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PubMed1981

Clonidine-induced hyperphagia in monkeys: evidence for alpha 2-noradrenergic receptor mediation.

The mechanism of clonidine-induced hyperphagia and weight gain in monkeys was studied in 11 Stumptail macaques. Clonidine induced a significant increase in food intake over baseline levels and a significant weight gain after the 3-day treatment period. Both changes induced by clonidine were antagonized by the alpha 2-noradrenergic antagonist yohimbine, but not by prazosin, an alpha 1-noradrenergic antagonist. These results suggest that clonidine-induced hyperphagia and weight gain in monkeys are mediated through alpha 2-noradrenergic receptors.

Animals↗
PubMed1987

Hyperphagia and obesity in rats with bilateral ibotenic acid-induced lesions of the ventromedial hypothalamic nucleus.

Macro-electrophoretic applications of the cellular neurotoxin ibotenic acid into the ventromedial hypothalamic nucleus (VMH) resulted in hyperphagia and obesity in male rats. Histological examination showed a reduction in the number of neuronal VMH cell bodies with glial proliferation without evidence of non-specific damage. This supports the hypothesis that hyperphagia and obesity after VMH lesions are related to destruction of neurons intrinsic to the VMH.

Animals↗
PubMed1996

Nitric oxide mediates hyperphagia of obese Zucker rats: relation to specific changes in the microstructure of feeding behavior.

The presence of a nitric oxide synthetase (NOS) was demonstrated in the rat brain. It has been demonstrated recently that NOS-inhibitors reduce food intake in mammals and this suggest that nitric oxide (NO) might be a physiological mediator involved in the mechanisms controlling feeding behavior. Actually, there is no information about the acute central and peripheral effects of NOS-inhibitors on feeding behavior in obese and lean Zucker rats. That is why we investigated the acute dose-dependent activity of NG-Nitro-Arginine-Methyl-Ester (L-NAME) on food intake and feeding behavior in these rats. When given peripherally in the obese rats, L-NAME produced a dose-dependent decrease in food intake (p<0.001). The calculated MED and the ED 50 were 0.50 mg/kg IP and 3.46 mg/kg IP, respectively. These effects could not be reproduced in the lean Zucker rats whatever the dose used (p=0.59). The anorectic properties of L-NAME were very well translated into the microstructure of the feeding behavior. Time spent to eat (p<0.001), meal duration (p<0.01) and meal number (p<0.01) were reduced in the obese rats. Interestingly, L-NAME produced the same effects in the lean rats, but meal size increased in a compensatory manner. Central administration of L-NAME reproduced the same effects in the obese rats, but lean rats still remained insensitive. Central aminergic and/or peptidergic defects associated with the expression of hyperphagia might explain the differences observed between these lean and the obese animals. These results indicate a role of nitric oxide in the expression of hyperphagia and show that it might be a physiological mediator involved in the mechanisms controlling feeding behavior.

Animals↗
PubMed1981

Metabolic effects of hypothalamic hyperphagia.

In order to test the hypothesis that the enhanced gluconeogenesis of hypothalamic obesity remains responsive to changed in food intake, we have measured gluconeogenesis in two modes of hypothalamic obesity under both hyperphagic and normophagic conditions. The results show that hyperphagia partially decreases gluconeogenesis and fully restores liver glycogen in both modes. The discussion section relates our present findings to the enhanced glucose utilization previously noted after VMH destruction and to the recent hypothesis that hyperphagia is a response to body protein depletion.

Animals↗
PubMed1984

Characteristics of insulin-induced hyperphagia in the golden hamster.

Two experiments were performed to investigate in some detail the behavioural and metabolic effects of the administration of regular insulin to golden hamsters. In Experiment 1 dose-response curves describing the effects of insulin upon both food intake and plasma glucose (PG) were generated. Dosages of less than 20 units/kg did not cause increases in food intake, while dosages of 10 units/kg or greater produced significant hypoglycemia at +6 hr post-injection. There was also a significant inverse linear relationship (r = -.528) between individual hamsters' food intakes and PG levels over the range of insulin dosages. In Experiment 2, insulin (30 units/kg) caused increases in meal frequency but not in meal size, and hyperphagia developed within +3 hr of insulin administration. When food was not available, insulin caused PG levels to fall below control levels at +1 hr and to remain depressed until at least +6 hr post-injection. However when hamsters were allowed to eat, PG did not fall significantly below control levels until +3 hr and began to recover at +5 hr post-injection. Results are discussed in relation to several apparent peculiarities in the hamster's behavioural response to regular insulin, specifically the small magnitude and the slow development of insulin-induced hyperphagia, and the hamster's relative insensitivity to the hyperphagic effect of insulin.

