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PubMed1983

Hypothalamic astrocytoma. Syndrome of hyperphagia, obesity, and disturbances of behavior and endocrine and autonomic function.

A 26-year-old woman had hyperphagia, obesity, aggressive behavior, visual hallucinations, reversal of wake-sleep patterns, hypothermia, hypothyroidism, and amenorrhea. She died of pancreatitis, probably secondary to hypothermia. Autopsy revealed a low-grade astrocytoma in the third ventricle and medial anterior and mid hypothalamus, primarily on the right. Although she exhibited thyroid and ovarian hypofunction, the patient had intact median eminence and pituitary function, suggesting end-organ failure, possibly of an autoimmune nature.

Adult↗
PubMed1998

An investigation of satiety in ageing, dementia, and hyperphagia.

OBJECTIVE: To investigate satiety in young, middle-aged, and elderly healthy adults, and in nonhyperphagic and hyperphagic elderly people with dementia. Previous work suggested hyperphagia in dementia was due to increased hunger and absence of satiation. METHODS: The primary measure of satiety was the amount of food eaten in an ad libitum meal, given 1 hr after a fixed preload. Three types of preload were used, high- and low-energy milkshakes and water. The effect of age was investigated by comparing the three groups of healthy adults. The effect of dementia was investigated by comparing the two demented groups with healthy elderly. RESULTS: Measurements suggested that accuracy of compensation for preload energy differences decreased with age and was absent in people with dementia. DISCUSSION: Lack of compensatory response in the elderly, particularly those with dementia, indicates the need for monitoring food intake to prevent over- or undereating.

Adult↗
PubMed2006

Hyperphagia and obesity of OLETF rats lacking CCK1 receptors: developmental aspects.

Otsuka Long Evans Tokushima Fatty (OLETF) rats have a deletion in the gene encoding the cholecystokinin-1 (CCK1) receptor. This deletion prevents protein expression, making the OLETF rat a CCK1 receptor knockout model. Consistent with the absence of CCK1 receptors, OLETF rats do not reduce their food intake in response to exogenously administered CCK and consume larger than normal meals. This deficit in within-meal feedback signaling is evident in liquid as well as solid meals. Neonatal OLETF rats show similar differences in independent ingestion tests. Intake is higher and is reflected in greater licking behavior. Neonatal OLETF rats also have diminished latencies to consume and higher initial ingestion rats. Adult OLETF rats are hyperphagic and obese. Although arcuate nucleus peptide gene expression is apparently normal in OLETF rats, when obesity is prevented through pair-feeding to amounts consumed by control Long Evans Tokushima Otsuka (LETO) rats, dorsomedial hypothalamic NPY mRNA expression is significantly elevated in OLETF rats. NPY overexpression is also evident in preobese, juvenile OLETF rats suggesting a causal role for this overexpression in the hyperphagia and obesity. Running wheel exercise normalizes food intake and body weight in OLETF rats. When access to exercise is provided at a time when OLETF rats are obese, the effects are limited to the period of exercise. When running wheel access is available to younger, preobese OLETF rats, exercise results in long lasting reductions in food intake and body weight and improved glucose regulation. These lasting metabolic effects of exercise may be secondary to an exercise induced reduction in DMH NPY mRNA expression.

Animals↗
PubMed1993

Time-dependent effects of progressive gamma-linolenate feeding on hyperphagia, weight gain, and erythrocyte fatty acid composition during growth of Zucker obese rats.

