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At least 19 recordsLinked to original sources
PubMed1991

High-fat diets stimulate transient hyperphagia whereas wet diets stimulate prolonged hyperphagia in Fischer rats.

The effectiveness of several different kinds of diets in stimulating hyperphagia in Fischer strain rats was compared. Of three different high-fat diets examined, only one stimulated significant hyperphagia and stimulated weight gain; this diet was high in both fat and carbohydrate. However, this hyperphagia and increased weight gain was transient, lasting less than four weeks. A high-sucrose diet stimulated energy intake for only one week. In contrast, adding water to a high-starch diet or adding saccharin to a wet diet stimulated energy intake and weight gain for at least ten weeks. Once water or saccharin were removed from these diets, hyperphagia subsided or even turned into hypophagia, until body weights approached control levels. The degree of hyperphagia during the first week did not correlate with subsequent hyperphagia or weight gain. These results suggest that wet diets act by different mechanisms than do dry high-fat and high-sucrose diets.

Animals↗
PubMed1997

Hyperphagia in dementia: 1. The use of an objective and reliable method for measuring hyperphagia in people with dementia.

Up to one third of dementia sufferers eat an increased quantity of food, compared with their premorbid intake, at some stage during the dementia. A proportion of these eat extraordinarily large quantities if food intake is not restricted. In order to investigate this phenomenon in detail, a reliable and standardized method of quantifying the degree of hyperphagia is required. We report the development of such a method. Twenty-six people with dementia, who were reported by their carers to be hyperphagic, were compared with 14 matched non-hyperphagic controls with dementia and 14 matched normal elderly. Subjects were offered two standardized meals, under specified conditions, ad libitum. One meal consisted of a single food, the other of a mixture of foods. The total energy intake provided a reliable measure of the degree of hyperphagia. The single food meal was more reliable but the mixed meal was a more sensitive measure of the hyperphagia.

Aged↗
PubMed1997

Hyperphagia in dementia: 2. Food choices and their macronutrient contents in hyperphagia, dementia and ageing.

Up to one third of dementia sufferers eat an increased quantity of food compared with their premorbid intake, at some stage during the dementia. In addition, over half of people with dementia are reported, by their carers, to show a marked change in food choice, particularly an increased liking for sweet food. The macronutrient content of foods chosen and the ratio of sweet to savoury foods were investigated experimentally using a standardized mixed meal. Three subject groups were studied: 17 people with dementia who were reported by their carers to overeat and who ate excessively under experimental conditions; 14 people with dementia who ate a normal amount; and, normal, non-demented controls (18 under 50 years old and 14 over 50 years old). The results showed that the normal elderly people chose a lower proportion of high-protein food than the young. The proportion of protein eaten was lower in people with dementia than in age-matched controls and was even lower in the hyperphagic dementia group. The proportion of sweet food eaten was higher in people with dementia and even higher in people with dementia who were hyperphagic. Various mechanisms to account for the results are discussed.

Adult↗
PubMed1997

Increased receptor sensitivity to neuropeptide Y in the hypothalamus may underlie transient hyperphagia and body weight gain.

Disruption of neural signaling by microinjection of a neurotoxin, colchicine (COL), in the ventromedial hypothalamus (VMH) of rats results in rapid and transient hyperphagia and body weight gain. Since neuropeptide Y (NPY) is a potent hypothalamic orexigenic signal and continuous NPY receptor activation by intracerebroventricular (icv) NPY infusion results in hyperphagia and obesity, we tested the hypothesis that altered NPYergic signaling may underlie the transient hyperphagia in COL-injected rats. Immediately following COL (4 microg) microinjections in the ventromedial nucleus (VMN) rats displayed hyperphagia both during the lights-on and lights-off periods. Concomitant with hyperphagia, preproNPY mRNA levels in the arcuate nucleus and NPY levels in the paraventricular nucleus decreased in a time-dependent manner. However, food intake in response to intracerebroventricular injections of NPY (29, 117 and 470 pmole) was significantly higher in COL-injected rats and the latency to initiation of feeding was markedly reduced as compared to controls. The smallest dose of NPY which was virtually ineffective in control rats, evoked near maximal intake in COL-injected rats. This enhanced response lasted for only 4 days paralleling the transient hyperphagia. The NPY Y1 receptor antagonist 1229U91 (5 or 30 microg/rat, icv) significantly suppressed feeding in COL-treated rats thereby indicating that hyperphagia in these rats was dependent upon endogenous NPY. Overall, these studies demonstrate that not only high levels, but low levels of NPY may also result in hyperphagia and increased body weight and this hyperphagia may be attributed to the rapid development of NPY Y1 receptor hypersensitivity.

