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PubMed1986

Loss of morphine hyperphagia following neonatal monosodium glutamate treatment in rats.

Morphine stimulates food intake in mildly-deprived and nondeprived rats. Neonatal administration of monosodium glutamate (MSG) destroys the medial-basal hypothalamus and other circumventricular organs, including cells containing beta-endorphin that project to other hypothalamic nuclei proposed in the modulation of morphine hyperphagia. Food intake of MSG-treated and control rats were assessed following vehicle and morphine (1.0-5.0 mg/kg, sc) treatment in a mild (5h) food deprivation paradigm. Morphine hyperphagia was found to be absent in MSG-treated rats, although they responded normally to mild deprivation following vehicle treatment. These results add to the types of ingestive deficits observed in the MSG-treated rat, and suggest that the circumventricular system in general, and opioid medial-basal hypothalamic cells in particular may be implicated in morphine hyperphagia.

Animals↗
PubMed1982

Effects of dopamine-depleting brain lesions on experimental hyperphagia in rats.

Dopamine (DA)-depleting brain lesions of various sizes were produced in rats either by intracerebroventricular injections of 6-hydroxydopamine (6-HDA) or by electrolytic lesions of the lateral hypothalamic (LH) area. Among 30 animals that became aphagic and adipsic for at least four days after large LH or 6-HDA-induced brain lesions, only three developed hyperphagia after electrolytic lesions of the ventromedial hypothalamus (VMH) or daily injections of long-acting protamine-zinc insulin (PZI). In 20 rats with smaller LH or 6-HDA-induced lesions, which had not shown marked initial behavioral dysfunctions, only three gained as much weight after VMH lesions as the control animals. Similarly, 6 of 10 rats with smaller LH lesions could not tolerate a 15-day series of PZI treatments, although 14 of 17 rats with smaller 6-HDA-induced lesions increased their food intake and gained weight during the PZI treatments as did control animals. These results indicate that hypothalamic hyperphagia can be blocked by DA-depleting brain lesions that neither produce an initial period of aphagia and adipsia nor involve hypothalamic tissue. They further indicate that even small LH lesions may prevent the development of hyperphagia elicited by PZI, whereas only very large 6-HDA-induced lesions consistently have this effect.

Animals↗
PubMed1981

Naltrexone suppresses hyperphagia induced in the rat by a highly palatable diet.

A highly palatable diet (ordinary chow supplemented with 4 highly palatable items changes every day) (HPD) provokes hyperphagia and overweight in the rat. After 17 weeks of such a diet, naltrexone (0.5 or 2.5 mg/kg IP) and opiate antagonist, was injected at the beginning of the dark period, and a food intake test was performed during the 3 following hours. Naltrexone does not modify the energy intake in control rats receiving ordinary chow but suppresses HPD induced hyperphagia. The involvement of the beta-endorphin system in this type of hyperphagia is discussed.

Animals↗
PubMed1985

Benzodiazepine-induced hyperphagia in the nondeprived rat: comparisons with CL 218,872, zopiclone, tracazolate and phenobarbital.

Nondeprived male rats were familiarized with 30 min daily access to a highly palatable diet. Clonazepam, midazolam and chlordiazepoxide each produced significant dose-dependent increases in food consumption. Clonazepam was the most potent, and a significant hyperphagic effect was detected following 0.078 mg/kg (IP). Amongst novel non-benzodiazepine anxiolytics, zopiclone and CL 218,872 also produced significant increases in food intake. The smallest doses to produce significant hyperphagia for these two drugs were 10.0 and 2.5 mg/kg (IP) respectively. In contrast, tracazolate caused only a reduction in feeding, evident at 20 and 40 mg/kg (IP). Previous reports indicate that although benzodiazepines, zopiclone and CL 218,872 displace [3H] flunitrazepam binding in rat cerebral cortex preparations, tracazolate enhances the binding. Our results are consistent with the drug-induced hyperphagia depending upon agonist actions at high-affinity benzodiazepine sites. They also provide pharmacological evidence for a dissociation between hyperphagic and anxiolytic drug effects. Phenobarbital (2.5-40.0 mg/kg), like the benzodiazepines, produced a strong stimulation of food intake, indicating that drug action at an alternative site in the benzodiazepine receptor-GABA receptor-chloride channel complex can also lead to hyperphagia.