Analysis of Variance↗
PubMed1990

Hyperphagia in rats produced by a mixture of fat and sugar.

The hyperphagic and weight-promoting effects of feeding rats a sugar-fat mixture were compared to those of presenting only one of the two nutrients. Experimental groups were fed sugar (sucrose), fat (corn oil), or a sugar-fat mixture as an option to chow; options were in the form of water solutions or emulsions. The control group was fed only chow. The sugar-fat group displayed a robust hyperphagia (greater than 36%), relative to the control group; the hyperphagic response was greater than that observed in the fat group but not in the sugar group. The sugar-fat group selected more calories from the option than the other two experimental groups. Body weight gains were also greater in the sugar-fat group than in the fat and sugar groups. Addition of saccharin to the fat emulsion increased fat and total intakes to levels close to those of the sugar-fat mixture. In a second experiment, the relative palatability of the plain and sweet fat emulsions was assessed with two-bottle preference tests. The sugar-fat mixture was preferred to the saccharin-fat mixture, which in turn was preferred to the plain-fat emulsion. These results suggest that the sweetness of the sugar-fat mixture contributed to the pronounced hyperphagia and obesity obtained with this diet option.

Animals↗
PubMed1993

Hyperphagia and obesity in female rats with temporal lobe lesions.

Damage to the temporal lobes in cats, dogs, and primates has long been known to result in hyperphagia and obesity, but research into the role of this area of the brain in feeding behavior has largely been neglected because of an inability to produce similar results in rats. The present study reports hyperphagia and obesity in female rats with small electrolytic lesions centered in the posterodorsal amygdala. Daily food intake more than doubled in the first few days after surgery and mean weight gain was more than four times that observed in animals with sham lesions during the first 26 days. The rats with lesions were not hyperresponsive to a switch in diets (lab chow to high-fat, and back). In all animals that gained abnormal amounts of weight, the posterior extent of the lesions extended through the amygdalohippocampal area into the ventral hippocampal formation. The results suggest that the temporal lobe is an important extrahypothalamic site for the regulation of food intake in rodents.

Animals↗
PubMed1985

Clonazepam-induced hyperphagia in nondeprived rats: tests of pharmacological specificity with Ro5-4864, Ro5-3663, Ro15-1788 and CGS 9896.

Nondeprived male rats were familiarised with daily 60 min access to a highly palatable diet, consisting of powdered rat diet, sweetened condensed milk and water. Clonazepam (0.625-5.0 mg/kg, IP) produced a substantial increase in food consumption within the first 30 min of access. The increase was similar across all dose conditions, suggesting that a maximal effect may have been achieved with a dose as small as 0.625 mg/kg. The hyperphagia induced by clonazepam was reversed by the benzodiazepine receptor antagonist, Ro15-1788 (5.0-20.0 mg/kg), indicating that the effect was benzodiazepine receptor-mediated. Treatments with the peripheral-type benzodiazepine agonist, Ro5-4864, did not induce a hyperphagic response. Instead, food consumption was significantly depressed following the administration of Ro5-4864 at 20 and 40 mg/kg, IP. A comparison of the clonazepam and Ro5-4864 data suggests that benzodiazepine-induced hyperphagia is mediated by central-type benzodiazepine binding sites. The pyrazoloquinoline, CGS 9896, binds with high affinity to benzodiazepine sites and has recently been described as a nonsedating anxiolytic. CGS 9896 (2.5-20.0 mg/kg, administered either IP or PO) did not affect consumption of the highly palatable diet. In consequence, anxiolytic and hyperphagic effects of drug actions at benzodiazepine receptors may be dissociated in the case of this compound. The atypical 1,4-benzodiazepine, Ro5-3663, a GABA antagonist which may act at the picrotoxinin site, produced a dose-related reduction in food consumption. Comparison with the results for Ro5-4864 rules out an interpretation for the anorexia in terms of anxiogenic effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Benzodiazepine-induced hyperphagia: a test of the hunger-mimetic model.