Animals↗
PubMed1991

Possible involvement of dopamine D-1 and D-2 receptors in diazepam-induced hyperphagia in rats.

Possible involvement of dopamine receptors in diazepam-induced (1 mg/kg, subcutaneous (sc] hyperphagia was studied in nondeprived rats. Pretreatment with the selective D-1 antagonist, SCH23390 (0.03 mg/kg, sc) inhibited diazepam-induced hyperphagia. In addition, pretreatment with the preferential D-2 antagonists, haloperidol (0.1 to 0.3 mg/kg, sc) and clebopride (0.1 to 0.3 mg/kg, sc) inhibited diazepam-induced hyperphagia in a dose-dependent manner. Pretreatment with co-administration of SCH23390 (0.1 mg/kg, sc) and clebopride (0.03 mg/kg, sc) completely inhibited this hyperphagia. The selective D-2 antagonist, sulpiride (40 mg/kg, sc) and the peripheral D-2 antagonist, domperidone (10 mg/kg, sc) did not affect diazepam-induced hyperphagia. However, sulpiride (10 micrograms, icv) or domperidone (2 micrograms, icv) administered centrally inhibited this hyperphagia. The highest dose of haloperidol (0.3 mg/kg, sc) or clebopride (0.3 mg/kg, sc) and higher doses of SCH23390 (0.01 and 0.03 mg/kg, sc) or SCH23390/clebopride (0.01/0.03 and 0.01/0.1 mg/kg, sc) tended to decrease spontaneous feeding in non-deprived rats. In addition, the highest dose of haloperidol, clebopride or SCH23390/clebopride inhibited spontaneous feeding in deprived rats. Interestingly, diazepam-induced hyperphagia was inhibited significantly by doses of haloperidol (0.1 mg/kg, sc), clebopride (0.1 mg/kg, sc) and SCH23390/clebopride (0.003/0.03 and 0.003/0.1 mg/kg, sc) which did not affect spontaneous feeding in non-deprived or deprived rats. Pretreatment with alpha-methyl-p-tyrosine (40 mg/kg, IP x 2, 6 and 2 h prior to diazepam administration) failed to inhibit this hyperphagia. Furthermore, pretreatment with a large dose of haloperidol (5 mg/kg, sc, 4 days before diazepam administration) augmented the sub-hyperphagic effect to diazepam (0.5 mg/kg, sc). Thus, these findings suggest that hyperphagia to diazepam is mediated in part by both dopamine D-1 and D-2 receptors in non-deprived rats.

Animals↗
PubMed1998

Natural history of hyperphagia and other eating changes in dementia.

OBJECTIVE: To investigate the natural history of overeating (hyperphagia) and its elements during the course of dementia. DESIGN: Prospective longitudinal study of overeating (hyperphagia) in dementia. Two studies were carried out: (1) hyperphagia and associated eating changes were investigated as part of a larger prospective 10-year study into behaviour changes, using carers' reports; (2) an observational study to investigate hyperphagia quantitatively; this took place over the course of a year by means of direct observation of test meals in a normal environment. SETTING: Subjects with dementia living in Oxfordshire, UK. PARTICIPANTS: (1) 99 people with dementia, living at home with a carer, with data for more than 1 year. (2) Nine people with a diagnosis of Alzheimer's disease who were hyperphagic. MEASURES: (1) The Present Behavioural Examination was used at 4-monthly intervals to assess the subjects' behaviour and psychological functioning. (2) Food intake, macronutrient choice and the microstructure of eating were measured using a standardized test meal. RESULTS: (1) Severe or persistent hyperphagia was reported in 23% of the sample and carers reported a clear onset to hyperphagia with a median duration of 16 months. (2) From direct observation, each person who was hyperphagic was seen to maintain a constant eating rate in test meals during the course of a year but meals ended earlier as hyperphagia decreased. CONCLUSIONS: Hyperphagia is common in dementia, it occurs over a single restricted period, mainly during the middle stages of dementia, and is not significantly related to age, sex, diagnosis, medication or activity.

