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PubMed2004

Resource allocation, hyperphagia and compensatory growth.

Organisms often shown enhanced growth during recovery from starvation, and can even overtake continuously fed conspecifics (overcompensation). In an earlier paper (Ecology 84, 2777-2787), we studied the relative role played by hyperphagia and resource allocation in producing overcompensation in juvenile (non-reproductive) animals. We found that, although hyperphagia always produces growth compensation, overcompensation additionally requires protein allocation control which routes assimilate preferentially to structure during recovery. In this paper we extend our model to cover reproductively active individuals and demonstrate that growth rate overcompensation requires a similar combination of hyperphagia and allocation control which routes the part of enhanced assimilation not used for reproduction preferentially towards structural growth. We compare the properties of our dynamic energy budget model with an earlier proposal, due to Kooijman, which we extend to include hyperphagia. This formulation assumes that the rate of allocation to reserves is controlled by instantaneous feeding rate, and one would thus expect that an extension to include hyperphagia would not predict growth overcompensation. However, we show that a self-consistent representation of the hyperphagic response in Kooijman's model overrides its fundamental dynamics, leading to preferential allocation to structural growth during recovery and hence to growth overcompensation.

Animals↗
PubMed2005

Hyperphagia of hyperthyroidism: is neuropeptide Y involved?

The possible role of neuropeptide Y (NPY) was studied in rats with hypermetabolism and hyperphagia induced by thyroxine (50-100-200 microg/day s.c. for 3-4 weeks). Both metabolic rate and body temperature increased quickly with thyroxine treatment, while hyperphagia started to develop only after 2 weeks of treatment. The weight gain rate progressively decreased or stopped. The NPY-induced hyperphagia was not altered significantly during thyroxine treatment (in severe thyrotoxicosis it was rather suppressed); the fasting-induced hyperphagia was smaller than in controls following 1 week of treatment, and it became enhanced only after 3 weeks, when the deficit in body weight indicated a certain level of starvation already prior to the food deprivation. The NPY-antagonist D-Tyr27,36,D-Thr32-NPY27,36 suppressed this fasting-induced hyperphagia, suggesting that endogenous NPY is involved in this late phase. In conclusion, hyperthyroidism per se does not increase the NPY activity, instead the quickly developing hyperthermia may inhibit the NPY actions; NPY may, however, be activated by a concurrent hypermetabolism-induced starvation.

Animals↗
PubMed2000

Melanocortin signaling is decreased during neurotoxin-induced transient hyperphagia and increased body-weight gain.

Hypothalamic neuropeptides play critical roles in the regulation of feeding behavior and body weight (BW). Disruption of signaling in the ventromedial nucleus by microinjection of the neurotoxin, colchicine (COL), produces transient hyperphagia with corresponding BW gain lasting for 4 days. Because the melanocortin system exerts an inhibitory control on food intake, we hypothesized that hyperphagia in COL-treated rats is due to decreased melanocortin-induced restraint on feeding. Melanocortin restraint is exerted through alpha-melanocortin-stimulating hormone derived from proopiomelanocortin (POMC) and is antagonized by agouti-related peptide produced in neurons located in the arcuate nucleus (ARC). COL (4 microg/0.5 microl saline) or saline was microinjected bilaterally into the ventromedial nucleus of adult male rats. In conjunction with BW gain, blood leptin levels were elevated, whereas POMC mRNA in the ARC was significantly decreased in COL-injected rats. Levels of alpha-melanocortin-stimulating hormone were also decreased in the micropunched paraventricular nucleus, dorsomedial nucleus, and perifornical hypothalamus, sites implicated in the control of food intake. That diminution in melanocortin signaling underlies hyperphagia was supported by the observation that intracerebroventricular injection of the MC3/MC4 melanocortin receptor agonist, MTII, prevented the hyperphagia and BW gain. Surprisingly, however, mRNA levels of the orexigenic peptide agouti-related peptide in the ARC were decreased perhaps due to the action of elevated leptin. These results show that transient hyperphagia and BW gain induced by disruption of signaling in the ventromedial nucleus results from two neurochemical rearrangements: development of leptin resistance in POMC neurons and diminution in melanocortin signaling as reflected by decreased POMC gene expression in the ARC and decreased availability of alpha-melanocortin-stimulating hormone for release in feeding relevant sites.

Agouti-Related Protein↗
PubMed1998

Hyperphagia induced by hypoglycemia in rats is independent of leptin and hypothalamic neuropeptide Y (NPY).