Animals↗
PubMed1986

Dopamine-norepinephrine interactions in the development of hyperphagia and obesity following medial hypothalamic lesions.

Conflicting evidence exists on the ability of central 6-hydroxydopamine (6-OHDA) injections to alter the subsequent development of hyperphagia and obesity following medial hypothalamic lesions (MHL) in rats. An initial study found no effects of prior intracisternal (IC) 6-OHDA on the subsequent development of this MHL syndrome, while later work reported that a dopamine (DA) depletions induced by intracerebral 6-OHDA effectively blocked it. The present study reexamined this issue by investigating the effects of depleting brain dopamine, norepinephrine (NE), or both DA and NE, on overeating and obesity induced by subsequent MH lesions. Different patterns of DA and NE depletions were achieved by IC 6-OHDA in combination with systemic pretreatments designed to protect central NE, DA, or neither amine, respectively. It was found that 6-OHDA regimens that selectively depleted forebrain DA did prevent the development of hyperphagia and obesity following MHL. However, when such forebrain DA depletions were accompanied by NE depletions no such blockade occurred. Manipulations which selectively depleted forebrain NE had no effect on MHL-induced hyperphagia and obesity. These results offer a framework for resolving previous discrepancies in the literature concerning brain monoamines and MHL effects. They also indicate that the effectiveness of brain DA depletions in blocking the MHL syndrome is critically dependent on the functional status of NE systems.

Animals↗
PubMed1993

Sertraline attenuates hyperphagia in rats following nicotine withdrawal.

Chronic nicotine administration can decrease food consumption and body weight. Abrupt withdrawal from nicotine can cause the reverse effect, hyperphagia and rapid weight gain. In the current study, the efficacy of sertraline, a serotonin reuptake inhibitor, on nicotine withdrawal-induced hyperphagia and rapid weight gain was assessed in rats. Sertraline was found to be effective in reversing the increase in feeding that occurred after withdrawal from chronic nicotine administration. Sertraline caused a dose-related decrease in food consumption in control rats not given nicotine. Doses of 5 and 10 mg/kg/day caused significant decreases while 2.5 mg/kg/day caused a slight though nonsignificant decrease in food consumption. Rats in which nicotine was abruptly withdrawn after 3 weeks of administration showed a significant increase in food consumption relative to controls. This increase was eliminated by the high dose of sertraline (10 mg/kg/day), but not by the lower two doses (2.5 and 5 mg/kg/day). Water consumption was affected in a similar fashion. Body weight gain was also affected by sertraline. During the first week after nicotine withdrawal, rats rapidly gained weight, but sertraline attenuated this. The 10-mg/kg dose of sertraline significantly attenuated the nicotine withdrawal-induced weight gain. These results suggest that sertraline can counteract the hyperphagia and rapid weight gain associated with nicotine withdrawal, and might therefore be a useful adjunct to smoking cessation.

1-Naphthylamine↗
PubMed1996

Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia.

The role of beta-adrenoreceptors in modulating feeding in glucoprivation- and lipoprivation-induced hyperphagias was studied in rats by measuring the efficacy of the selective beta2-adrenoreceptor agonist salbutamol to antagonize the hyperphagic response induced by injection of 2-deoxy-D-glucose (2-DG), insulin, or sodium mercaptoacetate (MA). 2-DG and insulin are blockers of glucose utilization, and their administration stimulates receptor cells that are selectively sensitive to central glucose availability. MA stimulates feeding in rats maintained on a fat-supplemented diet, by blocking fatty acid oxidation at different levels in the metabolic pathway. We found that salbutamol dose-dependently antagonized both the insulin- and MA-induced hyperphagia, with reductions in food intake up to 100% compared with rats treated with insulin or MA alone. On the contrary, salbutamol, even at the highest dose (15 mg/kg, IP), was completely ineffective against 2-DG-induced hyperphagia. The present results support the previously proposed notion that there are different neuronal or humoral circuits underlying the hyperphagic responses to the metabolic stimuli induced by glucoprivation (i.e., 2-DG and insulin administration), and they extend our knowledge on the effects of salbutamol on glucoprivic and lipoprivic control of feeding.

