Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral administration of the COOH-terminal octapeptide of cholecystokinin in doses from 1 to 100 micrograms per kilogram of body weight (0.25 to 25.0 micrograms per rat) significantly antagonized tail pinch-induced eating in rats, an animal model for stress-induced human hyperphagia. Centrally administered cholecystokinin was effective only in high doses (3 micrograms into the cerebral ventricle). The finding that the minimal effective dose of cholecystokinin in suppressing stress-induced appetitive behavior is smaller after peripheral than central administration suggests that the peptide is acting on peripheral, as opposed to central nervous system, substrates.
 ...
PMID:Cholecystokinin inhibits tail pinch-induced eating in rats. 56 35

Metabolic effects of 3 different sites of transplantation of cultured tumour cells from a radiation induced insulinoma (28 X 10(6) viable cells per rat) were examined in 15-18 weeks old male NEDH rats. Subscapular implantation consistently produced a highly vascularised encapsulated tumour associated with hyperinsulinaemia, hyperphagia and hypoglycaemia by 21 days, which progressed to fatal neuroglycopaenic coma at 37 +/- 3 days (mean +/- SEM). Implantation of tumour cells into the hepatic portal vein resulted in a multilobular hepatic tumour in two out of nine rats, with hyperinsulinaemia and fatal hypoglycaemia by 49-54 days. Irregularities of glucose homeostasis were observed in a further three rats by 62 days. Intrapancreatic implantation consistently produced a similar tumour to that observed at the subscapular site. Implantation into the pancreas produced the most rapid onset of hyperinsulinaemia, hyperphagia and hypoglycaemia, with survival for only 28 +/- 3 days. The results demonstrate an important effect of transplantation site on the function and metabolic consequences of the NEDH rat insulinoma.
 ...
PMID:Metabolic effects of radiation induced rat insulinoma at pancreatic, hepatic and subscapular transplantation sites. 287 15

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.
 ...
PMID:Viewing the ventromedial hypothalamus from the adrenal gland. 632 Jun 67

From the pathophysiological viewpoint, feeding responses to various stimuli were examined in Zucker fatty rats and their lean littermates. Intraventricular administration of norepinephrine (NE, 10 micrograms/rat) stimulated food intake in both rats. Intraventricular administration of 2-deoxy-D-glucose (2DG, 3.8 mg/rat) induced hyperphagia and concomitant hyperglycemia in lean rats. However, in fatty rats, the blood glucose was elevated but food intake was unaltered after 2DG administration. Subcutaneous administration of insulin (2 or 8 U/kg) stimulated food intake of both rats. Streptozotocin (STZ)-induced hypoinsulinemia produced transient reduction of food intake followed by sustained diabetic hyperphagia in lean rats. In fatty rats, the experimental hypoinsulinemia caused transient aphagia but not sustained diabetic hyperphagia. Daily injection of insulin (5 U/rat) restored energy assimilation in both diabetic rats. An increase in food intake due to insulin injection was remarkable only in diabetic fatty rats. From these findings, the regulatory system of food intake in fatty rats appears to be sensitive to changes in the circulating insulin level but insensitive to either glucoprivation or changes in body storage of energy.
 ...
PMID:Feeding responses of Zucker fatty rat to 2-deoxy-D-glucose, norepinephrine, and insulin. 700 24

We investigated the effects of intrahypothalamic administrations of the opioid agonists morphine (MOR) and ketocyclazocine (KCZ) and antagonists naltrexone (NALTX) and Mr2266 on food intake (FI) during light and dark phases of the diurnal cycle, after acute or chronic administration in rats. Acute intralateral hypothalamic (LH) administration of MOR or KCZ (1 microgram/rat) enhanced FI during dark and light phases, respectively, whereas intraventromedial hypothalamic (VMH) injections resulted in moderate hyperphagia during dark phases by both mu and kappa agonists. The receptor specificity was evident from blockade of the responses to MOR or KCZ by the respective antagonists NALTX and Mr2266. After repeated administrations of MOR and KCZ, FI responses to the test dose of these agonists injected in LH were modulated in opposite directions. However, the adaptative changes in FI after intra-VMH injection of KCZ were similar to those seen with MOR. These results are discussed in light of a differential opioid receptor involvement and their possible functional interactions within the hypothalamus during food intake.
 ...
PMID:Differential effects of intrahypothalamic administration of opioids on food intake in naive and tolerant rats. 858 6

