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)

Too often neglected, dosage of phosphatemia should yet be kept on mind. The role of phosphorus in bone mineralisation and regulation of acid-base balance is well known. Phosphorus is also an energy purveyor during numerous biologic reactions, and depp deprivation may lead to a lot of pathologic situations, sometimes severe. Mild hypophosphatemia is not rare and occurs in various clinical or therapeutic circumstances; deep hypophosphatemia is rather uncommon, occuring chiefly during hyperalimentation or realimentation of starving patients, especially alcoolics. Deep hypophosphatemia (by depletion or transfert) mainly induces clinical and pathological manifestations; they are subsequent to alterations of glucose metabolism, leading to a failure in ATP and 2,3 DPG synthesis. these metabolic events particularly explain muscular and hematological manifestations of hypophosphatemia. Phosphorus loading per os, or in severe cases intravenously corrects the biological abnormalities and improves clinical manifestations.
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PMID:[Hypophosphatemia (author's transl)]. 39 93

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

The effect of glucose hyperalimentation on energy metabolism in the cirrhotic rat liver after 70% hepatectomy was studied. After resection, rats received either 30 kcal/kg per day (group I) or 200 kcal/kg per day (group II) of glucose for 48 h. In both groups, hepatic mitochondrial ATP synthesis was accelerated when palmitic acid was used as substrate and suppressed when pyruvate was used. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose. Hepatic energy charge was within normal limits in group I, but decreased significantly in group II after hepatectomy. An abundance of glucose in the early postoperative period, therefore, caused a hepatic energy derangement by suppressing fatty acids utilization; this suppression was corroborated by the findings of lower immunoreactive glucagon and non-esterified fatty-acid concentrations in group II. To determine optimal glucose administration, the predicted value of glucose disposal rate (GDR) was calculated after an intravenous glucose tolerance test. GDR decreased significantly after hepatectomy and did not increase appreciably even with a large dose of insulin administration. These results suggest that glucose administration should be tailored to the GDR values after resection of the cirrhotic liver.
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PMID:Glucose overload and hepatic energy metabolism after resection of the cirrhotic liver in rats. 178 71

Too often neglected, dosage of phosphatemia should yet be kept on mind. The role of phosphorus in bone mineralization and regulation of acid-base balance is well known. Phosphorus is also an energy purveyor during numerous biologic reactions, and deep deprivation may lead to a lot of pathologic situations, sometimes severe. Mild hypophosphatemia is not rare and occurs in various clinical or therapeutic circumstances; deep hypophosphatemia is rather uncommon, occuring chiefly during hyperalimentation or realimentation of starving patients, especially alcoholics. Deep hypophosphatemia (by depletion or transfer) mainly induces clinical and pathological manifestations; they are subsequent to alterations of glucose metabolism, leading to a failure in ATP and 2,3 DPG synthesis. These metabolic events particularly explain muscular and hematological manifestations of hypophosphatemia. Phosphorus loading per os, or in severe cases intravenously corrects the biological abnormalities and improves clinical manifestations.
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PMID:[Hypophysphatemia (author's transl)]. 624 3

1,5-Anhydroglucitol (1-DG) has been known as an antimetabolic glucose analogue. Using gas chromatography, 1-DG was found to be physiologically present in rat serum. In order to investigate its direct and long-term effects on feeding, 1-DG was infused during the light period into the rat third ventricle in doses of 3.0, 6.0 and 12.0 mumol/rat. Its effects were then compared to those of similarly applied 2-deoxy-D-glucose (2-DG). Following initial hyperphagia, both of these glucose-analogues produced suppressive effects on feeding during the subsequent day throughout the light and dark periods. On the third day after 2-DG injection reduction of feeding did not recover completely to the pretreatment baseline levels, but it did recover after 1-DG. Both 1-DG and 2-DG caused linear dose-related hypophagia, with the slope for 1-DG being about half of that for 2-DG. It is suggested that the delayed hypophagia which followed the initial hyperphagia produced by deoxyglucose was a result of sustained inactivation of the Na-pump due to intracellular ATP deficiency caused by accumulation of deoxy-glucose-6-phosphate.
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PMID:Feeding suppression induced by intra-ventricle III infusion of 1,5-anhydroglucitol. 631 43

Clinical studies and experiments in rats were carried out to elucidate changes in fuel utilization after hepatectomy. In addition, the effect of glucose hyperalimentation on energy metabolism in the liver remnant was studied. Respiratory quotient (RQ) and substrate oxidation rate for fat and glucose were evaluated by indirect calorimetry in eight patients who had undergone liver resection. Patients had a reduced nonprotein RQ of approximately 0.85 and a reduced ratio of glucose to fat oxidation of approximately 2.0 on the 1st and 2nd postoperative days. After 80% hepatectomy, rats received either 30 kcal.kg-1.day-1 (group 1) or 200 kcal.kg-1.day-1 (group 2) of glucose for 48 h. In both rat groups, hepatic mitochondrial ATP synthesis 12 and 24 h after hepatectomy was accelerated when palmitic acid was used as the substrate and suppressed when pyruvate was used compared with sham-operated groups. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose, which seems to occur also in humans. Hepatic energy charge was within normal limits in group 1 (0.862 +/- 0.008) but decreased significantly in group 2 (0.818 +/- 0.006, p < 0.01) 12 h after hepatectomy. An abundance of glucose in the early postoperative period therefore caused a hepatic energy derangement by suppressing endogenous fat oxidation. This suppression was corroborated by the findings of lower immunoreactive glucagon and nonesterified fatty acid concentration in group 2. Therefore, glucose hyperalimentation in the early postoperative period after liver resection is not recommended.
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PMID:Fuel utilization and glucose hyperalimentation after liver resection. 781 53

