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

Obese Zucker rats were either pair-fed to their lean litter-mates or fed ad lib, to determine the effect of hyperphagia on serum hormone levels and tissue metabolism as indicated by enzyme activities and in vitro metabolite flux. Hyperphagia was shown to be non-essential for the elevation in serum insulin and suppression in serum growth hormone and prolactin in the genetically obese rat. It was also shown that the increased liver cell lipogenic rate was not dependent on hyperphagia in the obese rat and that adipose cell lipogenesis was not significantly altered in the pair-fed obese rat. The utilization of alanine for glucose synthesis in vitro was similar for both lean and obese rats, but its utilization for fatty acid synthesis was higher in the obese rat. Data is presented which suggest that the inhibitory effect of glucagon on liver lipogenesis is blunted in the obese rat.
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PMID:Serum hormone levels and tissue metabolism in pair-fed lean and obese Zucker rats. 19 81

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

In this paper two patients with uncommon syndromes, viz. acrodermatitis enteropathica-like eruption due to acute zinc deficiency, when on long-term intravenous hyperalimentation for Crohn's disease, and necrolytic migratory erythema as a consequence of a malignant glucagon secreting alpha-cell tumour of the pancreas (glucagonoma syndrome) are reported. Attention is paid to the many common features of the skin lesions in both syndromes. This is discussed in detail. Both patients passed through a catabolic stage. Laboratory investigations, however, failed to demonstrate a common biochemical mechanism which might be responsible for the skin lesions. Administration of zinc in the first patient and surgical treatment of the second patient results in rapid clearing of the skin lesions and other symptoms.
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PMID:Zinc deficiency syndrome versus glucagonoma syndrome. 53 35

Contrary to normal rats, diabetic rats are known to develop marked hypercholesterolemia when fed a cholesterol-enriched diet. The triggering factor involved in this hyperresponse has not been identified. With the aim of clarifying the role of the intestinal acyl-CoA:cholesterol acyltransferase (ACAT), we studied the effects of a high fat diet and the changes of intestinal ACAT activity during the early development of streptozotocin-diabetes in rats. Feeding diabetic rats with a diet enriched in cholesterol and saturated fat produced an increase in plasma and in tissue cholesterol as early as 3 days after streptozotocin injection in the absence of hyperphagia. Under these experimental conditions, treatment with insulin or with the ACAT inhibitor CL-277082 significantly reduced the plasma cholesterol to levels measured in nondiabetic rats fed the same high fat diet. An increase in [14C]cholesterol in plasma very low density lipoprotein was observed after oral administration of labeled cholesterol to 3-day diabetic rats. In parallel experiments, the direct measurement of small intestine microsomal ACAT activity revealed an increase, averaging 288% in diabetic rats 3 days after diabetes induction. This change in ACAT activity occurred simultaneously with an increase in plasma glucagon and was normalized by insulin treatment. The induction of intestinal ACAT activity in diabetic rats, its modulation by insulin, and the hypocholesterolemic effects of insulin or CL-277082 treatment clearly indicate that ACAT activity plays a major role in the initiation of diabetes-associated hypercholesterolemia.
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PMID:Role of the intestinal acyl-CoA:cholesterol acyltransferase activity in the hyperresponse of diabetic rats to dietary cholesterol. 143 72

Neuropeptide Y (NPY) concentrations were measured by radioimmunoassay in eight microdissected hypothalamic regions of obese (fa/fa) and lean (Fa/?) Zucker rats. Freely fed obese rats showed significant (40-100%) increases in NPY concentrations in several regions, notably the paraventricular, ventromedial, and dorsomedial nuclei and the arcuate nucleus/median eminence, compared with lean rats. Hypothalamic NPY concentrations were not affected in either obese or lean rats by food restriction, which caused 25% weight loss over 3 wk. Refeeding to initial weight significantly increased NPY levels in the ventromedial and dorsomedial nuclei in lean rats but did not significantly alter NPY concentrations in any hypothalamic region in obese rats. These observations indicate fundamental differences in the regulation of hypothalamic NPY between obese and lean Zucker rats. NPY injected into the paraventricular nucleus and other regions causes hyperphagia, obesity, and increased secretion of insulin, glucagon, ACTH, and corticosterone. These behavioral and neuroendocrine abnormalities all occur in the obese Zucker syndrome and may be due to increased NPY-ergic activity in the hypothalamus.
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PMID:Altered neuropeptide Y concentrations in specific hypothalamic regions of obese (fa/fa) Zucker rats. Possible relationship to obesity and neuroendocrine disturbances. 165 67