The 'hunger-mimetic' model is a prominent explanatory account of benzodiazepine-induced hyperphagia. A salient feature of food deprivation (hunger) in laboratory animals is 'finicky' eating, or an enhanced reactivity to the palatability of food. If the hunger-mimetic model is correct, a similar finicky pattern of increased eating should be observed both in hungry (food-deprived) rats and in benzodiazepine-treated, hyperphagic rats. Two groups of rats were matched on measures of ad lib baseline intake of both a highly palatable food (sweetened condensed milk) and a food low in palatability (milk adulterated with 37.5 mg% quinine). Subsequently one group was placed on a moderate food deprivation schedule while the second group was maintained on ad lib food but was injected (IP) with 5 mg/kg chlordiazepoxide (CDP) 30 min prior to food presentation tests. Single-bottle tests indicated that while the food deprived animals exhibited a greater augmentation of eating when given the high-palatability food, the animals pretreated with CDP exhibited an indiscriminate elevation of eating across both foods. Similarly, on two-bottle choice tests the food-deprived rats exhibited an enhanced preference for the high-palatability food, whereas the CDP-treated animals did not change from baseline food preference. These results fail to support the hunger-mimetic model of benzodiazepine-induced hyperphagia. Alternative models based on a perseverative, disinhibitory action of benzodiazepines are discussed.

Animals↗
PubMed1990

A contingent, conditioned suppression of eating following chronic benzodiazepine-induced hyperphagia.

While the hyperphagic effect of chloradizepoxide (CDP) has been reported by some to be enhanced with chronic drug treatment, the processes underlying this phenomenon are not well understood. In the present study, it was predicted that following chronic exposure to CDP-induced hyperphagia, animals given a placebo in place of their usual drug injection might be expected to exhibit evidence of a conditioned, drug-like response. Such a finding would then be consistent with an underlying process of behavioral sensitization. In Experiment 1a, Male Sprague-Dawley rats were randomly assigned to one of two groups receiving intraperitoneal (IP) injections of either 5 mg/kg CDP (Group CDP) or physiological saline (1 ml/kg; Group SAL) administered over 15 drug treatment days. Thirty minutes after each injection, all animals were given 30 min access to sweetened condensed milk. A significant enhancement of CDP-induced hyperphagia was observed over treatment sessions, confirming an earlier report. Unexpectedly, in the Placebo Test, the CDP animals exhibited a supression of milk consumption relative to that of the SAL group. Using the same animals, this finding was successfully replicated in Experiment 1b. In Experiment 2, it was hypothesized that if this conditioned, drug-opposite response were to reflect the involvement of some underlying compensatory, homeostatic mechanism, then it should only be observable under food-contingent conditions of chronic drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Potentiation of 2-deoxy-D-glucose antinociception, but not hyperphagia by zolantidine, a histamine (H2) receptor antagonist.

Antagonism of the histamine (H2) receptor reduces antinociception induced by naloxone-resistant foot-shock, naloxone-sensitive foot-shock, and morphine with a rank-order potency similar to their H2 antagonism. The antimetabolic glucose analog 2-deoxy-D-glucose (2DG) produces antinociceptive and hyperphagic responses that dissociate from each other and are in part mediated by opioid systems. The present study determined the effects of the brain-penetrating H2 receptor antagonist zolantidine (ZOL) on 2DG antinociception on the tail-flick and jump tests, as well as on 2DG hyperphagia, in rats. ZOL (0.01-1 mg/kg) potentiated the antinociceptive responses induced by a moderate (450 mg/kg) dose of 2DG, but had lesser effects upon antinociception induced by a lower (100 mg/kg) 2DG dose. ZOL itself slightly increased jump thresholds, but not tail-flick latencies. Combinations of ZOL and 2DG produced supraadditive antinociception, even though ZOL failed to significantly shift the 2DG dose-response curve to the left. In contrast, ZOL failed to alter basal intake or 2DG hyperphagia, supporting previous evidence implicating the H1 but not the H2 receptor in these effects. These results further dissociate the antinociceptive and hyperphagic effects of 2DG, and also support previous results indicating both pro- and antinociceptive roles for H2 receptors.

Animals↗
PubMed1987

Exercise-induced hyperphagia in the hamster is associated with elevated plasma somatostatin-like immunoreactivity.