Obese Zucker rats (fa/fa) have low levels of arachidonic acid (AA) in liver phospholipids (PL). We have previously shown that a 70% gamma-linolenate concentrate (GLA; an AA intermediate) fed at a fixed dose (0.07 g/day) normalized hepatic PL AA and reduced weight gain selectively in the obese animals. In a follow-up study, 16 obese (fa/fa) and 16 lean (Fa/Fa) 4-week-old male rats were randomized into 4 groups of 8 each and gavaged daily with soybean oil (SOY) containing 55% 18:2omega6 (an AA precursor) or GLA, using a progressive dose (< or = 5% of total calories) based on body weight. A defined diet with 11% of energy as SOY was fed ad libitum for 60 days. GLA obese had lower body weight (p<0.0001) and 60-day cumulative food intake (p<0.05) compared to SOY obese, but neither parameter differed between the lean groups. For the last twenty days cumulative food intake was identical for GLA obese and SOY lean, whereas SOY obese consumed 18% more (p<0.05). Thus the progressive dose of GLA selectively suppressed hyperphagia in obese Zucker rats. Erythrocytes collected at 15-day intervals showed parallel increases in AA in both genotypes over time, suggesting normal AA availability during rapid growth. Thus, the reduced PL AA in the livers from the obese rats probably reflects impaired distribution in selected tissues rather than reduced hepatic production. Due to the potential health risks of enriching tissue lipids with AA, great caution is advised in considering GLA as therapy for human obesity.

Adipose Tissue↗
PubMed2002

Glucocorticoids and parental hyperphagia in ring doves (Streptopelia risoria).

These studies explored the possibility that glucocorticoids promote parental care in ring doves by mediating, at least in part, the pronounced increase in food consumption that parent doves exhibit while provisioning their young. Plasma concentrations of the endogenous glucocorticoid corticosterone were found to be significantly higher in breeding females during the posthatching phase than during the incubation period. These differences were not observed in male breeding partners, but sex differences in daily activity rhythms are well documented in breeding doves, and blood sampling at different times of day would be required to adequately characterize the pattern of corticosterone in males during these breeding stages. In studies on nonbreeding doves, twice-daily intracerebroventricular (icv) injections of the synthetic glucocorticoid dexamethasone (DEX) increased food intake by 25-50% in both sexes, and further studies in males revealed that the increase was directly related to the dose of DEX administered. The highest dose of DEX given icv (1.0 microg/day) was not effective in stimulating feeding when given systemically, thereby suggesting that the hyperphagic action of DEX is exerted directly on the central nervous system. The icv infusion of the selective glucocorticoid receptor antagonist RU38486 blocked the hyperphagic effects of twice-daily icv injections of DEX in both sexes. Collectively, these data support the hypothesis that corticosterone contributes to the parental hyperphagia exhibited by breeding doves during the posthatching period. They also suggest that these orexigenic effects are mediated in part by CNS binding sites that resemble mammalian glucocorticoid receptors.

Animals↗
PubMed1993

Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions.

A case of childhood post-traumatic akinetic mutism is presented. The patient showed a hyperphagic condition while recovering from akinetic mutism. He had lesions in the left interlaminal nucleus of the thalamus, right globus pallidus, and right dorsomedial nucleus of the hypothalamus. Laboratory data indicated slightly disturbed hypothalamic functions. In general, akinetic mutism can be seen with bilateral destructive lesions, while hyperphagia may occur after destruction of dorsomedial hypothalamic nucleus, but it is very rare. This is the first reported case of akinetic mutism caused by a unilateral lesion.

Akinetic Mutism↗
PubMed1993

Striatal regulation of morphine-induced hyperphagia: an anatomical mapping study.

Both systemic and intracranial administration of morphine can result in spontaneous feeding in non-deprived rats. The present investigation was conducted to examine the involvement of the striatum in this phenomenon. Morphine sulfate (0, 0.5, 1.0, 5.0, 10.0, and 20.0 micrograms/0.5 microliters) was microinjected into five discrete striatal subregions in non-deprived rats: the nucleus accumbens, the ventromedial striatum, the ventrolateral striatum, the anterior dorsal striatum, and the posterior dorsal striatum. Feeding, drinking, locomotion, rearing, and food intake were measured over 4 h after infusion. Results indicate that the striatum is a heterogeneous structure with regard to the regulation of opiate-induced feeding behavior and locomotor activity. Morphine infusion into anteroventromedial regions including the nucleus accumbens resulted in a marked hyperphagia that was generally delayed in onset; much smaller increases or no change in feeding occurred after administration into more dorsal, lateral and posterior areas. It is hypothesized that there may exist within the striatum an anatomical gradient that is most sensitive to opiate-induced feeding within the anteroventromedial sector. Since this area has extensive connections with other brain sites sensitive to opiate-induced feeding, it may be a critical part of an opiatergic feeding system within the brain. In addition, a possible role for the anteroventromedial striatum in compulsive feeding and bulimia is discussed.

