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

A new strain of genetically obese mouse, the dbPas mouse, has been studied in terms of fat pad cellularity, serum parameters and thermogenesis. This obesity was observed in the inbred DW strain of mice at the Institut Pasteur-France, and is due to a recessive mutation on chromosome 4 at the diabetes locus. The mice became grossly obese, gaining weight until at least 16 mo of age. By 6 mo of age they exhibited hyperphagia, hypercholesterolemia, severe hyperinsulinemia, hypertrophy and hyperplasia of adipocytes, and impaired fertility. In contrast with other diabetic strains of mice, glycemia was normal in females and slightly elevated in males. This result indicates that the mutation of the db locus does not necessarily lead to a frank diabetes. Body temperature was normal either at 22 degrees C or after a cold exposure at 4 degrees C. GDP (guanosine diphosphate) binding to brown adipose tissue mitochondria was normal in obese mice as compared to lean. These data differentiate this model from other genetic obesities in mice and rats. This new model of genetic obesity offers interesting characteristics for the study of obesity.
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PMID:Description of a new model of genetic obesity: the dbPas mouse. 388 10

Obesity resulting from lesions of the ventromedial hypothalamus (VMH) has often been attributed to ablation-induced disinhibition of insulin release. However, lesion studies have generally employed electrolyzing anodal current with stainless steel electrodes, which results not only in tissue ablation but deposits of metallic ions that can chronically irritate surrounding tissue. The present study compared the effects of irritative and nonirritative VMH lesions on plasma insulin levels and obesity in female rats. Blood samples were obtained after a 4-h fast and 17 min after the initiation of a meal (6 ml of sweetened milk in 7 min) during a period when VMH rats were food restricted to the level of sham-operated animals and again when all animals were fed ad libitum. Irritative lesions (anodal electrolytic with stainless steel electrodes) caused heavy metallic ion deposition at the lesion site, marked obesity, and hyperinsulinemia both during food restriction and ad libitum feeding. Nonirritative lesions (cathodal electrolytic with platinum electrodes) resulted in no metallic ion deposition in seven of nine animals. These seven rats, which displayed 65% of the weight gain of animals with irritative lesions (significantly greater than sham rats), had significantly elevated insulin levels only under the postabsorptive condition during ad libitum feeding. In addition, only the animals with irritative lesions displayed emotional hyperreactivity to capture and handling. It is concluded that obesity produced by anodal electrolytic lesions with stainless steel electrodes is a result of both a destructive component resulting in hyperphagia with secondary hyperinsulinemia and an irritative component (accounting for up to 40% of the weight gain in female rats) resulting in basal hyperinsulinemia independent of hyperphagia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonirritative lesions of VMH: effects on plasma insulin, obesity, and hyperreactivity. 389 May 56

Insulin binding was measured in membrane particles prepared from the liver and several brain regions of 4-month-old female Zucker fa/fa (obese), Fa/fa (heterozygous), and Fa/Fa (lean) rats. High affinity insulin binding was decreased in the olfactory bulb of fatty (0.23 pmol bound/mg protein) and heterozygous (0.16 pmol/mg) rats compared with that in the lean controls (0.64 pmol/mg). Total binding was not changed in the cerebral cortex or hypothalamus. High affinity insulin binding was also decreased in the liver of both fatty (0.44 +/- 0.22 pmol/mg; P less than 0.01) and heterozygous (0.75 +/- 0.35 pmol/mg) animals compared with that in the lean rats (2.10 +/- 1.55 pmol/mg). This decreased binding is probably not due to down-regulation of receptors in the heterozygous rats, as they do not exhibit the hyperinsulinemia observed in the fatty rats. Rather, our findings suggest that there is a gene-related alteration in insulin binding in the Zucker rat, as low binding was observed in rats carrying either one (Fa/fa) or two (fa/fa) doses of the gene. We postulate that this central defect in insulin binding may contribute to inadequate perception of a central insulin feedback signal and to the hyperphagia observed in the obese rats.
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PMID:Brain and liver insulin binding is decreased in Zucker rats carrying the 'fa' gene. 389 61

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.
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PMID:Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats. 390 Mar 13

The present study was undertaken to determine the relative contributions of altered metabolic responses and excess food intake to the obesity and hyperinsulinemia of the ventromedial hypothalamic (VMH) syndrome. This experiment, employing an intragastric hyperalimentation protocol, was also designed to address the related issue of whether altered energy utilization serves as a compensatory strategy for reducing energy retention in the face of excess intake. Separate groups of VMH-lesioned and sham-lesioned female rats were fed, either orally or intragastrically, up to 200% of the calories ingested by a normally feeding intact rat. Both VMH-lesioned and intact rats became obese and hyperinsulinemic when hyperalimented for 30 days, but rats with lesions deposited 25% more fat than intact animals receiving an identical number of calories. Estimates of total carcass energy indicated that rats with lesions required 11% less calories than intact rats to retain identical levels of energy. Furthermore, intact hyperalimented rats failed to evidence the caloric wastage that has been reported to occur in orally fed rats that overeat cafeteria diets.
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PMID:Effects of intragastric hyperalimentation on pair-fed rats with ventromedial hypothalamic lesions. 391 63

Several different single gene mutations are known to cause similar diabetes-obesity syndromes in mice. Our studies with two mutations, obese (ob) and diabetes (db) have shown that each syndrome develops similarly. Symptoms include hyperinsulinemia, hyperglycemia, hyperphagia, diabetes, and obesity coupled with similar, and large increases, in the efficiency of food utilization. Even when maintained on 50 percent of normal food intake, mutants still become obese. This increase in metabolic efficiency has been suggested to be due to a failure of mutant mice to thermoregulate. Our studies indicate that any defect in thermoregulation is not severe enough to conserve sufficient calories to account for the large increase in metabolic efficiency observed in each mutant and the increased efficiency seen in mutants must be a result of other mechanisms. More critical studies in both normal and obese mice should lead to information defining the contribution of the many different potential energy saving mechanisms available.
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PMID:Increased metabolic efficiency in obese mutant mice. 406 38