The effects of acute and chronic morphine administration and the interaction with oxytocin and vasopressin on food intake response were investigated at various intervals during a 24-h schedule in rats. Acute morphine (5 mg/kg, IP) produced a generalized hyperphagic effect in both light (0-6 h) and dark (6-24 h) phases, the most marked effects being at 0-1 h, 1-3 h and 6-24 h. Chronic morphine (7 days) in an escalating dose schedule (5-35 mg/kg/day) produced (a) an enhancement of the hyperphagic effect in the light phase and (b) an attenuation of the food intake response during the dark phase. Neither oxytocin nor vasopressin had any significant influence on food intake, per se, after either acute or chronic administrations. However, both OXY and AVP reduced the hyperphagic response to acute morphine throughout the 24-h observation period. Further, on chronic administration, both neurohypophyseal peptides blocked the enhancements of morphine-induced hyperphagia (reverse tolerance) during light phase, whereas only vasopressin was effective in attenuating the reduction of hyperphagia (tolerance) during dark phase. These results are discussed in light of complex opiate-oxytocin/vasopressin interactions in the regulation of food intake.
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PMID:Effects of acute and chronic morphine on food intake in rats: modulation by oxytocin and vasopressin. 178 Mar 42

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

Forty obese subjects with normal glucose tolerance test (NGTT) thirteen diabetic obese subjects and sixteen normal subjects were studied to evaluate the possible interactions between beta-endorphin (B-Ep) and glucose homeostasis. On the basis of baseline B-Ep levels, two subgroups were selected: one group with normal mean values of B-Ep (7.02 +/- 0.59 pmol/l); another group with elevated mean values of B-Ep (18.95 +/- 1.52 pmol/l). No differences between these subgroups were found as regards body mass index (BMI), insulin and glucagon levels. Normal B-Ep values were found in diabetic obese subjects. No significant correlation was found between B-Ep and BMI, insulin or glucagon. Considering that B-Ep is involved in eating behavior and on the basis of our results, we suggest that elevated B-Ep levels can be found only in those obese NGTT subjects whose obesity is probably related to an abnormal modulation of food intake, such as hyperphagia.
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PMID:[Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. 202 70

Two-month hyperphagia after injury inflicted to the ventromedial hypothalamus in rats led to the development of marked obesity in an essential increase of the content of immunoreactive insulin, glucagon, and C-peptide in the blood. Increase of excessive body weight was attended by gradual diminution of the organisms sensitivity to exogenous insulin given in a dose of 0.03 U/100 g and maintenance of normal sensitivity to 0.1 U/100 g of exogenous insulin. It is most likely, therefore, that despite the increased function of the pancreatic islets and hyperinsulinemia, glucose tolerance decreased significantly due to diminished sensitivity of the peripheral tissues to insulin.
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PMID:[Insulin sensitivity of the body in experimental hypothalamic obesity]. 208 61

The metabolic effects and secretory properties of a radiation-induced transplantable insulinoma were examined in 16-17 week old NEDH rats. Subcutaneous subscapular implantation of tumour fragments resulted in hyperphagia, increased body weight gain, marked hyperinsulinaemia and severe hypoglycaemia, with the resulting death of the recipient by 27 days. Ultimate tumour size was 2.1 +/- 0.4 g (mean +/- SEM). At 3 days after transplantation, plasma glucose and insulin responses to intraperitoneal glucose, insulin, arginine and adrenaline were similar to control rats. At 20 days, plasma glucose concentrations of insulinoma-bearing rats remained low throughout glucose tolerance tests, and insulin responsiveness to glucose stimulation was absent. 2-Deoxy-D-glucose produced only a small rise of glucose concentrations in tumour-bearing rats. Insulin sensitivity was not appreciably impaired at 20 days despite severe hyperinsulinaemia and hypoglycaemia. The ability of adrenaline and propranolol to suppress plasma insulin and raise plasma glucose concentrations was also retained. At 20 days, glucagon evoked a marked plasma insulin response with no change in plasma glucose concentrations. In contrast, arginine and glibenclamide failed to stimulate insulin above high basal concentrations.
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PMID:Metabolic effects and secretory properties of a radiation-induced transplantable rat insulinoma. 288 53


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