Aged↗
PubMed1990

Diet composition determines course of hyperphagia in developing Zucker obese rats.

Previous observations from this laboratory indicate that, during growth, the hyperphagia of the male genetically obese Zucker rat reaches a peak or "breakpoint" and then declines. To examine the effect of dietary macronutrient content on the course of hyperphagia, groups of male lean and obese rats were maintained from 5-28 weeks of age on powdered chow, or isocaloric diets (3.6 kcal/g) containing 72% of calories as corn oil, dextrose, or soy isolate protein (n = 5 lean and obese rats/diet). On chow, hyperphagia was maintained at a level of 7-8 g above lean control intake until a "breakpoint" was reached at 17 weeks, and obese intake declined to lean control level. On the fat diet, hyperphagia was increased to 10 g/day when a breakpoint was reached at 8 weeks. On the dextrose and protein diets, hyperphagia at a level of 3-4 g/day reached breakpoints at weeks 18 and 16, respectively. On all diets, the intakes of obese rats were precisely equal to the intakes of lean control rats by weeks 19-20. These data show that the magnitude and duration of hyperphagia in the developing obese rat are influenced by diet composition. Previously, we have proposed that the obese rat's hyperphagia arises from rapid adipocyte filling. Since high-fat diets facilitate adipocyte enlargement, the early "breakpoint" of hyperphagia seen with the high-fat diet may indicate that this feeding stimulation decreases as the fat cells of the obese rat approach maximal size.

Adipose Tissue↗
PubMed1999

Hyperphagia in neonates withdrawing from methadone.

AIMS: To examine whether hyperphagia is a clinically significant problem in infants born to women receiving methadone maintenance. METHODS: The volume of feeds, changes in infant body weight, as well as occurrence of adverse clinical effects in infants withdrawing from methadone were studied during the first month of life. A retrospective chart review was conducted for all infants at San Francisco General between 1992 and 1995, born to women receiving methadone maintenance during their pregnancy. Forty four infants were identified and the data obtained from hospital medical records. The daily oral intake of these infants was recorded during the first month of life. The incidence of hyperphagia (oral intake > 190 cc/kg/day) was measured. Associations between infant oral intake and maternal methadone dose were studied using correlation analysis as well as Anova for repeated measures. Adverse clinical symptoms were also recorded. A subset of premature infants was studied separately. RESULTS: The incidence of hyperphagia was 26% by day 8 and 56% by day 16 of life in the infants. Hyperphagia was not associated with maternal methadone dose or with infant withdrawal scores. Infants who were hyperphagic lost significantly more weight during the first week of life than those who were not. Despite significantly greater intake, the hyperphagic infants did not gain weight more rapidly during the first month of life compared with those infants with lower oral intake. Infants who were hyperphagic (maximum intake of 290 cc/kg/day) did not experience increased vomiting, aspiration, diarrhoea, or abdominal distention. CONCLUSIONS: Hyperphagia is commonly found in infants withdrawing from methadone and can be persistent in a significant number. Hyperphagia was not associated with either increased neonatal weight gain or with adverse gastrointestinal consequences. Hyperphagia may occur in infants withdrawing from methadone who have high metabolic demands due to clinical signs not controlled by opiate treatment.

Adult↗
PubMed1982

Gold thioglucose-induced hypothalamic damage, hyperphagia, and obesity: dependence on the adrenal gland.

Previous studies from our laboratory suggested that adrenal hormones may participate, directly or indirectly, in the hypothalamic mechanism involved in the regulation of food intake. In the present studies, the effect of adrenalectomy on the development of gold thioglucose (GTG)-induced hyperphagia and obesity in mice was investigated. As expected, damage to the ventromedial hypothalamus by GTG was followed by hyperphagia and obesity. Ablation of the adrenal glands after the administration of GTG prevented the onset and development of hyperphagia and obesity. The administration of cortisone completely restored the hyperphagia and weight gain of GTG-treated adrenalectomized mice. The administration of desoxycorticosterone not only failed to restore the hyperphagia and obesity in these mice but, rather, led to a suppression of food intake, weight loss, and death. It is concluded that 1) GTG-induced hypothalamic hyperphagia and obesity are dependent on adrenal glucocorticoids, and 2) the ability of adrenal glucocorticoids to restore hyperphagia and obesity in hypothalamic lesioned adrenalectomized mice indicates that adrenal glucocorticoids can act on compounds outside of the ventromedial hypothalamus involved in the control of food intake.