Hypoglycemia causes hyperphagia and weight gain, through unknown peripheral and central signals. We investigated the effect of hypoglycemia on NPY and leptin expression and the ability of leptin to inhibit hypoglycemia-induced hyperphagia. Acute hypoglycemia (60 U/kg SC insulin; n = 8) increased food intake (p < 0.01) compared with controls (n = 8). Insulin- and leptin-treated rats (300 microg/kg IP leptin; n = 8) had reduced hyperphagia (p < 0.05 vs. controls; p < 0.05 vs. insulin alone) and a 15% fall in NPY mRNA levels compared with controls (p < 0.01). Chronic hypoglycemia, (20-60 U/kg/day insulin; n = 8) increased food intake compared with vehicle-treated controls (p < 0.01). Leptin and insulin administration (300 microg/kg/day IP leptin; n = 8) reduced hyperphagia (p < 0.01 vs. controls, p < 0.05 vs. insulin alone), and NPY mRNA fell by 18% vs. controls (p < 0.01). We conclude that hypoglycemia-induced hyperphagia is not mediated by either a fall in leptin or an increase in hypothalamic NPY mRNA. Leptin can inhibit feeding in hyperphagic hypoglycemic rats, and this may partly be attributable to its inhibition of the NPY neurons.

Acute Disease↗
PubMed1986

Central nervous system control of hyperphagia in hypothalamic obesity: dependence on adrenal glucocorticoids.

Gold thioglucose (GTG)-treated hyperphagic obese mice exhibit a pronounced anorexia upon adrenalectomy which is reversed by the systemic administration of adrenal glucocorticoids. To determine whether the return of hyperphagia was mediated by an action of the hormones on the central nervous system, food intake and body weight were monitored in anorexic GTG-treated obese adrenalectomized mice which received a single intracerebroventricular (icv) injection of very small amounts of adrenal glucocorticoids, including cortisone, corticosterone, and dexamethasone. The responses of untreated controls and adrenalectomized control mice were also studied. To rule out possible systemic effects of icv injections of adrenal glucocorticoids, food intake and body weight were also monitored in similar mice given a single ip injection of the hormones. We found that hyperphagia was restored and weight loss abolished in anorexic GTG-treated obese adrenalectomized mice after a single icv injection of adrenal glucocorticoids; the dose of cortisone required was found to be 1/60th of that previously shown to be needed systemically to restore hyperphagia. A single ip injection of these adrenal hormones in the small amounts given icv failed to induce hyperphagia in these mice. The icv and ip injections of the adrenal glucocorticoids did not significantly affect food intake or body weight of untreated controls and adrenalectomized control mice. These findings indicate that adrenal glucocorticoids act via the central nervous system in restoring hyperphagia in anorexic GTG-treated obese adrenalectomized mice.

Adrenal Glands↗
PubMed2001

The 5-HT2C/2B receptor agonist m-chlorophenylpiperazine (mCPP) inhibits 2-deoxy-D-glucose (2-DG)-induced hyperphagia in rats.

Effects of the 5-HT2C2/2B receptor agonist m-chlorophenylpiperazine (mCPP) on hyperphagia elicited by 2-deoxy-D-glucose (2-DG) were investigated in rats. mCPP apparently reduced 2-DG-induced hyperphagia. Suppressive effects of mCPP on hyperphagia induced by 2-DG were inhibited by the 5-HT2A/2B/2C receptor antagonist, ritanserin, although the 5-HT2, receptor antagonist ketanserin was without effect. Thus, inhibitory effects of mCPP on 2-DG-induced hyperphagia are mediated by the 5-HT2C/2B receptor. Our results demonstrate that mCPP can inhibit the bulimia model, 2-DG-induced hyperphagia.

Animals↗
PubMed1996

[Characteristics of dementia patients with hyperphagia].

Research into dementia has tended to concentrate on memory loss and other cognitive impairment, but attention has recently turned to the associated psychiatric symptoms and behavioral abnormalities. Among them, increases in the amount eaten or hyperphagia are not uncommon in dementia. This problem is of clinical importance since it not only jeopardizes patient's health, but also is a cause of caregiver burden. The aim of this study was to assess the prevalence of hyperphagia in dementia. Additionally, possible mechanisms underlying this problem were reviewed and related to the demographic data, cognitive function test, radiological findings and other psychiatric symptoms. Out of a sample of 91 demented inpatients, hyperphagia was present in 30.8%. Hyperphagia was significantly associated with delusion, misidentification, aggressive behavior, hoarding behavior and pica phenomena. But these patients did not show difference in cognitive function, radiological abnormalities, repetitive behavior and depressed mood when compared with other demented patients. The possible etiologies were discussed, including physiological and psychological factors. Hyperphagia is a complex phenomenon, better understanding of the underlying pathogenesis may highlight specific pharmacological or behavioral methods for the management this troublesome behavior.