Animals↗
PubMed1998

Hyperphagia and self-mutilation in Prader-Willi syndrome: psychopharmacological issues.

This study focused in the treatment of two major Prader-Willi symptoms: hyperphagia and self-injurious behavior (SIB). Four patients participated in a four-year study with monthly follow-ups. Patients lived in a behaviorally structured environment, and were treated with selective serotonin reuptake blockers and phenothiazines. Psychopharmacological intervention improved SIB symptoms, but was ineffective to control appetite satiation.

Adult↗
PubMed2005

A comparative proteomic analysis of the rat brain during rebound hyperphagia induced by space-restriction.

Although neurochemical changes have been reported in the brain in animal models of binge eating, biochemical changes of specific proteins in the brain are unknown. Our aim was to elucidate brain proteins altered in rats during enhanced rebound hyperphargia. Rats were deprived of food for 22 h/day for 6 days, then allowed free access to food for 24 h in normal cages (rebound hyperphargia) or in space-restricted cages (enhanced rebound hyperphargia). Proteins extracted from the rat brain were separated by two-dimensional gel electrophoresis, and compared with those from control rats freely fed for 7 days in normal cages. Proteins expressed differently from controls were identified by N-terminal amino acid sequencing and mass fingerprinting using a MALDI-TOF mass spectrometer. Among proteins in the corpus striatum, frontal lobe, hippocampus and thalamus/hypothalamus, ubiquitin C-terminal hydrolase L1 and peroxiredoxin 2 decreased in the hippocampus and phosphatidylethanolamine-binding protein increased in the thalamus/hypothalamus of rats with the enhanced rebound hyperphargia induced by space-restriction. In this study, we first demonstrated that three brain proteins changed in rats during enhanced rebound hyperphagia. These proteins might have pathophysiologic relevance to binge eating.

Animals↗
PubMed1986

Components of hypothalamic obesity: bipiperidyl-mustard lesions add hyperphagia to monosodium glutamate-induced hyperinsulinemia.

Rats with bilateral electrolytic lesions in the general region of the ventromedial hypothalamic (VMH) nucleus develop hyperinsulinemia, excessive food intake and obesity. Monosodium glutamate (MSG) destroys neurons of the arcuate hypothalamic (AH) nucleus and produces hyperinsulinemic but hypophagic obesity. Bipiperidyl mustard (BPM) primarily destroys VMH neurons, but has produced only a slight obesity even when rats were maintained on high-fat diets. In the present study, rats treated with MSG (AH lesion) were hyperinsulinemic, moderately obese and hypophagic; BPM rats (primarily VMH lesion) were not different from controls when fed standard chow diets. However, MSG/BPM rats (AH + VMH lesion) were hyperinsulinemic, massively obese and hyperphagic. Thus, two components of the electrolytic lesion syndrome previously attributed to VMH damage (hyperinsulinemia and obesity) were reproduced simply by MSG treatment alone. The third component (hyperphagia) occurred only when both AH and VMH were lesioned, suggesting that neurons in both nuclei may perform a satiety function and may be able to substitute for one another in this respect. Since MSG treatment is required for all components of both obesity syndromes described here, this underscores the importance of MSG-sensitive neurons in mechanisms of obesity. The combined treatment approach also represents the first rat model of hyperinsulinemic, hyperphagic obesity that can be entirely produced by systemic administration of neurotoxins.

Animals↗
PubMed1993

Functional mapping of neural sites mediating prolactin-induced hyperphagia in doves.

