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)

Chronic administration of scopolamine methyl nitrate, at doses much greater than required to block vagally mediated insulin secretion, reduced static phase VMH obesity by only 31%. At least 59% of the obesity persisted even when the initially effective dose (0.15 mg/Kg, 4 times/day) was increased eight-fold. The larger dose also did not prevent VMH hyperphagia and weight gain when scopolamine treatment was begun before the lesion. By ten days after the lesion, reduced gastrointestinal motility apparently prevented further weight gain. These results suggest that much of the obesity caused by VMH lesions is independent of vagally mediated insulin secretion or other excess vagal efferent activity. The doses used in this experiment were large in order to provide strong evidence for this conclusion.
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PMID:VMH obesity reduced but not reversed by scopolamine methyl nitrate. 52 52

Three series of experiments investigated the role of hyperinsulinemia and the vagus nerve in the hyperphagia and obesity syndrome produced in female rats by knife cuts in the ventromedial hypothalamus (VMH). The findings of the first series revealed that VMH cuts do not produce hyperinsulinemia when the rats are prevented from overeating, but insulin levels are elevated in rats allowed to overeat. The second series of experiments demonstrated that VMH-cut rats overconsume sweet sugar solutions during daily short-term tests, and that pharmacological blockade of vagal efferent activity with atropine methyl nitrate fails to inhibit this overconsumption. The third study revealed that subdiaphragmatic vagotomy completely blocks VMH hyperphagia and obesity on a chow diet, but does not prevent overeating and rapid weight gain in rats fed an assortment of highly palatable food. These findings indicate that vagally mediated insulin release is not an essential component to the VMH knife cut syndrome.
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PMID:The role of hyperinsulinema and the vagus nerve in hypothalamic hyperphagia reexamined. 701 36

Adult female rats given bilateral parasagittal knife cuts in the medial hypothalamus (VMH group) were hyperphagic and became obese on a chow diet, compared with sham-operated controls. The VMH rats also overconsumed, relative to controls, sucrose and glucose solutions during 30 min/day tests. Pretreating the VMH and control rats with atropine methyl nitrate (1.0, 5.0, or 10.0 mg/kg) reduced their intake of the sugar solutions in three out of five experiments, and in all experiments it suppressed their 24-hr chow intake. However, the VMH rats continued to drink more of the sugar solutions than did the controls after all atropine treatments, and in three out of four experiments their hyperphagia on the chow diet was not blocked by the atropine. The results do not support the hypothesis that vagally stimulated insulin release or other cholinergically mediated cephalic responses of digestion are essential for the expression of hypothalamic hyperphagia and finickiness.
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PMID:Atropine fails to block the overconsumption of sugar solutions by hypothalamic hyperphagic rats. 703 Nov 3

Nitric oxide (NO) has been suggested to be involved in the regulation of food intake. In the present study, NO metabolite (nitrite and nitrate, NOx) levels in the hypothalamus were determined in hyperphagic mice. In normal mice, NOx levels were higher in the hypothalamus than those in frontal cortex. Although 2-deoxy-D-glucose (2-DG) is known to induce hyperphagia by inhibiting glucose utilization, it did not affect NOx levels in the hypothalamus of mice. NOx concentration in the hypothalamus decreased in 48 h-food deprived mice. In the frontal cortex, neither 2-DG nor food deprivation affected NOx levels. These results suggest that NO production in the hypothalamus does not increase in 2-DG-elicited hyperphagia and that food deprivation reduces hypothalamic NO, probably by inhibiting NO synthase.
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PMID:Nitric oxide production in hypothalamus of 2-deoxy-D-glucose-treated and food deprived mice. 1209 47