The obese Zucker rat is an animal model of genetically inherited obesity demonstrating remarkable hyperphagia. In the present study, to try to clarify the relationship between obesity and gastric function including gastric mucosal integrity, the gastric acid secretion, emptying, and mucosal resistance against ulcerogenic agents were compared in lean and obese Zucker rats. Male lean and obese Zucker rats were housed at 25 degrees C under 12-hr/12-hr lighting cycle (on at 7:00 AM). The gastric acid output of obese Zucker rats was markedly smaller than that of lean Zucker rats, whereas there was no significant difference in gastric emptying in both groups. The degree of mucosal lesion formation induced by ulcerogenic agents was assessed by measuring the total length of all mucosal lesions observed (ulcer index; mm). The intragastric administration of indomethacin (20 mg/kg) produced hemorrhagic mucosal lesions in both lean and obese groups of Zucker rats, but the ulcer index was remarkably smaller in obese Zucker rats than that of their lean littermates (5.2 +/- 1.2 mm vs. 17.5 +/- 3.5 mm, mean +/- SEM, P < 0.01). In addition obese Zucker rats exhibited stronger resistance against the intragastric challenge of absolute ethanol (1 ml/rat), a necrotizing agent, with its ulcer index being 8.5 +/- 2.7 mm, compared with lean Zucker rats whose ulcer index was 26.4 +/- 5.4 mm (P < 0.01). The bilateral subdiaphragmatic vagotomy decreased both gastric acid secretion and the ulcer index of indomethacin-induced gastric injury observed in both obese and lean Zucker rats, whereas there was no significant difference in the ulcer index of ethanol-induced gastric injury. These results suggest that obese Zucker rats exhibit enhanced resistance against ulcerogens and decreased acid output. It is also speculated that the vagal system might be involved in inhibition of acid secretion and formation of indomethacin ulcers in obese Zucker rats.
 ...
PMID:[Pathophysiological study on the mucosal defense system of genetically obese Zucker rats]. 899 42

Effects of exogenous acidic fibroblast growth factor (aFGF), which is increased in the brain by food intake, on the plasma levels of catecholamines and on sympathetic efferent outflow were examined in anesthetized rats. A guide cannula was inserted into the cerebral third ventricle, and a vascular indwelling catheter was inserted into the right atrium from the jugular vein. Plasma epinephrine (Epi) and norepinephrine (NE) increased markedly in a dose-dependent manner for up to 120 min after intracerebroventricular or intravenous administration of aFGF (6-667 fmol/rat). Concomitant increases occurred in the efferent activity in the sympathetic nerves supplying the adrenal, spleen, and interscapular brown adipose tissue after the above administrations of aFGF. Both intravenous and intracerebroventricular administration of 10 ng basic FGF (bFGF) also increased sympathetic adrenal efferent activity and plasma Epi and NE concentrations. However, the increases induced by 10 ng bFGF were smaller than those induced by 10 ng aFGF. Bilateral splanchnicotomy completely prevented the increases in Epi induced by intracerebroventricular or intravenous aFGF but had less effect on the increases in NE. Pretreatment with an antibody against corticotropin-releasing factor (CRF), given via the intracerebroventricular route, significantly attenuated the increases in Epi and NE evoked by intracerebroventricular or intravenous administration of aFGF. Hepatic vagotomy also greatly reduced the increases in both catecholamines and the increases in sympathetic efferent firing rates evoked by intravenous administration of aFGF. These findings indicate that 1) aFGF administered intracerebroventricularly activates adrenomedullary secretion and sympathetic outflow via CRF release and 2) aFGF injected intravenously also induces sympathoadrenomedullary activation via centrally released CRF. The idea is discussed that sympathetic activation induced either by endogenous aFGF after feeding or by exogenously administered aFGF may play roles both in energy expenditure after overeating and in the modulation of immune functions.
 ...
PMID:Acidic fibroblast growth factor activates adrenomedullary secretion and sympathetic outflow in rats. 975 28

