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PubMed1988

Involvement of dopaminergic systems in the ventromedial hypothalamic hyperphagia.

The effect of chronic dopamine receptor blockage on ventro-medial hypothalamic lesion induced hyperphagia and obesity was studied. Rats with electrolytic ventromedial hypothalamic (VMH) lesions were treated chronically with either haloperidol (DA antagonist) or vehicle solution. Food intake of rats with VMH lesions fell well below baseline levels. Additionally, these animals started losing body weight within 24 hours of the initiation of treatment and continued to lose weight throughout the treatment period. When the treatment was discontinued these animals resumed overeating and regained body weights. The food intakes and body weights of unlesioned rats treated with either haloperidol or vehicle, and VMH lesioned rats treated with vehicle, were not affected by these treatments.

Animals↗
PubMed1987

Transient hyperphagia after sodium selenite injection in mice.

Injection (s.c.) of Na2SeO3 (SS, 20-30 mumol/kg) into male mice initiated eating, which began about 20 min after injection and continued for about 3 h. This initiation effect was observed for mice of different ages and at different times of the day. Other findings of this study were: (1) early morning injection (30 mumol/kg) caused increased food intake, as examined by gastric content 3 h after injection, compared to daytime injection; and (2) SS-induced transient hyperphagia was observed at ambient temperatures of 10 and 22 degrees C, but not at 37 degrees C. This paper discusses these results in relation to SS-induced hypothermia.

Animals↗
PubMed1990

Transient hypothermia and hyperphagia induced by selenium and tellurium compounds in mice.

The effects of sublethal doses of selenite, selenate, selenocystine (Se-Cys) and selenomethionine (Se-Met) as well as of tellurite on body temperature and feeding behavior were examined in male ICR mice. Ten or 30 mumol/kg of chemicals were injected subcutaneously and body temperature was measured up to 4 h. In a separate experiment, the gastric content was weighted 4 h after injection. All chemicals except Se-Met induced both hypothermia and hyperphagia, suggesting that: (a) these two effects are related to each other; (b) among the chemicals tested, Se-Cys appears to be the most potent hypothermia inducer; (c) Se-Met is unique in that it has neither effect.

Animals↗
PubMed2004

Partial leptin restoration increases hypothalamic-pituitary-adrenal activity while diminishing weight loss and hyperphagia in streptozotocin diabetic rats.

Chronic leptin administration at pharmacologic doses normalizes food intake and body weight in streptozotocin (STZ)-diabetic rats. We examined the metabolic effects of acute partial physiological leptin restoration in STZ-diabetic rats by using subcutaneous osmotic mini pumps. Groups: (1) Rats infused with vehicle (DV); (2) rats infused with recombinant murine methionine leptin (DL) at 4.5 microg . (kg body weight . d)(-1); (3)pair-fed rats (DP) given a food ration matching that consumed by the DL group. A fourth group of nondiabetic, normal (N) rats was also studied to assess normal metabolic efficiency, hypothalamic-pituitary-adrenal (HPA) activity and sympathoadrenal activity. Following leptin infusion, food consumption by DL rats was significantly lower than in DV rats. Paradoxically, despite a similar food intake to that of the DP group, which demonstrated a 40% reduction in body mass, DL rats increased their initial body weight by approximately 20% (P < .05). Plasma corticosterone and ACTH concentrations were elevated by 2-fold to 3-fold in DL versus N, DP, and DV rats. In the pars distalis, glucocorticoid receptor (GR) mRNA levels were significantly higher in DL and DP rats compared with N and DV rats. Our results suggest that partial restoration of physiologic leptin: (1) successfully reduces hyperphagia while allowing body weight gain in STZ-diabetic rats; (2) increases corticosterone levels in STZ-diabetic rats, which may in turn counteract the anorexic effects of diabetes; and (3) is associated with increased pituitary GR mRNA levels, despite elevated corticosterone levels, suggesting that leptin may interfere with the negative feedback regulation of the HPA axis.