The Zucker Diabetic Fatty (ZDF) rat is a model of impaired insulin sensitivity arising from hyperphagia owing to a mutation in the leptin receptor. In time, young ZDF rats, which are not initially diabetic, develop impaired pancreatic beta-cell function leading to apoptotic cell death. This results in an inability to fully compensate for the reduction in insulin sensitivity with hypersecretion of insulin. Young, pre-diabetic ZDF rats were treated, over a 4-week period, with the thiazolidinedione compound MCC-555, and the islet morphology studied in comparison to ZDF rats not given MCC-555. In particular, changes in the apoptotic incidence, as measured using TUNEL staining to localize apoptotic cells, were studied over the 4-week period. Changes in the induction of nitric oxide synthase and in the accumulation of nitrate/nitrite within the pancreas were also studied during the time course of administration of MCC-555. The study has demonstrated that the administration of MCC-555 significantly decreases the apoptotic incidence in the islets of Langerhans of pre-diabetic ZDF rats given the compound, as compared to those not given MCC-555, as well as decreasing the accumulation of nitrate/nitrite within the pancreas.
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PMID:Chronic treatment with the thiazolidinedione, MCC-555, is associated with reductions in nitric oxide synthase activity and beta-cell apoptosis in the pancreas of the Zucker Diabetic Fatty rat. 1280 Dec 82

1. The present study was designed to evaluate the protective effects of the nitric oxide (NO)-generating compounds L-arginine (L-Arg) and sodium nitroprusside (SNP) on oxidative stress markers in streptozotocin (STZ)-diabetic rats. 2. Diabetes was induced after a single intraperitoneal injection of STZ (60 mg/kg). Rats were divided into non-diabetic (control), diabetic and treated diabetic groups. The treated diabetic groups were supplemented with L-Arg (300 mg/kg), SNP (3 mg/kg per day) or glibenclamide (0.6 mg/kg per day) orally for 4 weeks. 3. At the end of the experiment, fasted rats were killed by cervical decapitation. Blood was collected for estimation of glucose, haemoglobin, glycosylated haemoglobin (HbA(1c)), total cholesterol, high-density lipoprotein-cholesterol and triglycerides. Thiobarbituric acid-reactive substances (TBARS; an index of lipid peroxidation), superoxide dismutase, glutathione peroxidase, catalase, nitrate/nitrite (NO(x)) and reduced glutathione (GSH) were estimated in liver and kidney homogenates. 4. A significant increase was observed in plasma glucose levels and HbA(1c), with a concomitant decrease in haemoglobin levels, in diabetic rats. These alterations reverted back to near normal after treatment with the NO-generating compounds. A loss of bodyweight, polydipsia, polyphagia and elevated levels of serum cholesterol and triglycerides were observed in diabetic rats. Hyperglycaemia was accompanied by a significant increase in tissue TBARS and a decrease in NO(x), GSH and anti-oxidant enzymes, whereas, supplementation with L-Arg and SNP significantly reduced TBARS levels and increased GSH and anti-oxidant enzyme activities. Linear regression analysis indicated that blood glucose and TBARS had a significant positive correlation with HbA(1c), whereas a negative correlation was observed between GSH and NO(x). 5. It is concluded that NO-generating compounds improve most of the biochemical abnormalities and anti-oxidant levels in diabetic rats. The beneficial effects of NO-generating compounds can be attributed to the generation of NO and/or enhanced anti-oxidant enzyme activities.
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PMID:Can nitric oxide-generating compounds improve the oxidative stress response in experimentally diabetic rats? 1758 Dec 13

Three series of experiments investigated the role of hyperinsulinemia and the vagus nerve in the hyperphagia and obesity syndrome produced in female rats by knife cuts in the ventromedial hypothalamus (VMH). The findings of the first series revealed that VMH cuts do not produce hyperinsulinemia when the rats are prevented from overeating, but insulin levels are elevated in rats allowed to overeat. The second series of experiments demonstrated that VMH-cut rats overconsume sweet sugar solutions during daily short-term tests, and that pharmacological blockade of vagal efferent activity with atropine methyl nitrate fails to inhibit this overconsumption. The third study revealed that subdiaphragmatic vagotomy completely blocks VMH hyperphagia and obesity on a chow diet, but does not prevent overeating and rapid weight gain in rats fed an assortment of highly palatable foods. These findings indicate that vagally mediated insulin release is not an essential component to the VMH knife cut syndrome.
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PMID:The role of hyperinsulinema and the vagus nerve in hypothalamic hyperphagia reexamined. 2794 28