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)

DALCE (1-40 micrograms, ICV), a short-acting agonist and long-acting antagonist at the delta opioid receptor, was examined for its effects upon food intake in rats under spontaneous, deprivation, glucoprivic and palatable conditions. DALCE (10 micrograms) significantly stimulated free feeding for up to 10 h but only minimally decreased (40 micrograms) food intake and body weight after 24-72 h. DALCE, administered prior to food deprivation (24 h), failed to affect subsequent 24-h intake and sporadically decreased intake and body weight change after 48-72 h. 2-Deoxy-D-glucose (650 mg/kg, IP) hyperphagia was transiently (2 h) decreased by long-term DALCE (10 micrograms) pretreatment. Hyperphagia following exposure to a high-fat diet was significantly potentiated by long-term DALCE (1 microgram) pretreatment. DALCE (10 micrograms) hyperphagia (2-10 h) was eliminated by central pretreatment with either naltrexone (20 micrograms) or the kappa antagonist, nor-binaltorphamine (20 micrograms) but was minimally affected by central pretreatment with the mu antagonist, beta-funaltrexamine (20 micrograms) or long-term DALCE (40 micrograms). The general inability of the antagonist actions of DALCE to alter these forms of feeding argues against a role for the delta opioid receptor in these responses.
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PMID:Ingestive behavior following central [D-Ala2, Leu5, Cys6]-enkephalin (DALCE), a short-acting agonist and long-acting antagonist at the delta opioid receptor. 165 17

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

2-Deoxy-D-glucose (2DG) analgesia, mediated in part by endogenous opiate and hypothalamo-hypophysial systems is presumably activated by its stress-related properties. Recently 2DG hyperphagia, but not 2DG hyperglycemia was reduced by central pretreatment with the pancreatic beta-cell toxin, alloxan; this deficit was eliminated by co-administration of 3M D-glucose. The present experiment examined whether intracerebroventricular pretreatment with alloxan (40 or 200 micrograms) altered 2DG analgesia (400 or 700 mg/kg, IP) on the tail-flick and jump tests, and whether 3M D-glucose co-administration ameliorated any deficits. Both alloxan doses significantly reduced 2DG analgesia (400 mg/kg) on both tests. 2DG analgesia (700 mg/kg) was significantly reduced by both alloxan doses on the jump test, but only by the higher alloxan pretreatment on the tail-flick test. 3M D-glucose co-administration ameliorated alloxan-induced analgesic deficits more effectively at the lower 2DG dose. Neither alloxan nor alloxan/3M D-glucose treatments altered basal thresholds. These data pertain both to alloxan's effects upon coding of 2DG effects as stressful, and to the role of diabetes and/or central glucoreceptors in analgesic processes.
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PMID:Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia. 339 8

5-Thio-D-glucose (200 and 500 mg/kg) produced hyperglycemia and significantly retarded emptying of the pregastric pouch of hamsters. 2-Deoxy-D-glucose did not affect stomach-emptying at either of the doses used (500 and 1000 mg/kg), but did cause hyperglycemia at the higher dose. These results are discussed in relation to the failure of these glucose analogs to produce hyperphagia in the golden hamster.
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PMID:Effects of 5-thio-D-glucose and 2-deoxy-D-glucose upon stomach-emptying in the golden hamster. 654 8

While opioid agonists administered into the hypothalamic paraventricular nucleus increase food intake in rats, naloxone reduces deprivation-induced intake. Ventricular administration of either mu (beta-funaltrexamine) or kappa (nor-binaltorphamine) opioid antagonists reduces spontaneous, deprivation, glucoprivic and palatable intake. The present study assessed whether microinjections of either general, mu or kappa opioid antagonists into the paraventricular nucleus altered either deprivation (24 h) intake, 2-deoxy-D-glucose hyperphagia or sucrose intake in rats. Deprivation intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 30-33%), beta-funaltrexamine (5 micrograms, 100 nmol, 26-29%) or naltrexone (10 micrograms, 260 nmol, 26%) in the paraventricular nucleus. 2-Deoxy-D-glucose hyperphagia was significantly reduced only after 2 h by naltrexone (10 micrograms, 260 nmol, 69%), norbinaltorphamine (20 micrograms, 272 nmol, 69%) or beta-funaltrexamine (20 micrograms, 400 nmol, 83%) in the paraventricular nucleus. Sucrose intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 27-36%), naltrexone (5-10 micrograms, 130-260 nmol, 18-31%) and beta-funaltrexamine (5 micrograms, 100 nmol, 20%) in the paraventricular nucleus. These data indicate that general, mu and kappa opioid antagonists administered into the hypothalamic paraventricular nucleus produce similar patterns of effects upon different forms of food intake as did ventricular administration, implicating this nucleus as part of the circuitry underlying opioid mediation of ingestion.
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PMID:Alterations in deprivation, glucoprivic and sucrose intake following general, mu and kappa opioid antagonists in the hypothalamic paraventricular nucleus of rats. 765 22