Adrenocorticotropic Hormone↗
PubMed2004

Intracerebroventricular administration of chicken motilin does not induce hyperphagia in meat-type chicks.

The effect of chicken motilin on food intake was investigated in meat-type chicks under ad libitum feeding, refeeding, and fasting conditions. We found that the intracerebroventricular injection of chicken motilin (0.1 and 0.2 microg) tended to increase food intake under ad libitum feeding and refeeding conditions at 60 min postinjection, but the differences were not significant (P>.05). On the other hand, central administration of chicken motilin (0.2 and 0.4 microg) showed a tendency to suppress feeding of fasted chicks as well as the result of high dose (5.0 microg) under ad libitum feeding conditions. Therefore, the results presented here suggest that central motilin alone does not induce hyperphagia in meat-type chicks.

Animals↗
PubMed1998

Effects of palatability-induced hyperphagia and food restriction on mRNA levels of neuropeptide-Y in the arcuate nucleus.

This study examined the effect of feeding either a bland cornstarch-based diet (BCD) or a highly palatable, high fat diet containing sucrose (HPD) on hypothalamic arcuate nucleus (ARC) gene expression for neuropeptide-Y (NPY). Male Sprague-Dawley rats received either BCD ad libitum, HPD ad libitum, HPD pair-fed to the caloric intake of the BCD, or the HPD at 60% of ad libitum HPD intake for 7 days. Animals receiving the HPD ad libitum consumed more calories and gained more weight than animals receiving the BCD (P<0.001). The HPD did not affect ARC NPY mRNA levels, whether the subjects were allowed to overeat or pair-fed to the BCD (P>0.05). However, feeding the HPD at 60% of ad libitum intake of the HPD, increased NPY mRNA levels in the ARC relative to the other treatments (P<0.01). The present data are consistent with the view that NPY in ARC responds to energy deficits rather than to hyperphagia stimuli related to palatability.

Animals↗
PubMed2000

A nitric oxide synthase inhibitor reduces hyperphagia induced in rats by the 5-HT(1A) receptor agonist, 8-OH-DPAT, independently of hypothalamic serotonin metabolism.

In rats, a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) inhibited the hyperphagia induced by the 5-hydroxytryptamine (5-HT)(1A) autoreceptor agonist, 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT). 8-OH-DPAT reduced 5-HT metabolism in the hypothalamus, and this was not blocked by pretreatment with L-NAME. L-NAME also did not affect basal hypothalamic 5-HT metabolism or reverse the decreases in 5-HT synthesis in hypothalamus. These results suggest that the hypophagic effects of L-NAME, which inhibits NO formation, are independent of 5-HT metabolism in the hypothalamus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1998

Hyperphagia in pre-fed rats following oral delta9-THC.

Using a pre-feed paradigm, the effects of orally-administered delta9-tetrahydrocannabinol (THC) on low baseline levels of nocturnal feeding were assessed. Following 2-h access to a palatable wet mash diet at dark onset, adult male Lister hooded rats (Charles River) were treated with either sesame seed oil vehicle or delta9- tetrahydrocannabinol (0.063, 0.12, 0.25, 0.5, 1.0, or 2.0 mg/kg). One hour later, rats were allowed ad libitum access to standard chow, and intakes were monitored over the subsequent 24 h. Doses of 0.5, 1.0, and 2.0 mg/kg produced substantial hyperphagia during the first hour of testing. Subsequently, rats compensated for their overconsumption so that 24-h intakes were similar in all conditions. The data confirm anecdotal reports of the orexigenic actions of exogenous cannabinoids and suggest a critical role for endogenous cannabinoid systems in the regulation of appetite.

Administration, Oral↗
PubMed1996

A new stress-related syndrome of growth failure and hyperphagia in children, associated with reversibility of growth-hormone insufficiency.