Aged↗
PubMed1997

Antisense mapping of the MOR-1 opioid receptor clone: modulation of hyperphagia induced by DAMGO.

The mu opioid receptor mediates ingestive behavior: mu-selective agonists stimulate food intake and antagonists reduce intake in many ingestive situations. Antisense oligodeoxynucleotides directed against each of the four exons of the MOR-1 clone were equally effective in reducing spontaneous food intake and body weight in rats. However, antisense probes directed against only exon 1 or 4 of the MOR-1 clone reduced mu-mediated analgesia. The present study examined whether central administration of antisense probes directed against each of the four exons of the MOR-1 clone or a missense control altered hyperphagia elicited by the mu agonist DAMGO across a range of doses. Antisense probes directed against only exon 1 or 4 blocked hyperphagia at agonist doses of 0.5 and 1.0 microg; this pattern was identical to that observed for mu-mediated analgesia. A missense control failed to exert significant effects, which suggests specificity of antisense actions. The effective antisense probes failed to reduce hyperphagia at a higher (5 microg) agonist dose, a result consistent with limitations in down-regulation of receptor proteins by antisense. The mu antagonist beta-funaltrexamine produced a similar pattern of effects on mu-mediated hyperphagia. The selective actions of antisense probes directed against different exons of the MOR-1 clone in reducing hyperphagia induced by DAMGO suggest that multiple splice variants of the MOR-1 clone exist and raise the possibility of further opioid receptor subclassifications.

Animals↗
PubMed1982

Inhibition by hypophysectomy of the hyperphagia and obesity following gold thioglucose.

The effect of hypophysectomy in mice previously treated with gold thioglucose (GTG) was studied with respect to changes in food intake and development of obesity. As expected, all mice treated with GTG alone exhibited lesions in the ventromedial hypothalamus (VMH), hyperphagia and obesity. Hypophysectomy of GTG treated mice prevented the appearance of hyperphagia and obesity. Daily administration of the adrenal corticoid, cortisone, completely restored the hyperphagia and obesity in GTG treated hypophysectomized mice. The amounts of cortisone used did not appreciably affect food intake or body weights of normal, hypophysectomized or GTG treated mice. These findings indicate that the hypothalamic hyperphagia and obesity which normally follows the administration of GTG is dependent on a functional pituitary gland. Furthermore, the specific ability of an adrenal corticoid to completely restore the hyperphagia and obesity of GTG treated hypophysectomized mice in the absence of other pituitary factors, suggests that the pituitary adrenal axis serves as an important link in the regulatory mechanism for control of feeding behavior in the mouse.

Adrenal Glands↗
PubMed1986

Failure to demonstrate schedule-induced hyperphagia with a fixed time 1-minute water delivery schedule.

The reduction of an animal's body weight to 80% of its Free Feeding Weight (FFW) is purported to be an important factor in the generation of schedule-induced behaviour. However, the importance of this factor in schedule-induced hyperphagia is unclear. Experimental studies in schedule-induced hyperphagia reported conflicting results. The aim of the present series of five experiments was to clarify the several conflicting factors in the generation of schedule-induced hyperphagia. Rats reduced to 80% FFW by water restriction and on a Fixed Time (FT) 1-min water delivery schedule showed that body weight reduction, water delivery schedule, size and distance of pellets, and order of schedule presentation were not important factors in the generation of schedule-induced hyperphagia. The failure of the present series of experiments to demonstrate schedule-induced hyperphagia suggests that this behaviour may be a specific class of schedule-induced behaviour that can only be demonstrated under the Bellingham, Wayner and Barone experimental paradigm.

Animals↗
PubMed1975

Chlorpromazine induced hyperphagia in the rat.

During a four month period, 20 rats treated with subcutaneous injections of chlorpromazine (CPZ), at any dose tested, gained less weight than saline treated controls. However, increased feeding did occur on the first day of CPZ treatment if the animal was drug free for at least two days prior to treatment. The "first day" hyperphagia was a time limited response that did not occur until 8 hours after CPZ injection and lasted only one day. During the period of hyperphagia, treated animals showed increased motivation to obtain food. Although sedation is a marked effect of CPZ and may be the reason for the delayed onset of hyperphagia, sedation with a different drug does not cause hyperphagia. It is suggested that accumulation of a metabolite of CPZ may interfere with the feeding response and cause the hyperphagia to disappear after the first day of treatment.

Animals↗
PubMed1994

Meal pattern of rats during hyperphagia induced by longterm food restriction is affected by diet composition.

