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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regulation of energy metabolism in obesity may differ from normal condition in several respects. The synthesis of lipids may be enhanced due to a greater production of insulin, estrogens and cortisol and to a lack of dehydroepiandrosterone. Lipolysis is reduced in obese subjects by a decreased secretion of catecholamines, growth hormone, adipsin and cachectin. Inadequate intake of food and stress modify the T3/rT3 ratio. Oxidative phosphorylation and the production of ATP is modified, thermogenesis decreases due to a reduced synthesis of thermogenin. A decreased activity of substrate cycles and of the Na-K ATPase, is expected. Most of these disorders are normalized in post-obese patients. Many common drugs interfere with energy metabolism, namely those used in psychiatry and all hormones and their antagonists mentioned above and used for a long time. Obesity should not be considered as a simple result of overeating and lack of physical activity.
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PMID:[Energy metabolism in obesity]. 158 28

Reversal of myocardial biochemical changes with insulin treatment (4 and 8 wk) was studied in 8 and 12 wk streptozotocin (STZ)-diabetic rats. STZ-induced diabetes was characterized by elevations in blood glucose, serum cholesterol, and triglycerides and depressed serum insulin levels. Insulin treatment for 4 and 8 wk completely restored the serum alterations to control values. The polyuria, polydipsia, and polyphagia were also markedly diminished by the insulin treatment. Diabetic rats had pronounced decreases in body, heart, and left ventricular weights, all of which were completely reversed by the insulin treatment. Hydroxyproline accumulation in diabetic rat hearts was only reversed by the 8-wk and not by the 4-wk insulin treatment. STZ produced a significant depletion of left ventricular magnesium content as well as depression of K+-stimulated sarcoplasmic reticulum and myofibrillar ATPase activities. Both the 4- and 8-wk insulin treatment produced a complete recovery of the myocardial magnesium content. No significant changes in sarcolemmal Na+-K+-ATPase and K+-stimulated p-nitrophenyl phosphatase activities were observed in diabetic animals compared with control. The decreased latency of the lysosomal hydrolase, N-acetyl-beta-glucosaminidase, and the increased collagen deposition observed in the diabetic hearts were only partially reversed by the 4-wk insulin treatment, but completely reversed by the 8-wk treatment period.
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PMID:Insulin reversal of biochemical changes in hearts from diabetic rats. 294 95

Metabolic responses to 20 days of overeating were examined in five healthy volunteers. Overfeeding caused a variable increase (1-18%) in basal metabolic rate but no change in metabolic rate during light exercise. Postprandial resting metabolic rate was 8-40% higher (mean 18%) during overeating. The increase in oxygen consumption during a norepinephrine infusion was the same before (20 +/- 2%) and after (17 +/- 3%) overfeeding. Overfeeding elevated basal insulin concentrations in all subjects and increased the insulin response to intravenous glucose in four of five subjects. Overfeeding did not significantly alter mean serum T3 concentrations or erythrocyte 86Rb uptake (an index of Na+,K+-ATPase activity). These data do not confirm reports that overfeeding increases metabolic rate more during exercise than during rest. They also suggest that the increase in resting metabolic rate during overfeeding is not caused by increased responsiveness to norepinephrine or increased serum T3 concentrations.
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PMID:Some metabolic effects of overeating in man. 353 42

When normal mice have their usual chow diets supplemented by free access to a solution of 10% sucrose, their caloric intake increases by about 30%. We have used this model to explore the effects of sucrose overfeeding on Na,K-ATPase-mediated cation transport. After 5 days of sucrose supplementation, Na,K-ATPase mediated K uptake is increased by 88% in liver slices and 26% in intact soleus muscles of these animals. Ob/ob mice are hyperphagic on an ad libitum chow diet, and they display even greater increments in caloric intake than do thin controls when similarly allowed access to sucrose. Despite hyperphagia while on a chow diet, Na,K-ATPase-mediated K uptake by liver slices of ob/ob mice is not significantly different from that of their thin littermates. In addition, Na,K-ATPase-mediated K uptake into liver slices of ob/ob mice does not significantly increase while on sucrose supplements. These findings demonstrate the influence of dietary factors on Na,K-ATPase-mediated ion transport in liver and muscle of normal mice, and suggest that ob/ob mice may have an impairment in such dietary control. These observations suggest an important role for nutritional factors in the overall regulation of monovalent cation transport, and may also have relevance for our understanding of the cellular mechanisms of dietary thermogenesis.
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PMID:Effect of sucrose overfeeding on Na,K-ATPase-mediated 86Rb uptake in normal and ob/ob mice. 627 18

A high-fat diet easily promotes hyperphagia giving an impression of an uncontrolled process. Fat digestion itself however provides control of fat intake through the digestion itself, carried out by pancreatic lipase and its protein cofactor colipase, and through enterostatin, a peptide released from procolipase during fat digestion. Procolipase (-/-) knockout mice have a severely reduced fat digestion and fat uptake, pointing to a major role of the digestive process itself. With a normal fat digestion, enterostatin basically restricts fat intake by preventing the overconsumption of fat. The mechanism for enterostatin might be an inhibition of a mu-opioid-mediated pathway, demonstrated through binding studies on SK-N-MC-cells and crude brain membranes. Another target protein of enterostatin is the beta-subunit of F1F0-ATPase, displaying a distinct binding of enterostatin, established through an aqueous two-phase partition system. The binding of enterostatin to F1-ATPase was partially displaced by beta-casomorphin, a peptide stimulating fat intake and acting competitively to enterostatin. We frame a hypothesis that regulation of fat intake through enterostatin contains a reward component, which is an F1-ATPase-mediated pathway, possibly complemented with an opioidergic pathway.
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PMID:Enterostatin and its target mechanisms during regulation of fat intake. 1562 Oct 68