BACKGROUND: Growth failure without organic aetiology but associated with behavioural disturbance and psychosocial stress has been termed psychosocial short stature. This condition is not a valid diagnostic entity, but encompasses failure to thrive, stunting secondary to chronic malnutrition, and idiopathic hypopituitarism. Some children show spontaneous catch-up growth when removed from the source of stress, without further treatment, but until now precise definition of this subgroup for the purpose of clinical identification has not been possible. METHODS: Hospital-referred children with growth failure unrelated to organic pathology, who came from stressful homes, were compared with children of short-normal stature identified from an epidemiological survey (n = 31). Growth-hormone dynamics were studied in the hospital group by a combination of diurnal profiles and provocation tests. The tests were repeated after a hospital stay of 3 weeks away from familial stress. Standard behavioural measures were obtained from home and school. FINDINGS: In a distinctive subgroup (n = 29), growth-hormone insufficiency was associated with characteristic behavioural features, especially hyperphagia and polydipsia, and a normal body-mass index. When the children were removed from their stressful home circumstances, growth-hormone insufficiency spontaneously resolved only in formerly hyperphagic subjects. 74% of the non-hyperphagic cases (n = 23) were anorexic, with a low body-mass index and normal growth-hormone responses to provocation tests. INTERPRETATION: We present explicit behavioural and developmental criteria by which the novel syndrome of hyperphagic short stature may be recognised clinically. Such children have a capacity for spontaneous recovery of growth-hormone production on removal from or reduction of stress. Discriminant and predictive validity of the core symptoms are demonstrated. Preliminary familial studies indicate a possible genetic predisposition.

Adolescent↗
PubMed2003

Pregnancy-induced hyperphagia is associated with increased gene expression of hypothalamic agouti-related peptide in rats.

Pregnancy is characterized by an increase in food intake that, in turn, produce a positive energy balance in order to face the considerable metabolic demands associated with the challenge of reproduction. Since hypothalamus is a key brain region involved in many peripheral signals and neuronal pathways that control energy homeostasis and food intake, we investigated if during pregnancy the increase in food intake is mediated by stimulating orexigenic and/or inhibiting anorexigenic neural pathways. We examined hypothalamic gene expressions of Ob-Rb, NPY, AgRP, POMC, MC4-R, and preproorexins in pregnant Wistar rats at day 19 of gestation. Food intake and body weight were increased progressively during the pregnancy. Visceral fat mass depots and serum leptin levels were also increased when compared with virgin animals. No differences were found in mRNA expression of Ob-Rb, POMC, MC4-R, NPY or preproorexin between virgin and pregnant animals. However, pregnancy produced a selective increase in AgRP mRNA levels. These results indicate that the positive energy balance that occurred during pregnancy can hardly be explained by changes in Ob-Rb despite hyperleptinemia associated with pregnancy. The enhanced expression of AgRP suggests the involvement of this neuropeptide in mediating pregnancy-associated hyperphagia.

Agouti-Related Protein↗
PubMed1999

Disruption of neural signaling within the hypothalamic ventromedial nucleus upregulates galanin gene expression in association with hyperphagia: an in situ hybridization analysis.