The insulin receptor was evaluated at different disease stages in the sand rat (Psammomys obesus), a model for nutrition-induced diabetes. Nondiabetic sand rats showed markedly low receptor number in liver compared with albino rats. Their receptor had an intact tyrosine kinase activity but a higher Km for ATP in the phosphorylation reaction of exogenous substrates. The initial effects of overeating (i.e., development of hyperinsulinemia without hyperglycemia) were associated in the sand rat with a dramatic decrease in in vitro and in vivo insulin-induced receptor tyrosine kinase activity in both liver and muscle. In muscle, this coincided with a decrease in receptor number and an increase in basal tyrosine kinase activity. Similar changes were observed upon development of hyperinsulinemia with hyperglycemia. Upon recovery from the diabetic state by diet restriction, the impaired receptor kinase activation was corrected. Complete restoration occurred only in animals that fully recovered from the diabetic state and became normoinsulinemic. These observations indicate that loss and gain of receptor tyrosine kinase activity were dependent on insulin levels. Thus, overeating may lead to the development of hyperinsulinemia through ineffective extraction of excess insulin by the scarce liver receptors. Hyperinsulinemia, in turn, causes a reversible reduction in receptor kinase activity, leading to insulin resistance. This sequence of events may be relevant to diet-related changes in human non-insulin-dependent diabetes mellitus.
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PMID:Hyperinsulinemia induces a reversible impairment in insulin receptor function leading to diabetes in the sand rat model of non-insulin-dependent diabetes mellitus. 812 94

Hyperphagia and anovulation are both triggered by prior food deprivation or other treatments that decrease intracellular availability of metabolic fuels in most species studied. Syrian hamsters fail to show compensatory hyperphagia, but do show anestrus in response to these energetic challenges. In the present experiments, we examined food intake, plasma glucose levels, and estrous cyclicity in Syrian hamsters in response to 2,5-anhydro-D-mannitol (2,5-AM), a fructose analog that is thought to trigger eating in rats by depleting intracellular levels of ATP. In experiment 1, female estrous cycling hamsters were treated with 100, 200, 400, or 800 mg/kg 2,5-AM or the vehicle by intraperitoneal injection. Food intake was measured 1, 2, 4, 8, and 24 h after treatment. There were no statistically significant increases in food intake in response to any dose of 2,5-AM. In experiment 2, blood samples were drawn at 0, 1, 3, 5, 7, and 25 h after hamsters were treated with 0 or 400 mg/kg 2,5-AM. 2,5-AM treatment resulted in a mild but significant decrease in plasma glucose levels similar to those seen in 2,5-AM-treated rats, suggesting that 2,5-AM has similar effects on fuel metabolism in rats and hamsters. In experiment 3, hamsters received 2,5-AM, 2,5-AM plus the fatty acid oxidation inhibitor methyl palmoxirate, or vehicle every 6 h over the first 48 h of the estrous cycle and were tested for indexes of estrous cyclicity at the end of the cycle. All hamsters showed normal estrous cycles, regardless of treatment. If 2,5-AM has similar metabolic consequences in rats and hamsters, the present results suggest that decreased intracellular levels of ATP and mild hypoglycemia do not increase food intake or inhibit estrous cyclicity in Syrian hamsters.
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PMID:Effects of the fructose analog, 2,5-anhydro-D-mannitol, on food intake and estrous cyclicity in Syrian hamsters. 908 57

Energy supply from foods and drinks depends upon carbohydrate, protein, lipid and alcohol content. Cells obtain the energy through a complex and integrated system of physico-chemical processes. The energy value of foods is applied for ATP formation, but also for nutrient utilization and turnover. Net energy from foods is expended for basal metabolism, thermic effect of food and physical activity. Total energy expenditure for human beings is displayed in different lists developed by national and international organisms and institutions. Energy balance and body weight are narrowly interrelated as well as body composition, which depends also of age, sex, exercise and neuroendocrine status. Obesity, is known as an excessive deposition of fat for height, and it is associated with cancer, dislipemias, endocrine abnormalities, diabetes, etc. Recent advances suggest that genetic and neuroendocrine factors are more involved in obesity rather than gluttony or sloth as previously reported.
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PMID:[Nutrition, energy balance, and obesity]. 1042 Sep 25

Obesity has reached epidemic proportions and has become one of the major health problems in developed countries. Current theories consider obesity a result of overeating and sedentary life style and most efforts to treat or prevent weight gain concentrate on exercise and food intake. This approach does not improve the situation as may be seen from the steep increase in the prevalence of obesity. This encouraged us to reanalyse existing information and look for biochemical basis of obesity. Our approach was to ignore current theories and concentrate on experimental data which are described in scientific journals and are available from several databases. We developed and applied a Knowledge Discovery in Databases procedure to analyse metabolic data. We began with the contradictory information: in obesity, more calories are consumed than used up, suggesting that obese people should have excess energy. On the other side, obese people experience fatigue and decreased physical endurance that indicates diminished energy supply in the body. The result of our work is a chain of metabolic events leading to obesity. The crucial event is the inhibition of the TCA cycle at the step of aconitase. It disturbs energy metabolism and results in ATP deficiency with simultaneous fat accumulation. Further steps in obesity development are the consequences of diminished energy supply: inhibition of beta-oxidation, leptin resistance, increase in appetite and food intake and a decrease in physical activity. Thus, our theory shows that obesity does not have to be caused by overeating and sedentary life-style but may be the result of the "obese" change in metabolism which is forcing people to overeat and save energy to sustain metabolic functions of cells. This "obese" change is caused by environmental factors that activate chronic low-grade inflammatory process in the body linking obesity with the environment of developed countries.
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PMID:Decreased energy levels can cause and sustain obesity. 1455 57


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