Microinjections of prolactin (PRL) into the ventromedial nucleus of the hypothalamus (VMN) or the preoptic area (POA) have been previously shown to increase food intake and body weight in ring doves. In an attempt to corroborate these results and to provide a more complete map of PRL-sensitive brain sites mediating the orexigenic action of PRL, a microinjection procedure was employed in the present study that delivered PRL or saline vehicle in extremely small volumes (10 nl/injection) to a variety of diencephalic sites in dove brain that had been previously demonstrated to contain high concentrations of PRL receptors. Estimates obtained from one female subject given a single 10 nl injection of [125I]ovine PRL into the VMN supported the claim that such injection volumes resulted in limited diffusion, as 80% of the tissue radioactivity was found within a 280 mm area surrounding the injection site at 30 min after injection. Food intake of cannulated male doves in the mapping study was monitored daily during a 6 day baseline period, an initial 4 day treatment period, a 6-12 day post-treatment recovery period, and a second 4 day treatment period. Approximately half of the birds received PRL injections (50 ng/10 nl twice daily) and saine vehicle injections (10 nl twice daily) during the first and second treatment periods, respectively, while remaining birds received these treatments in the reverse order. No significant changes in food intake across baseline, vehicle, post-treatment, or PRL treatment periods were observed in birds with injection sites in the lateral POA, paraventricular nucleus of the hypothalamus (PVN), or the medial-basal hypothalamic region between the tuberal hypothalamus (TU) and VMN. In contrast, injections of PRL into the VMN area, medial POA, or TU resulted in average daily food intake values that significantly exceeded those recorded during other periods. The most robust feeding response was seen in the VMN group, where PRL injections resulted in a 58% increase in food intake over that recorded during injection of vehicle. This increase was significantly greater than that observed following PRL injections into the mPOA (26%) or the TU (32%). These findings suggest that the VMN may be a primary site of PRL action in promoting hyperphagia in this species, although PRL effects at other diencephalic loci, such as the mPOA and TU, may also contribute to the orexigenic action of this hormone.

Animals↗
PubMed1996

Stimulation of 5-HT2A receptors in the paraventricular hypothalamus attenuates neuropeptide Y-induced hyperphagia through activation of corticotropin releasing factor.

The effect of 5-HT1 and 5-HT2 receptor agonists administered into the paraventricular hypothalamus was studied on the hyperphagia caused by neuropeptide Y (NPY) injected into the same area. The 5-HT2A/2C receptor agonist DOI (10-20 nmol/0.5 microliter) significantly reduced NPY overeating while the 5-HT1A/1B receptor agonist RU 24969 (3.5-14 nmol/0.5 microliter) and the 5-HT1B/2C receptor agonist mCPP (5-20 nmol/0.5 microliter) had no such effect. The 5-HT2A receptor antagonist spiperone (5 microgram/0.5 microliter) and the corticotropin releasing factor antagonist alpha-helical-CRF9-41 (0.5-1 micrograms/0.5 microliter) completely antagonized the effect of 10 nmol DOI.

Amphetamines↗
PubMed1989

Glutathione depletion by hyperphagia-induced obesity.

Reduced glutathione (GSH) levels in freeze-clamped livers of rats and mice in which hyperphagia is induced by cafeteria diet are 45% lower than in controls. Freshly isolated hepatocytes from mice fed cafeteria diet show a 45% decrease in GSH concentration and a 54% decrease in oxidized glutathione (GSSG) concentration when compared with controls. The rate of GSH synthesis in isolated hepatocytes from control mice is significantly higher than in those from mice fed cafeteria diet. Oral GSH is effective to prevent the decrease in hepatic GSH levels found in cafeteria fed mice.

Animals↗
PubMed1985

Hyperphagia induced by 2-deoxy-D-glucose in the presence of the delta-opioid antagonist ICI 174,864.

The effect of the selective delta-opioid antagonist ICI 174,864 (N,N-bisallyl-Tyr-Aib-Aib-Phe-Leu-OH: Aib=alpha-aminoisobutyric acid) on the hyperphagia induced by 2-deoxy-D-glucose (2-DG) was investigated in non-deprived rats. The increase in food intake produced by 2-DG (500 mg/kg i.p.) was not reduced by ICI 174,864 at a dose (3 micrograms/rat i.c.v.) which totally abolished the feeding response to the delta-agonist D-Ala2-D-Leu5-enkephalin (10 micrograms/rat i.c.v.). These findings suggest that the appetitive effects of 2-DG are not mediated by an enkephalinergic/delta-receptor system. They do not, however, preclude the possible involvement of endogenous opioids acting at other sub-types of opioid receptor in this glucoprivic ingestional response, which is suppressed by less specific opioid antagonists such as naloxone.

