Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes of colonic temperature were investigated to examine a mechanism of hypothermia in the obese rats which received subcutaneous administration of intermediate type-insulin (8 U/day) for 8 weeks. Although diurnal rhythmicity of colonic temperature levels was maintained similarly with those of vehicle-injected controls, the overall colonic temperature levels were significantly lowered in insulin-treated animals. In the condition of cold exposure at 5 degrees C, colonic temperature levels of insulin-treated animals were immediately and significantly decreased at 60 minutes after the start of cold exposure. The data obtained herein demonstrated that hyperinsulinemia accompanying with hyperphagia should be profoundly involved in hypothermia, observed in various experimental models of obesity.
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PMID:Hypothermia in insulin-treated obese rats. 163 26

The hyperphagic properties of insulin (10 U/kg, s.c.) were transiently (2h) and dose-dependently inhibited (30%) by central pretreatment with naltrexone (20-50 micrograms, i.c.v.). The irreversible mu opioid antagonist, beta-funaltrexamine (B-FNA, 20 micrograms, i.c.v.) significantly inhibited insulin hyperphagia by 28-54% over the 6-h time course. In contrast, insulin hyperphagia was only transiently (2 h) inhibited (27-30%) by either the irreversible mu 1 antagonist, naloxonazine (50 micrograms, i.c.v.) or the selective kappa antagonist, nor-binaltorphamine (NorBNI, 20 micrograms, i.c.v.). The delta-antagonistic actions of [D-Ala2, Leu5, Cys6]-enkephalin (DALCE, 40 micrograms, i.c.v.) failed to affect insulin hyperphagia. These data suggest that the mu 2 opioid receptor subtype modulates insulin hyperphagia.
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PMID:Mediation of insulin hyperphagia by specific central opiate receptor antagonists. 165 80

Neuropeptide Y (NPY) is an important hypothalamic regulator of feeding behavior. In this study we have investigated the regulation of the expression of preproNPY mRNA in male obese and lean Zucker rats by in situ hybridization. These animals represent a model of genetic obesity with hyperphagia, hyperinsulinemia and altered endocrine functions. Obese Zucker rats, treated for 12 days with 0.9% saline, had about 210% higher level of basal preproNPY mRNA expression in the arcuate nucleus when compared to their lean littermate controls. Repeated administrations of 8-hydroxy-dipropylaminotetralin (8-OH-DPAT), a serotonergic 5-HT1A agonist, or mifepristone, a glucocorticoid receptor antagonist, did not modify the basal expression of preproNPY mRNA in the Zucker phenotypes. The 8-OH-DPAT treatment significantly reduced hyperinsulinemia in obese Zucker rats without changing plasma glucose levels. The mifepristone treatment significantly increased plasma corticosterone levels in lean animals, but not in obese animals. The present study demonstrates enhanced expression of preproNPY mRNA in the arcuate nucleus in obese Zucker rats suggesting an involvement of NPY in the pathophysiology of the hyperphagic syndrome and genetically determined obesity in Zucker rats. Neither the antagonism of glucocorticoid receptors by mifepristone, nor repeated treatment with 8-OH-DPAT resulting in reduced insulin levels in obese Zucker rats, modified the basal expression of preproNPY mRNA in the arcuate nucleus.
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PMID:Effects of repeated administration of mifepristone and 8-OH-DPAT on expression of preproneuropeptide Y mRNA in the arcuate nucleus of obese Zucker rats. 165 93