Adrenergic beta-Agonists↗
PubMed1988

Ventromedial hypothalamic and paraventricular nucleus lesions damage a common system to produce hyperphagia.

We investigated the anatomical basis of paraventricular (PVN) and ventromedial (VMH) hypothalamic hyperphagia. Asymmetrical electrolytic lesions, damaging the VMH and PVN contralaterally, produced significant hyperphagia and weight gains (mean = 257.2 g) almost three times those of controls (89.8 g) during 56 postsurgical days. Weight gain in these rats was not significantly different from that in rats with bilateral lesions of the VMH (277.2 g) or PVN (188.2 g). Combined bilateral destruction of the PVN and VMH produced weight gain (272.8 g) almost identical to that seen after bilateral VMH lesions alone. The lack of additivity of these combined lesions and the effectiveness of the asymmetrical lesions are consistent with the hypothesis that lesions of either of these two regions damage a longitudinally running system to produce elevated food intake and body weight. Cell bodies of this system may lie within the PVN and send efferent projections through the VMH. Hyperinsulinemia developed only in rats with bilateral damage in the VMH. Thus, hypothalamic hyperphagia and hyperinsulinemia appear to be dissociable, reflecting damage to separate neural systems.

Animals↗
PubMed1998

Evidence that dark-phase hyperphagia induced by neurotoxin 6-hydroxydopamine may be due to decreased leptin and increased neuropeptide Y signaling.

Hyperphagia and obesity can be experimentally induced in rodents by microinjection of 6-hydroxydopamine (6-OHDA) into the ventral noradrenergic bundle (VNAB) to interrupt efferent catecholaminergic pathways to the hypothalamus. Since hypothalamic neuropeptide Y (NPY) is implicated in the control of ingestive behavior, we evaluated hypothalamic NPY activity in this model of obesity. Adult male rats injected bilaterally with 12 microg of 6-OHDA in the VNAB displayed an enhanced rate of body weight gain and selective dark-phase hyperphagia that started at about 10 days postinjection and persisted for the entire duration of the experiment. NPY gene expression, assessed by ribonuclease protection assay, was significantly higher in the hypothalami of 6-OHDA-treated hyperphagic rats during the dark phase (p < 0.01 vs. levels during the light phase and in control, vehicle-injected rats). We also evaluated gene expression of NPY Y and Y5 receptors, receptor subtypes reported to mediate NPY-induced feeding. The dark-phase increase in NPY mRNA was accompanied by the concomitant upregulation of NPY Y5R gene expression, but not of Y1R mRNA levels. Leptin, the peripheral hormone secreted by adipocytes, is believed to maintain body weight and inhibit food intake, most likely by suppressing hypothalamic NPY activity. Evaluation of leptin gene expression in the epididymal fat revealed that the upregulation of leptin mRNA noted during the dark phase in control rats did not occur in 6-OHDA-treated rats. These observations implied that the normal restraint on NPY and feeding exercised by leptin in control rats may be abrogated in 6-OHDA-treated hyperphagic rats due to insufficient levels of leptin. If so, administration of leptin should inhibit food intake in these rats. Indeed, injection of leptin (2 mg/kg, intraperitoneally (i.p.)) on 2 consecutive days reduced 24-h food intake by 25% and significantly reduced body weight. These results suggest that the nocturnal hyperphagia and resultant obesity induced by 6-OHDA injected into the VNAB may be attributed to leptin deficiency concomitant with increased hypothalamic NPY.

Adrenergic Agents↗
PubMed1984

Hyperinsulinemia in rats with ventromedial hypothalamic lesions: role of hyperphagia.