Hypothalamic neuropeptides play critical roles in the regulation of appetite and body weight. We recently reported that disruption of neural signaling in the ventromedial nucleus (VMN) by microinjection of the neurotoxin, colchicine (COL), produced transient hyperphagia with attendant body weight gain lasting for 4 days. The neural mechanism(s) underlying this temporary shift in energy homeostasis is still unknown. Galanin (GAL) is produced in several hypothalamic nuclei and since microinjection of GAL into these sites stimulates feeding, we tested the hypothesis that galaninergic signaling is upregulated in COL-treated rats. COL (4 microgram in 0.5 microliter saline) or saline alone was microinjected into the VMN of adult male rats and GAL mRNA was evaluated in the basal hypothalamus by ribonuclease protection assay on day 1, day 2 and day 4 after injection. Whereas in saline-treated rats body weight and GAL mRNA remained unaffected, they were significantly increased in COL-injected rats through the period of observation. To identify the specific neuronal subpopulations involved, GAL mRNA levels were analyzed in feeding-related hypothalamic nuclei using semiquantitative in situ hybridization histochemistry on day 4 after microinjection of COL or saline into the VMN. In COL-treated rats, GAL mRNA levels increased dramatically over controls in the supraoptic nucleus, paraventricular nucleus (PVN), dorsomedial nucleus (DMN), arcuate nucleus (ARC) and lateral hypothalamic area (LHA); no significant change was observed in the central nucleus of amygdala. These results indicated that disruption of neurotransmission in the VMN upregulated GAL gene expression in those hypothalamic sites (PVN, DMN, LHA and ARC) that are implicated in regulation of feeding, and since GAL stimulates feeding, this neurochemical rearrangement may contribute to the over-eating in these animals. These results also suggest that, normally, neurons in the VMN may suppress GAL neurotransmission in feeding-regulating hypothalamic neural circuits.

Animals↗
PubMed1998

Neuropeptide Y release in the paraventricular nucleus is decreased during transient hyperphagia induced by microinjection of colchicine into the ventromedial nucleus of rats.

Disruption of neural signaling in the ventromedial nucleus (VMN) of rats by microinjection of the neurotoxin colchicine (COL) results in transient hyperphagia accompanied by enhanced weight gain. We tested the hypothesis that release of neuropeptide Y (NPY), a potent orexigenic signal is augmented within the paraventricular nucleus (PVN) of COL-treated hyperphagic rats. Adult male rats were microinjected bilaterally with either COL (4 microg/0.5 microl in saline) or saline in the VMN and a push-pull guide cannula aimed at the PVN was implanted for analysis of extra-cellular NPY. COL-injected rats gained 37.8+/-6.1 g while the saline-injected rats lost 9.3+/-3.4 g during the 4 days following surgery. On day 4, post-injection, the PVN of these rats was perfused with artificial cerebrospinal fluid via the push-pull cannula. NPY levels in perfusates collected at 10 min intervals from hyperphagic, COL-injected rats were markedly diminished. Cumulative NPY efflux over the 180 min sampling period was significantly less in COL-treated (27.7+/-6.0 pg) versus saline-injected control rats (110.6+/-32.2 pg; P < 0.05). These results show that impairment of neural signaling in the VMN by COL suppressed NPY release in the PVN. These observations taken together with previous studies showing diminution in preproNPY mRNA in the arcuate nucleus (ARC) and NPY levels in the PVN are in accordance with the thesis that the VMN normally exerts a facilitatory influence on NPYergic signaling in the ARC-PVN axis.

Animals↗
PubMed1998

Leptin-independent hyperphagia and type 2 diabetes in mice with a mutated serotonin 5-HT2C receptor gene.

Brain serotonin and leptin signaling contribute substantially to the regulation of feeding and energy expenditure. Here we show that young adult mice with a targeted mutation of the serotonin 5-HT2C receptor gene consume more food despite normal responses to exogenous leptin administration. Chronic hyperphagia leads to a 'middle-aged'-onset obesity associated with a partial leptin resistance of late onset. In addition, older mice develop insulin resistance and impaired glucose tolerance. Mutant mice also responded more to high-fat feeding, leading to hyperglycemia without hyperlipidemia. These findings demonstrate a dissociation of serotonin and leptin signaling in the regulation of feeding and indicate that a perturbation of brain serotonin systems can predispose to type 2 diabetes.

Animals↗
PubMed2000

Dopamine is required for hyperphagia in Lep(ob/ob) mice.