Adrenal Glands↗
PubMed1998

Morphine-6beta-glucuronide-induced hyperphagia: characterization of opioid action by selective antagonists and antisense mapping in rats.

Opiate drugs such as morphine stimulate food intake in rats. The morphine metabolite, morphine-6beta-glucuronide (M6G), is more active than morphine in analgesic assays, and appears to act through distinct receptors. Thus, although morphine analgesia is decreased by antisense oligodeoxynucleotides (AS ODNs) targeting exons 1 and 4 of the MOR-1 clone, M6G analgesia is reduced by probes targeting exons 2 and 3 of the MOR-1 clone. Our study examined whether central administration of M6G increased food intake in rats, and characterized this response using either selective mu, kappa1, delta1 and delta2 antagonists, or antisense directed against the various cloned opioid receptors. Central M6G (10-1000 ng) significantly and dose-dependently increased intake after 4 hr. Whereas mu antagonism with betaFNA significantly and dose-dependently reduced M6G-induced hyperphagia, equimolar doses of delta1, delta2, and kappa1 antagonists were ineffective. AS ODNs directed against either exons 2 or 3 of the MOR-1 clone blocked M6G-induced hyperphagia, whereas either AS ODNs directed against exons 1 or 4, or a MS ODN directed against exon 2 were ineffective. In contrast, an AS ODN probe directed against exon 1, but not exon 2, of the MOR-1 clone reduced morphine-induced hyperphagia, an effect identical to DAMGO-induced hyperphagia. Whereas M6G-induced hyperphagia was insensitive to antisense probes directed against the DOR-1, KOR-1 and KOR-3/ORL1 clones, these probes respectively reduced hyperphagia induced by deltorphin II, U50488H and nociceptin. Although pharmacological data indicate that M6G-induced hyperphagia acts through mu receptors, antisense data imply that the hyperphagic actions of M6G are mediated by a receptor distinct from traditional mu agonists, either as an alternative splice variant of the MOR-1 clone or a distinct gene.

Animals↗
PubMed2004

Diet-induced hyperphagia in the rat is influenced by sex and exercise.

Caloric intake is increased in rats fed a diet containing greater fat or sugar than that found in laboratory chow. Because such diet-induced hyperphagia has been studied primarily in sedentary male rats, our goal here was to investigate the effects of sex and exercise on caloric intake of a diet (chow supplemented with sweet milk) chosen for its ability to stimulate hyperphagia. Rats were housed individually in cages that provided access to running wheels, and daily caloric intake of chow alone and then chow plus sweet milk was monitored during sedentary and active conditions. In sedentary rats, chow intake was greater in males compared with females. Wheel running produced similar decreases in chow intake in both sexes. Availability of the chow plus milk diet increased caloric intake compared with that observed in chow-fed rats. This diet-induced hyperphagia was significantly greater in sedentary females (35.7 +/- 3.1% increase) relative to sedentary males (9.1 +/- 2.2% increase). In addition, 35% of sedentary females consuming the chow plus milk diet developed estrous cycle disruptions. Wheel running decreased intake of the chow plus milk diet in both sexes. In active males, diet-induced hyperphagia was abolished; caloric intake was reduced to that observed during chow feeding. In active female rats, diet-induced hyperphagia was attenuated but not abolished; caloric intake of the chow plus milk diet remained greater than that observed during chow feeding. We conclude that female rats are more vulnerable than male rats to this form of diet-induced hyperphagia.

Animals↗
PubMed2005

Development of insulin resistance and hyperphagia in Zucker fatty rats.