The effect of intracerebroventricular administration of dizocilpine on feeding behaviour and adrenal corticrotropic hormone (ACTH)-induced anorexia in elevated plus maze was examined. Dizocilpine (10, 20 and 40 nmol/rat, i.c.v.) showed a dose-dependent increase in food intake in 16 h food deprived rats. Dopamine receptor antagonists such as SCH 23390 (0.25 and 0.5 mg/kg, i.p.), pimozide (0.5 and 1 mg/kg, i.p.) and haloperidol (0.25 and 0.5 mg/kg, i.p.) dose-dependently blocked dizocilpine (40 nmol)-induced potentiation of food intake. Brain dopamine depletion by pretreatment with reserpine (5 mg/kg, i.p.) and alpha-methyl-p-tyrosine (200 mg/kg, i.p.) decreased food intake in rats. Similarly, pretreatment with reserpine and alpha-methyl-p-tyrosine (AMPT) reversed the hyperphagic effect of dizocilpine (20 and 40 nmol). Intracerebroventricular administration of ACTH (5 microgram/rat) produced significant diminution of feeding duration and increased tasting latency and feeding latency in elevated plus maze which was reversed by dizocilpine (40 nmol). SCH 23390 (0.25 mg/kg), pimozide (0.5 mg/kg) and haloperidol (0.25 mg/kg) reversed the effect of dizocilpine on ACTH-induced behaviours in elevated plus maze. The present observations support and extend the hypothesis that endogenous excitatory aminoacids (EAAs) play a role in the control of food intake. Further, dizocilpine-induced hyperphagia and dizocilpine-induced reversal of ACTH effect on feeding behaviour in elevated plus maze involve DAergic mediation.
 ...
PMID:Dopamine receptor sensitive effect of dizocilpine on feeding behaviour. 981

Melanin-concentrating hormone (MCH) and orexin-A are orexigenic peptidergic neurotransmitters produced primarily in the lateral hypothalamus. Because two other hypothalamic peptides, neuropeptide Y and agouti-related peptide, increase food intake by a mechanism that depends on activation of opioid receptors, we assessed whether MCH or orexin-A also elicits food intake via opioid receptor activation. A dose of naloxone (0.3 mg/kg, ip) that had no effect on its own reduced the acute orexigenic effect of third ventricular (i3vt) orexin-A (3 ng/rat). However, this same dose of naloxone had no effect on i3vt MCH (5 microg/rat)-induced hyperphagia. Because the opioid system has also been linked to food selection, we investigated whether MCH or orexin-A alters food choice when rats have simultaneous access to two diets differing in the relative amounts of fat and carbohydrate. Whereas i3vt MCH stimulated intake of both diets and did not alter food choice, i3vt orexin-A stimulated intake of only the high fat diet. These data indicate that despite several similarities between MCH and orexin-A, these two lateral hypothalamic area peptides stimulate food intake by recruiting different neural circuits and exert different effects on food choice.
 ...
PMID:Eating elicited by orexin-a, but not melanin-concentrating hormone, is opioid mediated. 1213 May 65

Sibutramine sensitivity assay in genetically obese (bombesin BB3 receptor (BRS-3)-deficient mice, KK-Ay mice, db/db mice and Zucker obese rat) and wild-type animals was examined. The sensitivity of Sibutramine (10 mg/kg, p.o.) in BRS-3-deficient mice was retained as well as normal animals; however, it was decreased in KK-Ay, db/db mice and Zucker obese rat. The suppression values of food intake in BRS-3-deficient, KK-Ay, db/db mice and Zucker obese rat were 49.8+/-5.8%, 16.1+/-4.7%, 0.1+/-2.8% and -2.0+/-2.2% (mean +/- S.E.), respectively. Next, we found that the contribution of hyperphagia was small in the progress of obesity in BRS-3-deficient mice by calculating energy efficiency. Our results indicate that there is an inverse relationship between the sensitivity to Sibutramine and the contribution of hyperphagia to the progress of obesity in animals.
 ...
PMID:Sibutramine sensitivity assay revealed a unique phenotype of bombesin BB3 receptor-deficient mice. 1287 36


1 2 Next >>