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Results for “Hyperphagia”

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At least 325 records · Page 18Linked to original sources
PubMed2006

Hypothalamic neuropeptide Y (NPY) and the attenuation of hyperphagia in streptozotocin diabetic rats treated with dopamine D1/D2 agonists.

1. Dopamine is an appetite suppressant, while neuropeptide Y (NPY), an appetite stimulant in the brain, is reported to be involved in anorectic action induced by a combined administration of D1/D2 agonists in normal rats. In diabetic rats, however, these factors have not been studied. 2. Rats (including normal, diabetic and insulin-treated diabetic rats) were given daily injections of saline or D1/D2 agonists for 6 days. Changes in food intake and hypothalamic NPY content of these rats were assessed and compared. 3. The D1/D2 agonist-induced anorectic responses were altered in diabetic rats compared to normal rats treated similarly. Both the anorectic response on the first day of dosing and the tolerant response on the subsequent days were attenuated. 4. This alteration was independent of the neuroendocrine disturbance on feeding behavior since the basic pattern of food intake during the time course of a 24-h day/night cycle was similar in normal and diabetic rats; the decrease of food intake following drug treatment was only shown at the initial interval of 0-6 h in both groups of rats. 5. However, this alteration coincided with changes in NPY content following D1/D2 coadministration. The replacement of insulin in diabetic rats could normalize both NPY content and D1/D2 agonist-induced anorexia. 6. It is demonstrated that the response of D1/D2 agonist-induced appetite suppression is attenuated in diabetic rats compared to normal rats and that elevated hypothalamic NPY content may contribute to this alteration.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Conditioned diminution of brain stimulation hyperphagia.

It is well established that electrical stimulation of the lateral hypothalamus (ESLH) can lead to stimulus-bound feeding in many different species. The present study examined the effect of a warning signal on ESLH-induced feeding. When rats are warned of ESLH (through Pavlovian conditioning), their latencies to start eating from ESLH onset are longer (approximately 2.5X) than when they are not warned. Thus, the rats are able to prepare for the maladaptive situation of eating when satiated.

Animals↗
PubMedDate not supplied

Seasonal hyperphagia does not reduce digestive efficiency in an Arctic grazer.

Muskoxen (Ovibos moschatus) consume fibrous plants that grow rapidly over the short Arctic summer. We studied responses of eight castrated male muskoxen to a diet of grass hay and mineral supplements during spring, autumn, and winter. Animals gained body mass in spring (239+/-39 kg) as body fat content increased from 26% to 38% of ingesta-free mass in winter without changes in lean mass and protein. Intakes of dry matter (DM) increased by 74% between spring and autumn as digestible energy increased from 554 to 923 kJ kg(-0.75) d(-1) during mass gain. Digestibility of cellulose (72%-76%) was not affected by increasing food intake between spring and autumn but was reduced to 65% in winter. Digestibility of nitrogen compounds was 61%-66%, even though intake increased by 134% between spring and autumn. Excess dietary nitrogen from hay and supplements increased urea concentrations in plasma and urine. High loads of solutes such as potassium did not affect plasma or urinary osmolality but were associated with increased rates of glomerular filtration and urinary excretion. Low intakes of sodium from grasses may limit intake and digestion during summer, but high food intakes can support deposition of nitrogen, calcium, magnesium, copper, and zinc in body tissue even when dietary concentrations are low. Seasonal increases in digestive and metabolic functions allow muskoxen to rapidly accumulate energy and nutrients in body tissue during the short season of plant growth.

Alaska↗
PubMed2001

Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus.

The bHLH-PAS transcription factor SIM1 is required for the development of the paraventricular nucleus (PVN) of the hypothalamus. Mice homozygous for a null allele of Sim1 (Sim1(-/-)) lack a PVN and die perinatally. In contrast, we show here that Sim1 heterozygous mice are viable but develop early-onset obesity, with increased linear growth, hyperinsulinemia and hyperleptinemia. Sim1(+/-) mice are hyperphagic but their energy expenditure is not decreased, distinguishing them from other mouse models of early-onset obesity such as deficiencies in leptin and melanocortin receptor 4. Quantitative histological comparison with normal littermates showed that the PVN of Sim1(+/-) mice contains on average 24% fewer cells without a selective loss of any identifiable major cell type. Since acquired lesions in the PVN also induce increased appetite without a decrease in energy expenditure, we propose that abnormalities of PVN development cause the obesity of Sim1(+/-) mice. Severe obesity was described recently in a patient with a balanced translocation disrupting SIM1. Pathways controlling the development of the PVN thus have the potential to cause obesity in both mice and humans.

Adipose Tissue↗
PubMed2006

Obesity, hyperphagia and increased metabolic efficiency in Pc1 mutant mice.

Prohormone convertase 1 (PC1) mutations lead to obesity in humans. However, Pc1 knockout mice do not become obese; in fact, they are runted due to a defect in growth-hormone releasing hormone processing, leading to the speculation that PC1 subserves different functions between mouse and human. Here, we report a novel allele of mouse Pc1 (N222D) that leads to obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity in Pc1(N222D/N222D) mice. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. The obesity is associated with impaired autocatalytic activation of mature PC1 and reduced hypothalamic alpha-MSH. This is the first characterization of Pc1 mutation in a model organism that mimics human PC1 deficiency.