The relation of hyperinsulinemia to hyperphagia was examined in rats with lesions of the ventromedial hypothalamus (VMH). Plasma insulin and glucose levels were assayed after a 4-hr fast and 17 min after the initiation of a meal (6 ml of sweetened milk in 7 min) in animals with sham lesions, VMH animals maintained at preoperative body weight by food restriction, and VMH animals fed ad lib. Both VMH groups displayed basal and postabsorptive hyperinsulinemia, compared with the sham-operated control group, but insulin levels were greatest under the ad lib feeding condition. It is suggested that VMH hyperinsulinemia is due both to a primary effect of the lesion and to hyperphagia and that marked obesity can result in the absence of basal hyperinsulinemia as a result of hyperphagia with consequent postabsorptive hyperinsulinemia.

Animals↗
PubMed1985

Opiates and medial hypothalamic knife cuts cause hyperphagia through different mechanisms.

Several experiments were performed to determine whether the hyperphagia caused by medial hypothalamic knife cuts and that induced by opiate agonists are mediated by a common mechanism. In the first set of experiments, male Sprague-Dawley rats were given bilateral parasagittal medial hypothalamic knife cuts or a sham procedure and fed a high-fat Crisco-chow diet. Knife-cut and sham-operated rats were approximately equally sensitive to the suppressive effects of naloxone on food intake. The kappa opiate receptor agonist ketocyclazocine generally increased daytime food intake in sham-operated rats; in contrast, the normal hyperphagia of knife-cut rats was in most cases either unchanged or decreased by ketocyclazocine. In a second set of experiments, neither diet composition nor hypothalamic knife cuts significantly affected the feeding responses to naloxone or the stimulatory effects of the kappa agonist butorphanol tartrate. It was hypothesized that the differential effects of ketocyclazocine in knife-cut and sham-operated rats are a consequence of the sedative effects of the drug combined with the elevated baseline of the knife-cut subjects. This hypothesis was supported by a third experiment, in which ketocyclazocine also reduced nocturnal intake in unoperated rats and butorphanol increased intake. That feeding responses to naloxone and butorphanol were essentially unchanged by hypothalamic knife cuts suggests that the opioid feeding system is independent of the longitudinal feeding inhibitory pathway believed to be involved in knife-cut-induced hyperphagia.

Animals↗
PubMed1981

Vagotomy blocks hypothalamic hyperphagia in rats on a chow diet and sucrose solution, but not on a palatable mixed diet.

Adult female rats were given ventromedial hypothalamic parasagittal knife cuts (VMH treatment) or control surgery (Con treatment), followed 10 days later by subdiaphragmatic vagotomy (Vag treatment) or sham vagotomy (Sham treatment). The hyperphagia and obesity produced by the VMH cuts to rats on a chow diet was completely blocked by vagotomy (VMH-Vag group). Vagotomy also inhibited the VMH rats' overconsumption of a 20% sucrose solution during 1 hr/day and 24 hr/day tests, which contrasts with the effects of atropine treatment. However, when offered a selection of palatable foods (cookies, sweet milk, high-fat ration) in addition to chow, the VMH-Vag rats overate and gained considerably more weight than did the Con-Vag rats or the Con-Sham rats. The Con-Vag rats, on the other hand, gained less weight than did the Con-Sham rats on the palatable diet. The results indicate that intact subdiaphragmatic vagi are not essential for the expression of VMH hyperphagia and finickiness, and they therefore question the role of vagally mediated cephalic responses in the hypothalamic hyperphagia syndrome. On the other hand, the results indicate that in brain-intact animals vagotomy suppresses the development of diet-induced obesity.

Animals↗
PubMed1988

Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition?

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.

Animals↗
PubMed1981

Induction of hyperphagia in rats by intracerebroventricular infusion of sodium pentobarbital. A method for testing anorexigenic compounds.