The influence of diet composition on feeding behavior during the hyperphagia induced by about 15% loss in body weight due to restricted feeding (5 g food/day for 7 days) was investigated in adult male rats. Rats were fed either a low-fat, high-carbohydrate diet (LF diet), a medium-fat diet (MF diet) or a carbohydrate-free, high-fat diet (HF diet). The transient hyperphagia resulting from food restriction was greater in LF- and MF-rats than in HF-rats, in which a mild hypophagia was observed following the hyperphagia. Recovery of body weight was imperfect in the HF-rats in comparison to the unrestricted controls. During the hyperphagia, the meal pattern of LF- and MF-rats was mainly characterized by an increase in meal size, whereas HF-rats showed an increase in meal frequency. These observations indicate that control of food intake by body weight in LF- and MF-rats occurs mainly by modulation of the mechanisms producing meal-ending satiety, whereas in HF-rats the mechanisms eliciting meal initiation seem to be affected by body weight.

Animals↗
PubMed2000

Naltrexone does not prevent the weight gain and hyperphagia induced by the antipsychotic drug sulpiride in rats.

Few pharmacological tools are currently available to counteract the excessive body weight gain often observed during prolonged administration of antipsychotic drugs. Most antipsychotic drugs block dopamine receptors, and both the brain dopaminergic and opioid systems appear to be involved in initiation and maintenance of feeding behavior, respectively. We evaluated whether the opioid antagonist naltrexone (NAL, 0.5-16 mg/kg/ip for 21 days) (a) affects body weight and food intake in gonadally-intact and drug-free female rats, (b) prevents obesity, hyperphagia, hyperprolactinemia and vaginal cycle disruption induced by long-term administration of the antipsychotic drug sulpiride (SUL, 20 mg/kg/ip for 21 days), or (c) reverses the acute hyperphagia induced by SUL (15 microg bilaterally), when directly applied in the perifornical lateral hypothalamus (PFLH). In drug-free rats, only NAL doses above 4 mg/kg, significantly decreased weight gain and food intake. Even though NAL (1 and 8 mg/kg) significantly attenuated SUL-induced hyperphagia and hyperprolactinemia, it did not reverse at any dose the weight gain and permanent diestrous induced by SUL. In addition, local NAL did not prevent the hyperphagia and polidypsia observed after acute intrahypothalamic SUL. Unexpectedly, the cumulative and 24 h food intake in SUL-treated rats was significantly increased by NAL. Collectively, these results do not support a role for endogenous opiates in the neural and endocrine mechanisms involved in weight gain during prolonged antipsychotic drug administration in rats.

Animals↗
PubMed2003

Hyperphagia modifies FA profiles of plasma phospholipids, plasma FFA, and adipose tissue TAG.

Hyperphagia was achieved by continuous intracerebroventricular infusion of a melanocortin receptor antagonist (HS024; Neosystem, Strasbourg, France) in rats. The effects of hyperphagia on FA composition and concentration of plasma phospholipids (PL), plasma FFA, and adipose tissue TAG were studied in rats for 8 d [short-term hyperphagia (STH); n = 8], or 28 d [long-term hyperphagia (LTH); n = 9]. The control rats were treated with artificial cerebrospinal fluid for 8 d (n = 8) or 28 d (n = 10). The rats were fed the same regular diet. In STH rats the plasma PL and fasting plasma FFA contained higher concentrations of saturated FA (SFA) and monounsaturated FA (MUFA), and plasma FFA contained lower n-6 PUFA than in the control rats. In LTH rats the plasma PL contained higher concentrations of SFA, MUFA, and n-3 PUFA and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. In LTH rats the abundant dietary intake of 18:2n-6 did not enrich 18:2n-6 of the plasma PL or adipose tissue TAG. In LTH rats the fasting plasma FFA contained more than twofold higher concentrations of SFA and MUFA, and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. This animal obesity model shows that LTH affects the FA composition and concentration of plasma PL, plasma FFA, and adipose tissue TAG, a result consistent with changes associated with increased risk of various diseases in humans. These results also demonstrate that LTH alters the FA composition of plasma PL and adipose tissue TAG in a way that does not reflect the FA composition of dietary fat.

Adipose Tissue↗
PubMed1984

The plasma amino acid response to cafeteria feeding in the rat: influence of hyperphagia, sucrose intake, and exercise.

