity, food intake, and reproductive traits in the domestic fowl. 267 24

Polygenic obese (M16) and nonobese (ICR) mice were fed ad libitum either a high-fat (FAT) or high-carbohydrate (CHO) diet from 6 to 10 weeks of age. After this four-week period, M16 exceeded (P less than 0.01) ICR mice and FAT-fed exceeded (P less than 0.01) CHO-fed mice in body energy percent, body fat percent, and weight and proportional weight of epididymal and subcutaneous fat pads. Fat cell size and number in both fat depots were greater (P less than 0.01) in the M16 than in the ICR line. Mice fed FAT had larger (P less than 0.01) fat cells in both depots compared with CHO-fed mice, but fat cell nuber was not altered significantly. M16 mice were hyperglycemic, hyperinsulinemic and hypercholesterolemic, Dietary treatment did not affect glucose or insulin levels, but cholesterol was greater (P less than 0.01) on FAT than on CHO diet. Lipoprotein lipase and fatty acid synthetase activities were greater in M16 than in ICR mice, while fatty acid synthetase activity was greater in mice fed CHO than in those fed FAT. Genotype by diet interactions were not important for the traits studied. Polygenic obese mice, developed by selection for increased growth rate, share many of the characteristics of the single gene obesity syndromes in rodents. The development of obesity in polygenic obese mice may be due, in part, to an acceleration of the normal developmental process of growth, in addition to hyperphagia and increased energetic efficiency.
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PMID:Adipose cellularity, serum glucose, insulin and cholesterol in polygenic obese mice fed high-fat or high-carbohydrate diets. 703 Aug 75

Mice overexpressing human UCP-3 in skeletal muscle (UCP-3tg) are lean despite overeating, have increased metabolic rate, and their skeletal muscle mitochondria show increased proton conductance. The true function of UCP-3 however, has yet to be determined. It is assumed that UCP-3tg mice have increased fatty acid beta-oxidation to fuel their increased metabolic rate. In this study we have quantified skeletal muscle mRNA levels of a number of genes involved in fatty acid metabolism. mRNA levels of uncoupling protein-2, carnitine palmitoyl transferase-1beta and fatty acid binding proteins, and transporters were unchanged when compared to wild-type mice. Lipoprotein lipase mRNA was slightly, but significantly, increased by 50%. The most notable change in gene expression was a threefold increase in mitochondrial thioesterase (MTE-1) expression. In the face of a chronic increase in mitochondrial uncoupling these changes suggest that increased flux of fatty acids through the beta-oxidation pathway does not necessarily require marked changes in expression of genes involved in fatty acid metabolism. The large increase in MTE-1 both confirms the importance of this gene in situations where mitochondrial beta-oxidation is increased and supports the hypothesis that UCP-3 exports fatty acids generated by MTE-1 in the mitochondrion.
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PMID:Overexpression of UCP-3 in skeletal muscle of mice results in increased expression of mitochondrial thioesterase mRNA. 1135 53