Neuropeptide Y (NPY) concentrations were measured by radioimmunoassay in eight microdissected hypothalamic regions of obese (fa/fa) and lean (Fa/?) Zucker rats. Freely fed obese rats showed significant (40-100%) increases in NPY concentrations in several regions, notably the paraventricular, ventromedial, and dorsomedial nuclei and the arcuate nucleus/median eminence, compared with lean rats. Hypothalamic NPY concentrations were not affected in either obese or lean rats by food restriction, which caused 25% weight loss over 3 wk. Refeeding to initial weight significantly increased NPY levels in the ventromedial and dorsomedial nuclei in lean rats but did not significantly alter NPY concentrations in any hypothalamic region in obese rats. These observations indicate fundamental differences in the regulation of hypothalamic NPY between obese and lean Zucker rats. NPY injected into the paraventricular nucleus and other regions causes hyperphagia, obesity, and increased secretion of insulin, glucagon, ACTH, and corticosterone. These behavioral and neuroendocrine abnormalities all occur in the obese Zucker syndrome and may be due to increased NPY-ergic activity in the hypothalamus.
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PMID:Altered neuropeptide Y concentrations in specific hypothalamic regions of obese (fa/fa) Zucker rats. Possible relationship to obesity and neuroendocrine disturbances. 165 67

Spontaneously diabetic rats with remarkable polyuria, polyphagia, and polydipsia were discovered in 1983 in an outbred colony of Long-Evans rats purchased from Charles River Canada in 1982. They have since been maintained at the Tokushima Research Institute (Otsuka Pharmaceutical, Tokushima, Japan). A strain of rats (Long-Evans Tokushima Lean [LETL]) with diabetes was bred from these rats. The characteristic features of the disease in LETL rats are 1) sudden onset of polyuria, polyphagia, hyperglycemia, and weight loss; 2) no sex differences in the rate of onset or severity; 3) lymphocyte infiltration into islets followed by destruction of beta-cells and disappearance of lymphocytes at the onset of diabetes; 4) no significant T lymphopenia; 5) lymphocyte infiltration into the salivary glands and lacrimal glands; and 6) at least two recessive genes involved in the pathogenesis of insulitis, one of which is closely linked with RT1u. These characteristics closely resemble those of human insulin-dependent diabetes mellitus (IDDM). Results suggest that the LETL rat is a useful animal model for analysis of genetic and immunologic factors relating to the pathogenesis of human IDDM.
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PMID:New inbred strain of Long-Evans Tokushima lean rats with IDDM without lymphopenia. 168 94

Insulin was chronically administered to rats to determine its effect on the daily changes in food intake and body weight. Animals received regular insulin via 14-day osmotic minipumps in doses of 0.0, 0.5, 1.0, 3.0, and 5.0 IU/day treated either with (+GLU) or without glutamic acid (-GLU). Previous studies have shown that glutamic acid prevents insulin aggregation in the minipumps to provide a more stable flow rate. Food intake and body weights were measured each day of treatment. Chronic insulin treatment was ineffective in promoting changes in animals receiving any dose of insulin except the highest dose. Animals receiving 5.0 IU/day insulin + GLU experienced a transient hyperphagia and weight gain followed by a suppression in food intake and body weight by Day 4 of treatment. Effects were attenuated in animals receiving insulin -GLU. Plasma insulin concentrations on Day 14 were similar for all doses, suggesting a compensation took place either in insulin degradation or endogenous insulin production. Results indicate that glutamic acid treatment enhances the effects of chronic insulin administration via osmotic minipumps.
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PMID:Effect of chronic insulin administration on food intake and body weight in rats. 168 90

Fluoxetine selectively inhibits serotonin uptake in vitro and in vivo and thus enhances serotonergic function, leading to a decrease in food intake beginning with the first dose and a decrease in body weight or in weight gain after multiple doses of fluoxetine. Fluoxetine and other drugs that increase serotonergic function decrease food intake with characteristics that make them attractive for use in weight reduction. In rats, for instance, fluoxetine and other serotonergic drugs suppress stress-induced eating, suppress carbohydrate consumption selectively, and suppress insulin-induced hyperphagia. Fluoxetine and other serotonergic drugs do not cause amphetamine-like behavioral stimulation in animals and have no known abuse or addiction liability. In obese yellow mice and in normal mice, as in rats, fluoxetine causes a sustained decrease in food intake and body weight. The pharmacologic effects of fluoxetine in animals suggest its potential use in weight-reduction programs in obese humans.
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PMID:Preclinical pharmacology of fluoxetine, a serotonergic drug for weight loss. 172 30