Amino Acid Sequence↗
PubMed2005

Adaptation to a high-fat diet leads to hyperphagia and diminished sensitivity to cholecystokinin in rats.

Rats fed high-fat (HF) diets exhibit reduced sensitivity to some peptide satiety signals. We hypothesized that reduced sensitivity to satiety signals might contribute to overconsumption of a high-energy food after adaptation to HF diets. To test this, we measured daily, 3-h intake of a high-energy, high-fat (HHF, 22.3 kJ/g) test food in rats fed either low-fat (LF) or HF, isoenergetic (16.2 kJ/g) diets. During testing, half of each group received the HHF test food (LF/HHF; HF/HHF), whereas the other half received their respective maintenance diet (LF/LF; HF/HF). Rats fed a HF diet ate more of the HHF food during the 3-h testing period than LF-fed rats (HF/HHF = 7.7 +/- 0.3 g vs. LF/HHF = 5.5 +/- 0.2 g; P = 0.003). Rats tested on their own maintenance diets had similar intakes (HF/HF = 3.2 +/- 0.2 g vs. LF/LF = 3.7 +/- 0.3 g), which were lower (P < or = 0.008) than intakes of rats tested on HHF. HHF-tested rats did not differ in body weight by the end of wk 2 of testing. In a subsequent short-term choice preference test, rats exhibited an equal relative preference for HHF irrespective of their maintenance diets (HF = 63.1%, LF = 68.1%, P = 0.29). Finally, we examined the effect of intraperitoneal NaCl or cholecystokinin (CCK)-8 (100 and 250 ng/kg) injection on 1-h food intake. Both doses of CCK significantly suppressed food intake in LF-fed rats but not HF-fed rats. These results demonstrate that chronic ingestion of a HF diet leads to short-term overconsumption of a high-energy, high-fat food compared with LF-fed cohorts, which is associated with a decreased sensitivity to CCK.

Acclimatization↗
PubMed2003

A role for arcuate cocaine and amphetamine-regulated transcript in hyperphagia, thermogenesis, and cold adaptation.

We have recently shown that injection of the hypothalamic peptide cocaine and amphetamine regulated transcript (CART) into discrete hypothalamic nuclei stimulates food intake. This stimulation was particularly marked in the arcuate nucleus. Here we show that twice daily intra-arcuate injection of 0.2 nmole CART peptide for 7 days was associated with a 60% higher daytime food intake, an 85% higher thermogenic response to the beta3 agonist BRL 35135, and a 60% increase in brown adipose tissue UCP-1 mRNA. In a separate study, using stereotactically targeted gene transfer, a CART transgene was delivered by using polyethylenimine to the arcuate nucleus of adult rats. Food intake was increased significantly during ad libitum feeding and following periods of food withdrawal and food restriction in CART over-expressing animals. CART over-expressing animals lost 12% more weight than controls following a 24-h fast. Brown adipose tissue uncoupling protein-1 (UCP-1) mRNA levels (collected Day 25) were 80% higher in CART over-expressing animals. Finally, by using quantitative in situ hybridization, we found that chronic cold exposure (20 days at 4oC) increased arcuate nucleus CART mRNA by 124%. Together with the orexigenic and thermogenic effects of CART, this finding suggests a role for arcuate nucleus CART in cold adaptation.

Adaptation, Physiological↗
PubMed1989

Appetite-modulating drugs in dwarf goats, with special emphasis on benzodiazepine-induced hyperphagia and its antagonism by flumazenil and RO 15-3505.

In dwarf goats fasted for 2 h, i.v. administration of the benzodiazepine (BZ) agonists diazepam (60 micrograms/kg), brotizolam (2 and 4 micrograms/kg) and climazolam (100 micrograms/kg) induced hyperphagic effects, whereas i.v. injections of the BZ-antagonist flumazenil (R degrees 15-1788; 0.5 mg/kg), the anthelmintic ivermectin (0.1 mg/kg), the 5-HT2 antagonist ritanserine (0.1 mg/kg), ACTH (10 micrograms/kg) and prednisolone (1 mg/kg) were inactive in a 30-min feeding test. Both the BZ-antagonist R degrees 15-3505 (greater than or equal to 0.1 mg/kg) and the opiate receptor antagonist naloxone (0.1 mg/kg) had anorectic effects in dwarf goats given 30 min access to a palatable pelleted concentrate. The hyperphagic effects of climazolam and brotizolam were not antagonized by flumazenil, whereas similar doses of this drug completely reversed muscle incoordination and ataxia induced by much higher doses of these BZ-agonists. In the combination experiments with naloxone and BZ-agonists, naloxone antagonized the hyperphagic effects of both diazepam and brotizolam. Similarly, in the diazepam-R degrees 15-3505 study, there was a significant effect of diazepam and a significant inhibition of this effect by R degrees 15-3505 (50 micrograms/kg). In the diazepam-ivermectin combination experiment no evidence for drug potentiation was found. These results and the mode of action of the above mentioned drugs are discussed in relation to feeding behaviour.

Animals↗