Glucoprivic feeding induced by intraperitoneal (IP) injection of 2-deoxy-D-glucose (2-DG, 250 mg/kg body weight) in the middle of the light phase was investigated in old (age: 15-16 months) and young (age; 2.5-3.5 months) hepatic branch-vagotomized (HBV) and sham-vagotomized (SV) rats. Rats were fed either a carbohydrate-rich diet or a fat-enriched diet with a moderate carbohydrate content. The glucoprivic feeding response was greater in 13-h food-deprived old HBV rats than in 13-h food-deprived old SV rats on both diets. 2-Deoxy-D-glucose produced a greater feeding response when rats were fed the fat-enriched diet. Independent of the diet, the transient hyperphagia induced by 2-DG was followed by a long-term hypophagia in old SV rats, but not in old HBV rats. In 13-h food-deprived young rats, hepatic branch vagotomy did not affect the changes in food intake induced by 2-DG. In undeprived old and young rats, the feeding response to 2-DG, exceeding that of deprived rats, was also not affected by HBV. It is concluded that under certain conditions hepatic branch vagotomy eliminates a 2-DG-induced signal inhibiting food intake and thus enhances glucoprivic feeding. The feeding response to 2-DG therefore seems to depend on stimuli affecting food intake in an antagonistic manner.
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PMID:Hepatic branch vagotomy enhances glucoprivic feeding in food-deprived old rats. 837 18

Opioid receptor subtype antagonists differentially alter food intake under deprivation (24 h), glucoprivic (2-deoxy-D-glucose, 500 mg/kg, i.p.) or palatable (10% sucrose) conditions with mu (beta-funaltrexamine) and kappa (nor-binaltorphamine), but not delta1 ([D-Ala2,Leu5,Cys6]enkephalin) opioid antagonists reducing each form of intake following ventricular microinjection. Both mu and kappa opioid antagonists microinjected into either the hypothalamic paraventricular nucleus or the nucleus accumbens reduce intake under deprivation and glucoprivic conditions. Palatable intake is reduced by both antagonists in the paraventricular nucleus, but only mu antagonists are active in the accumbens. Food intake is stimulated by mu and delta, but not kappa, opioid agonists microinjected into the ventral tegmental area. The present study examined whether food intake under either deprivation, glucoprivic or palatable conditions was altered by bilateral administration of general (naltrexone), mu, kappa, delta1 or delta2 (naltrindole isothiocyanate) opioid antagonists into the ventral tegmental area. Deprivation (24 h)-induced feeding was significantly reduced by high (50 microg), but not lower (10-20 microg) doses of naltrexone (21%), and by delta2 (4 microg, 19%) antagonism in the ventral tegmental area. 2-Deoxy-D-glucose (500 mg/kg, i.p.)-induced hyperphagia was significantly reduced by high (50 microg), but not lower (20 microg) doses of naltrexone (64%), and by delta2 (4 microg, 27%) antagonism in the ventral tegmental area. Sucrose (10%) intake was significantly reduced by naltrexone (20-50 microg, 25-39%) and delta2 (4 microg, 25%) antagonism in the ventral tegmental area. Neither mu, kappa nor delta1 antagonists were effective in reducing any form of intake following microinjection into the ventral tegmental area. These data indicate that the ventral tegmental area plays a relatively minor role in the elicitation of these forms of food intake, and that delta2, rather than mu, kappa or delta1 opioid receptors appear responsible for mediation of these forms of intake by this nucleus.
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PMID:Evaluation of opioid receptor subtype antagonist effects in the ventral tegmental area upon food intake under deprivation, glucoprivic and palatable conditions. 936 10

2-Deoxy-D-glucose (2DG) elicits glucoprivic food intake whether administered centrally or systemically. Insulin, on the other hand, elicits glucoprivic food intake when administered systemically but reduces food intake when administered centrally. The purpose of these experiments was to determine the interaction of centrally administered insulin with systemically administered 2DG on feeding. In the experimental condition, male Sprague-Dawley rats were administered 5 mU insulin into the third cerebral ventricle (i3vt) followed 2 h later by a subcutaneous injection of 250 mg/kg of 2DG. Contrary to expectations, third ventricular insulin significantly increased 2DG-induced hyperphagia. A replication using doses of insulin ranging from 1 to 10 mU revealed a dose-dependent response. Whereas the lowest dose of insulin (1 mU) did not reliably change food intake, doses of 2.5, 5, and 10 mU significantly enhanced 2DG-induced feeding. Consistent with previous reports, centrally administered insulin, when given alone, caused a significant reduction of 24-h body weight and chow intake. To assess if the insulin-induced hyperphagia was a result of leakage from the ventricles, we peripherally administered 5 mU of insulin and observed, if anything, a slight decrease of food intake. These studies suggest that in the presence of central glucoprivation, a distinct anabolic action of centrally administered insulin overrides the normally observed catabolic response and increases the hyperphagic feeding response induced by 2DG.
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PMID:Central insulin potentiates eating elicited by 2-deoxy-D-glucose. 1257 32