The effect of glucose hyperalimentation on energy metabolism in the cirrhotic rat liver after 70% hepatectomy was studied. After resection, rats received either 30 kcal/kg per day (group I) or 200 kcal/kg per day (group II) of glucose for 48 h. In both groups, hepatic mitochondrial ATP synthesis was accelerated when palmitic acid was used as substrate and suppressed when pyruvate was used. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose. Hepatic energy charge was within normal limits in group I, but decreased significantly in group II after hepatectomy. An abundance of glucose in the early postoperative period, therefore, caused a hepatic energy derangement by suppressing fatty acids utilization; this suppression was corroborated by the findings of lower immunoreactive glucagon and non-esterified fatty-acid concentrations in group II. To determine optimal glucose administration, the predicted value of glucose disposal rate (GDR) was calculated after an intravenous glucose tolerance test. GDR decreased significantly after hepatectomy and did not increase appreciably even with a large dose of insulin administration. These results suggest that glucose administration should be tailored to the GDR values after resection of the cirrhotic liver.
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PMID:Glucose overload and hepatic energy metabolism after resection of the cirrhotic liver in rats. 178 71

Prematurity in Indian births is modeled, based on the hypothesis that reduced protein and glucose and aminoacids and maternal anemia and preeclampsia lead to placental dysfunction which is also affected by metabolic disturbance and fetal circulation related to cellular growth and questions about genetics. There may be an ethnic propensity for early maturation of the fetus which affects the higher stillbirth rates and perinatal mortality. It was observed that among, for instance, black and Indian racial groups there may be meconium release and fetal distress. The significance is that physicians should increase antenatal surveillance before 40 weeks. Maternal nutrition should be advanced and hyperalimentation by cordocentesis. Other interventions such as glucose, oxygen, and aspirin administration are still very experimental. The evidence that velocity of growth is different and low birth weight is due to abnormal growth and shortened gestation is currently being researched among different ethnic groups. The discussion is concerned with reports of ethnic variation among Indian and Malay babies in Singapore and babies of French or African ancestry in France. In these studies findings were that the Indians and Malays in Singapore vs. the Chinese had higher mortality, and black African ancestry in mixed ancestry babies was related to higher infant mortality. Another study on neonatal mortality in India led to the recommendation that 2000 gm be established as the limit for defining low birth weight. In the 1501- 2000 gm birth weight groups, 30-45% are preterm, and the remainder are term or postterm. Low birth weight may transcend generations in India even with emigration. Experimental studies show that intrauterine weight is related to placental volume. Reduced growth and lower fetal insulin/glucose ratio with elevated fetal glycine/valine ratio was found to be related to reduced glucose supply among fetuses with fetal hypertriglyceridemia. Fat seems to be lacking among low birth weight fetuses. Studies of somatomedin and somatostatin in metabolism are helping to provide greater understanding of fetal growth processes.
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PMID:The prematurity paradox of the small Indian baby. 180 Mar 24

Two experiments were conducted in order to see if dopamine satiety receptors in the lateral hypothalamus or satiety mechanisms in the ventromedial hypothalamus were involved in the hyperphagia and body weight increase induced by systemic sulpiride. In the first experiment, it was shown that systemic sulpiride (20 mg/kg) does not block the anorexia caused by intraperifornical injections of amphetamine. In the second experiment, sulpiride (20 mg/kg during 18 days) did not produce an additional increase in body weight in previously VMH-lesioned female rats. This last fact cannot be explained by a ceiling effect since insulin (5 U/day during 7 days) increased body weight in the same VMH rats in which sulpiride was not effective. These results do not support the hypothesis that systemic sulpiride reaches the perifornical dopamine D2 receptors to disinhibit feeding, but suggest instead an involvement of the ventromedial hypothalamus. This last suggestion is more in agreement with the hypothesis that sulpiride alters feeding and body weight gain through the induction of a functional gonadectomy.
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PMID:Ventromedial hypothalamus vs. lateral hypothalamic D2 satiety receptors in the body weight increase induced by systemic sulpiride. 183 76


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