Polydipsia, polyuria, polyphagia, and glucosuria followed the administration of streptozotocin to 6 nonpregnant and 15 pregnant monkeys (Macaca mulatta) in the first trimester of pregnancy. The diabetogenic action of the drug was also reflected in an induced but variable deterioration in maternal intravenous glucose tolerance and a marked attenuation of maternal plasma insulin responsiveness to intravenous glycemic stimuli. The products of conception were examined in 29 pregnancies. The neonates and the placentas of the streptozotocin-treated pregnant animals were significantly heavier than average for the period of gestation, polyhydramnios was consistently present, and there was an increase in the incidence of third trimester stillbirths. The fetal and maternal plasma glucose, insulin, and growth hormone concentrations were examined after the intravascular administration of glucose or a solution of mixed amino acids to the fetus in the third trimester. The neonatal plasma responses to similar insulinogenic stimuli were also examined.Fetal and neonatal base line plasma insulin concentrations were significantly elevated compared to those of the controls. The administration of intravascular glucose to the fetus, mother, or neonate was associated with a prompt 2-to 5-fold increase in fetal or neonatal plasma insulin concentrations. These findings contrast to the unresponsiveness of the pancreatic islet tissue we reported in normal subhuman primate pregnancy. The intravascular infusion of a relatively low concentration of mixed amino acids (2 mg/min) to the conceptii from the streptozotocin-treated pregnancies was associated with an elevation in fetal and neonatal plasma insulin levels, whereas normal monkey fetuses and neonates required a 10-fold greater concentration of amino acids in the infusate for similar responses. The induced hyperaminoacidemia or hyperglycemia did not consistently alter plasma growth hormone concentrations in the conceptii from normal or streptozotocin-treated pregnancies. These data provide evidence that maternal glucose intolerance during pregnancy is associated with enhanced fetal and neonatal pancreatic islet cell responsiveness to glucose and mixed amino acids. Although the specific mechanism(s) that alters both the sensitivity and responsiveness of the normal pancreatic fetal islet to insulinogenic stimuli remains unclear, the data do indicate that insulin-dependent maternal hyperglycemia and hyperaminoacidemia, separately or in combination could contribute to the fetal hyperinsulinemia of pregnancies complicated by diabetes mellitus. Moreover, the overall experiences with these streptozotocin-treated animals suggest that a subhuman primate model may be available to examine directly the antenatal pathophysiology of abnormal carbohydrate metabolism.
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PMID:Subhuman primate pregnancy complicated by streptozotocin-induced diabetes mellitus. 425 54

The relationships among food intake, insulin secretion, and adrenocortical function are reviewed. It is hypothesized that a major role of structures in, or passing through, the ventromedial hypothalamus is to inhibit food intake, insulin secretion, and adrenocortical function during the day (in the nocturnally active rat) and that this activity is normally driven by elements within the suprachiasmatic nuclei. Lesions of the ventromedial hypothalamus of rats result in nonrhythmic food intake, hyperinsulinemia, nonrhythmic adrenocortical function, and obesity. Adrenalectomy prevents or reverses the effects of lesions of the ventromedial hypothalamus on food intake, insulin secretion, and obesity, and corticosteroid replacement restores them. Because the actions of corticosteroids are both time- and dose-dependent, it is proposed that the effects of the tonic levels of corticosteroids observed after lesions of the ventromedial hypothalamus are to augment the hyperphagia, hyperinsulinemia, and substrate flow into fat to a greater extent than would occur if there were a normal circadian rhythm in adrenocortical function.
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PMID:Viewing the ventromedial hypothalamus from the adrenal gland. 632 Jun 67

Electrolytic lesions of the ventromedial hypothalamus including nucl. hypothalamicus inferior caused the cockerels to become hyperphagic. The plasma insulin level of the control birds was low before feeding and it increased after feeding, while that of the hyperphagic birds was higher before feeding and increased even more after feeding. Under the fasting condition on the 19th day, the insulin secretion of the hyperphagic birds remained at a high level, and there was a high correlation between the insulin value and the food consumption. Hyperactivity of insulin secretion in the hypothalamic hyperphagic birds was inhibited by administration of diazoxide and their insulin levels declined to a level similar to that of the controls. As a result the hyperphagia was interrupted and the daily food consumption declined to the same level as the controls. Therefore, the hyperinsulinemia seemed to be necessary for maintaining the hypothalamic hyperphagia in chickens. The role of glucagon in this phenomenon is also discussed.
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PMID:Hyperinsulinemia and its role in maintaining the hypothalamic hyperphagia in chickens. 634 54

Immunologically reactive insulin levels were determined in freely-moving normal rats offered three different test-meals. In test I, they were offered their normal diet for 4.5 min. In test II, they first ate the same diet for the same amount of time, then a cookie for 6 min, and finally they had free access to lard. In test III, the normal diet was followed by a synthetic sweetener and then by vaseline. It was shown that in a varied meal (tests II and III), the ingestion of each new food was immediately followed by a peak of insulin secretion superimposed on normal postprandial hyperinsulinemia. This resulted in an overall increase in insulinemia over the 15-min period measured. It is well known that in a varied meal more food is consumed. Thus, it may be that when a varied meal is offered, final satiety is postponed. This could be due to sensorially-triggered peaks of insulin secretion which would explain why the "cafeteria diet" induces hyperphagia and obesity.
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PMID:[Cephalic phase of insulin secretion and the variety of the food in rat feed]. 634 27


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