The onset of hyperphagia in the Zucker fatty (fa/fa) rat occurs on a single day in postnatal development and could be driven by an increase in insulin sensitivity. To test this hypothesis, we performed insulin tolerance tests at several points in development. In rapidly growing juvenile rats, fatty rats are as insulin sensitive as lean rats at 4 wk of age but become increasingly insulin resistant as they became obese. During the suckling to weaning transition, fatty rats are insulin resistant at 2 wk of age, when they are exclusively suckling; they are also insulin resistant at 3 wk of age, when they are suckling and consuming solid food, but not hyperphagic. By 4 wk of age, when fatty rats are hyperphagic, they are as insulin sensitive as their lean littermates. These data indicate that fatty rats experience two phases of insulin resistance, punctuated by a brief period of insulin sensitivity that follows the onset of hyperphagia. To determine whether the increase in insulin sensitivity could be driving the onset of hyperphagia, insulin tolerance tests were performed from 21 to 27 days of age. Obese and lean rats became increasingly insulin resistant from 21 to 23 days of age and then became as insulin sensitive as lean rats by 25 days of age. These data show that increased insulin resistance precedes the onset of hyperphagia and increased insulin sensitivity follows the onset of hyperphagia. This pattern suggests that developmental perturbations in insulin signaling are likely to be involved in the onset of hyperphagia.

Aging↗
PubMed1995

Evidence of a physiological role for neuropeptide Y in ventromedial hypothalamic lesion-induced hyperphagia.

We evaluated the role of neuropeptide Y (NPY), a potent endogenous orexigenic signal, in the ventromedial hypothalamic (VMH) lesion-induced hyperphagia in rats. To produce hyperphagia and excessive weight gain, adult female rats received bilateral electrolytic or sham lesions in the VMH. Concurrently, a permanent intracerebroventricular cannula was implanted in the third ventricle of the brain. After a recovery period, these rats were passively immunized against NPY to evaluate the role of endogenous NPY on hyperphagia. The results showed that intraventricular administration of NPY antibodies abolished the hyperphagia in VMH-lesioned rats. These revelations are in agreement with the notion that altered hypothalamic NPY release or action may underlie the hyperphagia and excessive weight gain seen in response to structural damage in the VMH.

Animals↗
PubMed1995

Relationship between histamine receptors in the brain and diazepam-induced hyperphagia in rats.

We investigated whether histaminergic neurons in the brain are involved in diazepam-induced hyperphagia in rats. Pretreatment with intracerebroventricular (ICV) injection of either histamine H1-receptor antagonist, pyrilamine (10 and 30 micrograms) or histamine H2-receptor antagonist, famotidine (3 and 10 micrograms) did not affect only diazepam (1 mg/kg, subcutaneous, SC)-induced hyperphagia in nondeprived rats, but also spontaneous feeding in food-deprived rats. In addition, pretreatment with ICV injection of histamine H3-receptor antagonist, thioperamide, and histamine H3-receptor agonist, (R) alpha methylhistamine, enhanced and inhibited diazepam-induced hyperphagia (1 mg/kg, SC) in nondeprived rats, respectively. However, thioperamide and (R) alpha methylhistamine did not affect spontaneous feeding in food-deprived rats. These findings suggest that histaminergic neurons are not directly involved in diazepam-induced hyperphagia in rats. Furthermore, enhancement or inhibition of diazepam-induced hyperphagia by histamine H3-receptor antagonist or agonist may occur via histamine H3-receptors localized in the other neurons in the rat brain.

Animals↗
PubMed1985

Patterns of hyperphagia in the Zucker obese rat: a role for fat cell size and number?

The hypothesis that adipocyte size and number influence feeding behavior, via as yet unidentified signals to the CNS, is reviewed. The proposal is made that, due to several metabolic alterations which favor lipid deposition, the genetically obese Zucker rat (fafa) may be an appropriate model in which to study feeding-adipose tissue relationships. Data from several studies are presented demonstrating that the developing male Zucker fatty rat displays hyperphagia during the growth period which reaches a peak, or "break point," and then declines such that intake of fatty and lean rats becomes comparable at approximately 20 weeks of age. Beyond week 20, cycles of hyperphagia of several weeks' duration can be detected in fatty rats. The above feeding changes are related to data showing that on a laboratory chow-type diet, adipocytes approach maximal size at 15-16 weeks in the fatty rat, while accelerated proliferation of adipocytes takes place following week 20. During growth, responding for food in an operant task by fatty rats varies in accord with the pattern of hyperphagia. Further studies in the fatty rat show that the duration and magnitude of developmental hyperphagia can be altered by manipulating the caloric density and macronutrient content of the diet, with fat containing diets leading to the earliest break point of developmental hyperphagia. Some theoretical problems with the notion of adipose tissue feedback control of feeding behavior are discussed.

Adipose Tissue↗