Animals↗
PubMed1989

Hyperphagia induced by pylorectomy in sheep.

In the hay-fed sheep, gastric (abomasal) contents are delivered continuously into the duodenal bulb at a mean flow rate of 210 ml per hour. The pylorus could behave as the site of origin of a feedback satiety signal by acting as a distal stomach sphincter limiting the abomasal emptying rate. This ability of the pyloric sphincter was confirmed by enhancement of abomasal outflow following either pylorectomy or pyloroplasty. In both cases, the subsequent reduction of the mean residence time of digesta in the abomasum was accompanied by an increase in the voluntary intake. The increase by 48% of food intake persisted several weeks after pylorectomy and was not only compensatory for the lower intake during recovery from surgery. Such an hyperphagia, obtained by removal of the ruminant herbivore pylorus, suggests the suppression at the antroduodenal junction level of a regulating factor affecting voluntary food intake by modulating the mean residence time of digesta in the abomasum.

Animals↗
PubMed1989

Hypothalamic and basal forebrain germinoma presenting with amnesia and hyperphagia.

Patients harboring primary intracranial germinomas usually have had Parinaud's syndrome and hydrocephalus (with pineal tumors) or hypopituitarism, visual loss, and diabetes insipidus (with suprasellar tumors) at presentation. The few reported cases of verified intraparenchymal hypothalamic germinomas all have been in prepubertal males with progressive neurologic deficits, altered levels of consciousness, or clinically apparent panhypopituitarism. The subject of this report was an endocrinologically normal, primiparous 24-year-old woman who presented with hydrocephalus followed by worsening anterograde amnesia and hyperphagia despite having a functioning ventriculoatrial shunt. Computed tomography scanning and magnetic resonance imaging demonstrated an anterior hypothalamic, thalamic, and basal forebrain mass, which stereotactic biopsy proved to be a germinoma. Intraaxial germinomas restricted to the anterior hypothalamus or thalamus rarely have been reported. The clinical features of the current patient may be unique.

Adult↗
PubMed1991

Reported hyperphagia in foster children.

In evaluating a large group of foster children from biological families with a high incidence of alcohol and/or drug abuse, there emerges a subsample of children with both atypical eating patterns as well as atypical behavior patterns. Their physical and behavioral characteristics are described. These children are neither obese nor "failure to thrive." They display an excessive appetite for food, a driven quality to their eating, an apparent lack of satiety, and frequent eating to the point of vomiting or gastric pain if food intake is not limited externally. All of these children have psychiatric disorders. Hyperphagia appears to be a marker for significant psychopathology.

Adaptation, Psychological↗
PubMed1994

Chronic cerebroventricular galanin does not induce sustained hyperphagia or obesity.

Acute central administration of galanin has been reported to increase fat consumption. These experiments were designed to test the hypothesis that repeated injections of galanin would elicit hyperphagia and weight gain and that this response would depend on the available diet. Male Sprague-Dawley rats were fed high (56% energy) or low (10% energy) fat diets. Galanin (300 pmol) or saline vehicle was injected into the third ventricle twice daily for 7 days and three times daily for another 6 days. On both the high-carbohydrate and high-fat diets, twice daily galanin increased daytime food intake, but there was a compensatory decrease in nighttime intake. The addition of a third, nighttime injection of galanin was ineffective in producing an increase in total 24-h intake. There was no significant increase in body weight during galanin treatment in rats eating either diet although animals eating the high-fat diet gained more weight as reflected by a significant increase in epididymal fat pad weight. Galanin treatment had no effects on serum insulin, glucose or corticosterone concentrations, measured at the end of the experiment. However, animals fed the high-fat diet had significantly higher insulin concentrations at the time of sacrifice. Although repeated central infusions of galanin reliably stimulated daytime intake of both diets, they failed to increase total daily energy intake or body weight.

Animals↗