The plasma amino acid response to voluntary hyperphagia was evaluated in rats fed a "cafeteria" diet for 4 to 8 weeks and compared to chow-fed controls. The influence of the sucrose content of the cafeteria diet was examined by studying rats given a low-sucrose, highly palatable, liquid diet (Magnacal). In a second series of studies the cafeteria diet was fed to rats housed in wheel cages and who ran 2.0 +/- 0.1 milles per day and compared with a sedentary cafeteria-fed group housed in standard cages. As expected, the cafeteria diet resulted in hyperphagia (45% to 55%) and in increased weight gain (35% to 50%). In response to cafeteria feeding there was an increase in plasma threonine, serine, proline, citrulline, alpha-amino butyric acid (ABA), and tyrosine. Significant decreases were observed in the branched chain amino acids (BCAA), valine and leucine. All of these changes were also observed when hyperphagia was induced with the low-sucrose diet, with the exception of the rise in ABA. In the exercised cafeteria-fed rats, excessive weight gain did not occur. Nevertheless, the amino acid response to the cafeteria diet was the same as in sedentary rats with excessive weight gain. The plasma amino acid pattern in those rats that developed glucose intolerance during cafeteria feeding and those that maintained normal glucose tolerance was similar. We conclude that hyperphagia induced by cafeteria feeding in the rat results in a specific plasma amino acid profile characterized by elevations in some amino acids (threonine, serine, proline, citrulline, ABA, and tyrosine) and reductions in the BCAA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1988

PVN-hindbrain pathway involved in the hypothalamic hyperphagia-obesity syndrome.

This study examined the involvement of caudal brainstem projections of the hypothalamic paraventricular nucleus (PVN) in the medial hypothalamic (MH) hyperphagia-obesity syndrome. Experiment 1 demonstrated that a unilateral parasagittal knife cut in the MH combined with a contralateral coronal knife cut in either the ventrolateral pons (vP) or ventrolateral medulla (vM) significantly increased food intake and body weight in adult female rats. Overeating and overweight were also produced by a unilateral MH knife cut combined with a contralateral oblique cut under the nucleus of the solitary tract and dorsal motor nucleus of the vagus complex (NST/DX). In contrast, an MH cut x dorsolateral medullary cut combination did not increase food intake or body weight compared to a MH cut alone or sham surgery. Experiment 2 demonstrated that the hyperphagia/obesity effect of MH x vP knife cuts was comparable to that obtained with bilateral PVN lesions, but less than that produced by bilateral MH knife cuts. Bilateral vP cuts also increased body weight but the effect was less than that obtained with the other experimental treatments. Feeding the rats a high-fat diet rather than chow potentiated the hyperphagia and obesity syndromes produced by the various lesion conditions. Taken together, these findings suggest that the medial hypothalamic hyperphagia and obesity syndrome is due, in part, to damage to PVN projections to the caudal brainstem, the NST/DX complex in particular. The functional significance of this PVN-hindbrain "feeding" pathway and the identity of extra-PVN components of the hyperphagia-obesity syndrome remain to be established.

Animals↗
PubMed1984

Stress and sucrose hyperphagia: role of endogenous opiates.

Two experimental situations induce hyperphagia in the rat: the cafeteria model and the tail-pinching model. In non-deprived rats which are offered for one hour a choice of 3 liquid cafeteria items in addition to ordinary chow and water, mild tail-pinching results in a preferential sucrose hyperphagia; naltrexone (2.5 mg/kg IP) suppresses this stress-induced hyperphagia; beta-endorphin (3 micrograms ICV) has the same effect. This apparent discrepancy is discussed: the antagonist may suppress the hyperphagia because it suppresses the reward provoked by the sucrose, the agonist because it makes it unnecessary.

Animals↗
PubMed1996

Probing the causes of high-fat diet hyperphagia: a mechanistic and behavioral dissection.

High-fat diets promote hyperphagia in both rats and humans; however, understanding of the process by which dietary fat increases intake is incomplete. Since altering the fat content of a diet simultaneously changes both its sensory properties and postingestive effects, it is unclear whether high-fat diet hyperphagia is driven by oral influences, postingestive factors, or both. Previous findings from both animal and human studies indicate that relatively "less palatable" high-fat diets are overeaten relative to high-carbohydrate diets, indicating that the postingestive effects of high-fat foods are sufficient to promote hyperphagia. A program of research on rats is described, which isolates and assesses the independent effects of sensory and postingestive influences on intake of liquid high-fat and high-carbohydrate diets. An integrated series of experiments investigates both short-term (meal size, postprandial satiety) and long-term (ad lib intake over weeks) effects of diet composition on intake in order to "dissect" the causes of high-fat diet hyperphagia. Preliminary findings from this approach indicate that the postingestive effects of a high-fat diet promote longer meal size, less postprandial satiety per calorie, and greater daily calorie intake than a high-carbohydrate diet.

Animals↗