Syrian golden hamsters when allowed free access to food and an exercise wheel will run long distances and develop hyperphagia and accelerated linear body growth with high circulating levels of growth hormone and insulin. Somatostatin, a widely distributed brain-gut neurohormonal peptide, modulates nutrient absorption and may regulate food intake. To examine the role of circulating plasma somatostatin-like immunoreactivity (SRIF-LI; pg/ml) in exercise induced hyperphagia 4 groups of animals were studied; an unrestricted exercise group (279.0 +/- 107.7, n = 10); a sedentary group (121.1 +/- 40.8, n = 8); a restricted exercise group (107.7 +/- 12.4, n = 6); and a restricted no exercise group (115.5 +/- 45.9, n = 9). Thus, the unrestricted exercise group has a significantly elevated SRIF-LI concentration (P less than 0.01) while there was no difference between the other 3 groups. The elevation of plasma SRIF-LI in the unrestricted exercise group may represent a response to modulate increased nutrient entry in this group or may represent an incompletely effective satiety signal.

Animals↗
PubMed1994

Differential effects of Tyr-MIF-1, MIF-1, and naloxone on peptide YY-induced hyperphagia.

Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) and MIF-1 (Pro-Leu-Gly-NH2) act as opiate antagonists in various behavioral systems including ingestion. Central injection of peptide YY (PYY) elicits a powerful feeding response in satiated rats, and the opioid antagonist naloxone decreases eating in a variety of conditions including PYY-stimulated eating. Therefore, the aim of this study was to examine the effects of Tyr-MIF-1 and MIF-1 as opiate antagonists on a naloxone-sensitive PYY model of hyperphagia. Naloxone at doses of 1.0 and 10.0 mg/kg, SC, decreased hyperphagia induced by 2.4 micrograms PYY injected in the PVN. MIF-1 and Tyr-MIF-1 had no effect on PYY-induced eating at doses comparable to naloxone (0.1 to 10.0 mg/kg, IP). These results suggest that in this model of eating behavior, Tyr-MIF-1 and MIF-1 do not act as opiate antagonists.

Animals↗
PubMed1994

Increased neuropeptide Y concentrations in specific hypothalamic regions of lactating rats: possible relationship to hyperphagia and adaptive changes in energy balance.

Lactation is accompanied by hyperphagia and a reduction in brown adipose tissue (BAT) thermogenesis, which are unexplained. Neuropeptide Y (NPY) powerfully stimulates feeding and inhibits BAT thermogenesis when injected into the paraventricular nucleus and other specific regions of the rat hypothalamus. We have tested the hypothesis that hypothalamic NPY activity is increased in lactating rats. Lactating rats consumed over four times as much food as nonlactating controls (n = 10; p < 0.001). Final plasma insulin concentrations in lactating rats were lower than in controls (6.8 +/- 0.8 vs. 11.7 +/- 2.1 pmol/l; p < 0.05) although plasma glucose and corticosterone concentrations were comparable (p > 0.05). Lactating rats showed significantly higher NPY levels than controls in specific hypothalamic regions, namely the arcuate nucleus-median eminence complex (a 41% rise; p < 0.001), paraventricular nucleus (35%; p < 0.001), ventromedial nucleus (66%; p = 0.003), and dorsomedial nucleus (78%; p < 0.001). Other hypothalamic regions showed no significant differences between groups. Increased NPY concentrations in specific hypothalamic regions, particularly the arcuate nucleus where NPY is synthesized, suggest increased activity of the hypothalamic NPYergic system in lactation. Neuropeptide Y may mediate hyperphagia and reduced BAT thermogenesis in lactation. Hypoinsulinemia may be a stimulus to hypothalamic NPY in lactation, as has been postulated in other conditions of negative energy balance.

Adaptation, Physiological↗
PubMed2006

Prader-Willi-like phenotype: investigation of 1p36 deletion in 41 patients with delayed psychomotor development, hypotonia, obesity and/or hyperphagia, learning disabilities and behavioral problems.

Monosomy 1p36 is one of the most commonly observed mental retardation (MR) syndromes that results in a clinically recognizable phenotype including delayed psychomotor development and/or MR, hypotonia, epilepsy, hearing loss, growth delay, microcephaly, deep-set eyes, flat nasal bridge and pointed chin. Besides, a Prader-Willi syndrome (PWS)-like phenotype has been described in patients with 1p36 monosomy. Forty-one patients presenting hypotonia, developmental delay, obesity and/or hyperphagia and behavioral problems who tested negative for PWS were investigated by FISH and/or microsatellite markers. Twenty-six were analyzed with a 1p-specific subtelomeric probe, and one terminal deletion was identified. Thirty patients (15 of which also studied by FISH) were investigated by microsatellite markers, and no interstitial 1p36 deletion was found. Our patient presenting the 1p36 deletion did not have the striking features of this monosomy, but her clinical and behavioral features were quite similar to those observed in patients with PWS, except for the presence of normal sucking at birth. The extent of the deletion could be limited to the most terminal 2.5 Mb of 1p36, within the chromosomal region 1p36.33-1p36.32, that is smaller than usually seen in monosomy 1p36 patients. Therefore, chromosome 1p36.33 deletion should be investigated in patients with hypotonia, developmental delay, obesity and/or hyperphagia and behavioral problems who test negative for PWS.