In rats hyperphagia could be reversibly induced by intracerebroventricular infusion of sodium pentobarbital. Hyperphagia was elicited in a dose dependent manner, the optimal infusion rate being 1000 micrograms/h sodium pentobarbital. At this rate, feeding behaviour was induced selectively, with only minor side effects being apparent. Systemic application of d-methamphetamine or propylhexedrine given prior to infusion resulted in a dose dependent reduction of hyperphagia. The method, therefore, could be useful for testing putative anorexigenic compounds in hyperphagic rats.

Animals↗
PubMed1981

Hyperphagia and obesity. Relationship to medial hypothalamic lesions.

Progressive left hemiparesis followed by face and trunk cutaneous vasodilation and hyperphagia developed in a 28-year-old man. He began eating five to six meals a day and gained 16 kg in 60 days. Computed tomography disclosed a neoplastic lesion involving the midline via the hypothalamus and reaching the contralateral lenticular nucleus. Findings from endocrine studies, including thyroid-stimulating hormone, growth hormone, prolactin, and cortisol serum levels, were normal. Hyperphagia and consequent obesity were associated with bilateral destruction of the ventromedial hypothalamic area; cutaneous vasodilation was related to involvement of the preoptic area.

Body Weight↗
PubMed1997

Mosaicism for deletion 1p36.33 in a patient with obesity and hyperphagia.

We report on a 4-year-old girl with obesity and hyperphagia whose peripheral blood cytogenetic analysis showed mosaicism for a deletion of band 1p36.33. Terminal 1p deletions are rarely reported and this patient represents the first identified case of mosaicism. Given the subtlety of the cytogenetic abnormality and the possibility of mosaicism, the incidence of such deletions has probably been underestimated. While a characteristic phenotype associated with this karyotypic abnormality was described recently, the present report highlights the additional clinical findings of obesity and hyperphagia and the overlap of manifestations with Prader-Willi syndrome.

Child, Preschool↗
PubMed2000

Changes in leptin levels during lactation: implications for lactational hyperphagia and anovulation.

In these studies we investigated the time course of changes in circulating leptin levels in lactating rats and the dependence of these changes on the energetic cost of lactation and evaluated the contribution of changes in leptin levels to lactational hyperphagia and infertility. In the first experiment, plasma leptin levels were measured on Days 5, 10, 15, 20, and 25 postpartum in freefeeding lactating rats and age-matched virgin females. Retroperitoneal and parametrial fat pads weights were obtained from the same females. In the second experiment the same measures, together with plasma insulin and prolactin levels, were taken on Days 15 and 20 postpartum from galactophore-cut and sham-operated females. In Experiments 3 and 4, the effects of exogenous leptin administration, either subcutaneously (sc) or intracerebroventricularly (icv), on lactational anovulation, maternal food intake, and dam and litter weights were examined. Circulating leptin levels decreased in lactating rats. Leptin levels were highly positively correlated with fat pad weight. Eliminating the energetic costs of lactation by preventing milk delivery induced dramatic increases in plasma leptin and insulin levels and also increased adiposity. Exogenous leptin administration did not affect length of lactational anovulation but reduced food intake, maternal body weight, and litter weight gain when given centrally and maternal body weight when given systemically. Together, these data show that the energetic costs of lactation are associated with a fall in circulating leptin levels but that these do not make a major contribution to the suppression of reproduction in lactating rats; however, they may be permissive to the hyperphagia of lactation.

Animals↗
PubMed1999

Involvement of nitric oxide in the 5-HT1A autoreceptor-mediated hyperphagia in rats.

Effects of nitric oxide synthase(NOS) inhibitors on 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT)-induced hyperphagia which is mediated by the 5-HT autoreceptor were investigated. The non-selective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI) clearly suppressed increases in food intake by 8-OH-DPAT. Both hypophagic effects of L-NAME and 7-NI were reversed by the nitric oxide precursor, L-arginine. The findings suggest that nitric oxide formed in the brain is involved in 8-OH-DPAT-induced hyperphagia.

8-Hydroxy-2-(di-n-propylamino)tetralin↗