Feeding is a complex process responsive to sensory information related to sight and smell of food, previous feeding experiences, satiety signals elicited by ingestion and hormonal signals related to energy balance. Dopamine released in specific brain regions is associated with pleasurable and rewarding events and may reinforce positive aspects of feeding. Dopamine also influences initiation and coordination of motor activity and is required for sensorimotor functions. Thus, dopamine may facilitate integration of sensory cues related to hunger, initiating the search for food and its consumption. Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens, where they modulate movement and reward. There are projections from the nucleus accumbens to the lateral hypothalamus that regulate feeding. Dopamine-deficient mice (Dbh(Th/+), Th-/-; hereafter DD mice) cannot synthesize dopamine in dopaminergic neurons. They gradually become aphagic and die of starvation. Daily treatment of DD mice with L-3,4-dihydroxyphenylalanine (L-DOPA) transiently restores brain dopamine, locomotion and feeding. Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia. As the hypothalamic leptin-melanocortin pathway appears to regulate appetite and metabolism, we generated mice lacking both dopamine and leptin (DD x Lep(ob/ob)) to determine if leptin deficiency overcomes the aphagia of DD mice. DD x Lep(ob/ob) mice became obese when treated daily with L-DOPA, but when L-DOPA treatment was terminated the double mutants were capable of movement, but did not feed. Our data show that dopamine is required for feeding in leptin-null mice.

Animals↗
PubMed2006

Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance.

Here we report the presence of hyperphagia, obesity and insulin resistance in knockout mice deficient in IL-18 or IL-18 receptor, and in mice transgenic for expression of IL-18 binding protein. Obesity of Il18-/- mice resulted from accumulation of fat tissue based on increased food intake. Il18-/- mice also had hyperinsulinemia, consistent with insulin resistance and hyperglycemia. Insulin resistance was secondary to obesity induced by increased food intake and occurred at the liver level as well as at the muscle and fat-tissue level. The molecular mechanisms responsible for the hepatic insulin resistance in the Il18-/- mice involved an enhanced expression of genes associated with gluconeogenesis in the liver of Il18-/- mice, resulting from defective phosphorylation of STAT3. Recombinant IL-18 (rIL-18) administered intracerebrally inhibited food intake. In addition, rIL-18 reversed hyperglycemia in Il18-/- mice through activation of STAT3 phosphorylation. These findings indicate a new role of IL-18 in the homeostasis of energy intake and insulin sensitivity.

Animals↗
PubMed2002

Decreasing hypothalamic insulin receptors causes hyperphagia and insulin resistance in rats.

We investigated the role of hypothalamic insulin signaling in the regulation of energy balance and insulin action in rats through selective decreases in insulin receptor expression in discrete hypothalamic nuclei. We generated an antisense oligodeoxynucleotide directed against the insulin receptor precursor protein and administered this directly into the third cerebral ventricle. Immunostaining of rat brains after 7-day administration of the oligodeoxynucleotide showed a selective decrease of insulin receptor protein within cells in the medial portion of the arcuate nucleus (decreased by approximately 80% as compared to rats treated with a control oligodeoxynucleotide). Insulin receptors in other hypothalamic and extra-hypothalamic areas were not affected. This selective decrease in hypothalamic insulin receptor protein was accompanied by rapid onset of hyperphagia and increased fat mass. During insulin-clamp studies, physiological hyperinsulinemia decreased glucose production by 55% in rats treated with control oligodeoxynucleotides but by only 25% in rats treated with insulin receptor antisense oligodeoxynucleotides. Thus, insulin receptors in discrete areas of the hypothalamus have a physiological role in the control of food intake, fat mass and hepatic action of insulin.

Adipose Tissue↗
PubMed2005

Hyperphagia and obesity in Na,K-ATPase alpha2 subunit-defective mice.