Adolescent↗
PubMed2005

Allopregnanolone produces hyperphagia by reducing neophobia without altering food palatability.

The neurosteroid allopregnanolone may increase feeding by altering food palatability; however, it may also increase feeding by reducing anxiety (neophobia). Moreover, it is unclear whether this induced hyperphagia is selective to safe, palatable foods only. Male rats were injected with allopregnanolone 20 min prior to behavioral testing. The taste reactivity test was used to examine possible shifts in the palatability of a 0.3 M sucrose solution. A lickometer was used to monitor intake and licking of either a sucrose or sucrose-quinine solution. Sucrose palatability was not enhanced; however, allopregnanolone significantly increased sucrose intake and licking on Test Day 1 when the solution was novel, but not on Test Day 2 when the solution was familiar. Sucrose-quinine intake was not enhanced. Allopregnanolone-induced hyperphagia is not a result of altered sucrose palatability, but rather reflects a reduction in the neophobia elicited by a novel solution; an effect that further seems to be selective to safe, palatable foods.

Analysis of Variance↗
PubMed2006

Role for dopamine-3 receptor in the hyperphagia of an unanticipated high-fat meal in rats.

Behavioral studies have indicated that midbrain dopamine projections arising in the ventral tegmental area and substantia nigra play a central role in integrating violations of expectancy in reward-related paradigms. The present study was designed to assess violations of dietary expectation and the role the dopamine-3 receptor plays in integrating reward-related food intake in violations of expectancy. Two groups of rats were conditioned to a meal-feeding schedule (3 h of access to food per day) in which they received either standard rodent chow or a preferable, high-fat diet. Animals either received the diet they had access to during the training period (no contrast) or the opposite diet (negative and positive contrast). As predicted, animals in the positive contrast condition were hyperphagic compared to no contrast animals. Animals in the negative contrast (high fat to chow) condition were hypophagic compared to no contrast animals. A dopamine agonist specific to the dopamine three receptor, ((+/-)-7-Hydroxy-dipropylaminotetralin HBr) and the dopamine-2 receptor antagonist raclopride were administered in equimolar doses peripherally to assess the involvement of the dopamine receptor subtypes in the violation of expectancy food intake effects. 7-Hydroxy-dipropylaminotetralin HBr blocked the hyperphagia associated with positive contrast and did not disrupt intake in the negative contrast or no contrast paradigm. Raclopride was ineffective at disrupting food intake. These results support the hypothesis that the dopamine-3 receptor is involved in the hyperphagia of an unexpected high fat meal.

Animals↗
PubMed2005

Effect of CCK-8 on insulin-induced hyperphagia and hypothalamic orexigenic neuropeptide expression in the rat.

The influence of cholecystokinin octapeptide (CCK-8) on normal and insulin-induced feeding and expression of orexigenic hypothalamic neuropeptides was investigated in male rats. CCK-8, administered during meals (4 microg/kg) or continuously (32 microg/kg over 60 min), blunted the stimulating effect of insulin (50 IU/kg) on feeding by reducing meal size (-60%; P<0.05 or -86%; P<0.0001, respectively). Rats without access to food and injected with IP insulin (50 IU/kg) showed increased hypothalamic mRNA levels of orexin (+30%; P<0.05) and melanin-concentrating hormone (+52%; P<0.05), as compared with ad libitum-fed and saline-injected control rats. Continuous IP infusion of CCK-8 (32 microg/kg) blunted these increases. Our results suggest that both orexin and melanin-concentrating hormone participate in the response to insulin hypoglycemia without food being present; these neurons may be involved in mechanisms related to insulin-induced hyperphagia. Signals triggered by peripheral CCK-8 act to decrease the expression of orexin and melanin-concentrating hormone. This may be associated with a reduction in hyperphagia.

Animals↗