OBJECTIVE: The Na,K-ATPase alpha2 subunit gene (Atp1a2) is expressed in the brain, skeletal muscles, heart, and adipocytes. Specific function of the alpha2 subunit, such as involvement in differentiation and function of adipocytes, has not been addressed. The aim of this study was to examine whether Atp1a2-defective heterozygous mice show obesity and reveal the mechanisms underlying the obesity. RESEARCH METHODS AND PROCEDURES: We measured the differentiation and glucose uptake function of in vitro-differentiated adipocytes derived from embryonic fibroblasts of Atp1a2-defective mice. Food intake, body temperature, metabolic rate, and spontaneous activity and mRNA levels of neuropeptide genes were compared between the heterozygous and wild-type adult mice. RESULTS: Atp1a2 heterozygous female mice developed obesity after middle age. The time course of in vitro adipocyte differentiation of embryonic fibroblasts isolated from wild type, heterozygous, and homozygous mice was not different, glucose and Rb uptake activities of the in vitro-differentiated adipocytes were not altered, and the effects of insulin on glucose uptake and those of monensin and ouabain on Rb uptake were similar among the genotypes. However, food intake in the light phase was significantly greater in the heterozygous mice than the wild type in the 24-hour dark-light cycle, whereas it was similar under constant-light condition. Body temperature, metabolic rate at rest, and spontaneous motor activity of the heterozygous mice were similar to those of the wild type. Orexin mRNA level was lower in heterozygous than wild-type mice. DISCUSSION: The Na,K-ATPase alpha2 subunit is not involved in the differentiation or in glucose and Rb uptake function of in vitro-differentiated adipocytes. Hyperphagia is the likely primary cause of obesity in Atp1a2 heterozygous mice.

Adipocytes↗
PubMed2001

Insulin-sensitizing action of rosiglitazone is enhanced by preventing hyperphagia.

AIM: We investigated whether pair-feeding to prevent hyperphagia would potentiate the insulin-sensitizing effect of rosiglitazone in chow-fed and insulin-resistant dietary obese rats, and studied the role of leptin and hypothalamic neuropeptide Y as mediators of weight gain during treatment. METHODS: Dietary obese and chow-fed rats (575 +/- 10 vs. 536 +/- 7 g; p < 0.01) were given rosiglitazone (30 mg/kg p.o.) or vehicle daily for 14 days. RESULTS: Energy intake and weight gain were greater in rosiglitazone-treated ad-lib-fed rats (body weight: chow + 24 +/- 2 g, rosiglitazone-treated + 55 +/- 2 g, p < 0.001; dietary obese + 34 +/- 2 g, rosiglitazone-treated + 74 +/- 7 g, p < 0.001). Half of each rosiglitazone-treated group were pair-fed to vehicle-treated controls. Rosiglitazone normalized circulating free fatty acids (FFAs) and insulin sensitivity in dietary obese rats (homeostasis model assessment (HOMA): chow-fed controls, 3.9 +/- 0.3; dietary obese controls, 6.7 +/- 0.7; rosiglitazone-treated, ad lib-fed dietary obese, 4.2 +/- 0.5; both p < 0.01). Insulin sensitivity improved further with pair-feeding (HOMA: 2.9 +/- 0.4; p < 0.05 vs. rosiglitazone-treated, ad lib-fed dietary obese), despite unchanged FFAs. Qualitatively similar findings were made in chow-fed rats. Pair-feeding prevented rosiglitazone-related weight gain in chow-fed, but not dietary obese rats (body weight: + 49 +/- 5 g, p < 0.001 vs. untreated dietary obese controls). Adipose tissue OB mRNA was elevated in dietary obese rats, reduced 49% (p < 0.01) by rosiglitazone treatment, and further (by 16%) with pair-feeding (p < 0.0001). Plasma leptin, however, only fell in the pair-fed group. Hypothalamic neuropeptide Y mRNA was unchanged throughout, suggesting that weight gain associated with high-dose rosiglitazone treatment is independent of hypothalamic neuropeptide Y. CONCLUSIONS: Food restriction potentiates the insulin-sensitizing effect of rosiglitazone in rats, and this effect is independent of a fall in FFAs.

Animals↗