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

Meals increase the activity of the sympathetic nervous system (SNS) above the activity level observed in the postabsorptive state. Pharmacologic blockade of the thermogenic effect of norepinephrine, the primary neurotransmitter of the SNS, suggests that this response accounts for approximately 20% of the thermic response to food. Energy expenditure increases after several days of sustained overeating. There is no convincing evidence that this response is mediated by increased SNS activity in humans, as it is in some animals. Energy expenditure decreases within a few days of energy deprivation. When sodium balance is maintained, energy deprivation also reduces SNS activity. The reduced SNS activity may contribute to the decreased energy expenditure, but cannot explain it completely. The contribution of the SNS to total energy expenditure is small in normal subjects consuming a weight-maintenance diet, probably < 5%. A few studies have suggested that SNS activity is reduced in obese humans, suggesting that low energy expenditure associated with reduced SNS activity may contribute to obesity. However, a critical evaluation of the available evidence indicates that this hypothesis is untenable.
 ...
PMID:Sympathetic nervous system response to intake. 748 30

Drugs, such as sodium mercaptoacetate and methylpalmoxirate, which block fatty acid oxidation at different levels in the metabolic pathway, stimulate feeding. It is well known that selective centrally induced stimulation of dopamine, serotonin (5-hydroxytryptamine, 5-HT) and beta-adrenoceptors, or inhibition of the opiatergic system substantially decrease food intake in rats trained to eat 4 h a day. The results of the present study show that centrally acting dopaminergic and serotoninergic anorectic drugs, the opiate receptor antagonist naloxone, the alpha-adrenoceptor blocking drug phentolamine, and peripherally administered 5-HT counteract the overeating induced by mercaptoacetate. Comparing these effects to those described in 2-deoxy-D-glucose- and insulin-induced feeding, our data support the proposition that distinct neural circuits are involved in the hyperphagic responses to diverse metabolic stimuli.
 ...
PMID:Pharmacological antagonism of lipoprivic feeding induced by sodium mercaptoacetate. 760 Dec 16

The weight gain and hyperphagia induced by chronic administration of sulpiride in female rats were not prevented by the concomitant administration of an extra source of sodium. In addition, serum sodium levels were not affected, but potassium levels were significantly reduced by sulpiride administered for 1 week. These results suggest that sulpiride-induced obesity in rats is not related to sodium imbalance. The mechanism for the decrease in serum potassium levels and its relation with sulpiride-induced weight gain warrant further investigation.
 ...
PMID:Hyponatremia and neuroleptic-induced obesity in rats. 799 68

Vanadate treatment can lower glycemia in diabetic rats. This action is generally attributed to vanadate's insulinomimetic properties, but vanadate also inhibits feeding, which could lower blood glucose. We therefore assessed the contribution of hypophagia to vanadate's antihyperglycemic action in a 3-week study of streptozocin-induced (STZ) diabetic rats. Untreated diabetic rats (n = 8) ate 54% more food than nondiabetic control rats (P < 0.001). Diabetic rats given sodium metavanadate (0.5 mg in 0.5 ml of water by gavage twice daily; n = 8) had significantly lower food intakes (P < 0.001) than untreated diabetic rats. In vanadate-treated diabetic rats, blood glucose levels were significantly lower than in untreated diabetic rats (P < 0.001). Untreated diabetic rats pair-fed to the food intake of the vanadate-treated diabetic rats (n = 8) showed virtually identical blood glucose falls (P > 0.05 vs. vanadate-treated diabetic rats). Vanadate treatment did not affect plasma insulin concentrations in diabetic rats. In nondiabetic rats (n = 8), vanadate treatment significantly reduced food intake (P < 0.05) and also lowered plasma insulin concentrations (P < 0.05) without significantly affecting glycemia. To investigate the mechanism of vanadate's hypophagic effect, we also measured regional hypothalamic levels of neuropeptide Y (NPY), a potent central appetite stimulant that is thought to drive hyperphagia in STZ-induced diabetes. Hypothalamic NPY concentrations rise markedly in diabetes and are normalized by insulin replacement. Unlike insulin, vanadate treatment did not normalize regional hypothalamic NPY concentrations in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of chronic vanadate administration in the STZ-induced diabetic rat. The antihyperglycemic action of vanadate is attributable entirely to its suppression of feeding. 792 99

It has been shown that improvement of glucose homeostasis by oral vanadate or vanadyl treatment in streptozotocin-induced diabetic rats is accompanied by severe negative side effects (some deaths, decreased weight gain, alteration in renal function as well as tissue vanadium accumulation) which argue against the use of vanadium compounds in diabetes treatment. The present study was undertaken to assess the effectiveness in alleviating some signs of diabetes in streptozotocin-treated rats with oral therapy with sodium metavanadate (NaVO3) and sodium 4,5 dihydroxybenzene-1,3-disulfonate (Tiron), a chelating agent effective in mobilizing vanadium. In a preliminary experiment, diabetic rats were given aqueous solutions of 0.20 mg NaVO3/ml for 4 days. Vanadium-treated rats which showed blood glucose levels significantly lower (p < 0.001) than vanadate-untreated diabetic rats were selected for subsequent experiments. These animals were given 0.20 mg NaVO3/ml in drinking water and 0, 125.6, 314 or 628 mg Tiron/kg/d by gavage for 2 w. Although most of the animals did not become normoglycemic, several characteristic signs of diabetes (hyperglycemia, hyperphagia and polydipsia) were alleviated by the NaVO3 treatment. The administration of 314 mg Tiron/kg/d (approximately 1 NaVO3: 5 Tiron, mole ratio) did not diminish the ameliorative effects of NaVO3 with respect to diabetes, but significantly decreased the level of vanadium accumulation in target organs. These results show that some of the beneficial effects of NaVO3 are maintained in diabetic animals given Tiron, while the administration of the chelator results in a significant decrease in tissue vanadium accumulation. Accordingly, this would diminish the possibility of toxic side effects derived from prolonged oral vanadium administration.
 ...
PMID:Oral vanadate and Tiron in treatment of diabetes mellitus in rats: improvement of glucose homeostasis and negative side-effects. 830 15

Rumen-fistulated lactating cows were individually fed on hay or silage and intakes were monitored during 3 h treatment periods and for 2 h after. Each experiment used five, six or seven animals and the treatments were applied in a Latin Square design. Sodium acetate infusions of 1.8-11.0 mol in 4.5 litres water caused a dose-related depression in hay intake, the extent being 82 g dry matter (DM)/mol infused (P < 0.01). Sodium acetate infusions of 6.0-15.0 mol in 4.5 litres water caused a dose-related depression in silage intake of 118 g DM/mol infused. Rumen fluid pH for both diets was unaffected by treatment. Acetate and Na concentrations were increased and significantly negatively correlated with intake of both diets. Infusions of 2-8 mol sodium propionate caused a dose-related depression of hay intake which was significant when cow and day effects were accounted for. Sodium propionate infusions of 4-8 mol significantly depressed silage intake by 140 g DM/mol infused (P < 0.001). Rumen fluid pH was unaffected by treatment while propionate and Na concentrations were elevated and significantly negatively correlated with intake for both diets. Inflation of a rubber balloon in the rumen with 12.5-20 litres warm water resulted in a dose-dependent depression in hay intake of 66 g DM/l distension (P < 0.05). There was significant overeating during the 2 h following the 20 litre treatment. With silage, 15-25 litres of balloon distension for 3 h resulted in a dose-dependent depression in intake of 28 g DM/l distension (P < 0.001). There was no significant overeating during the 2 h following distension. When given in physiological amounts, at the lower end of the range used in these experiments, acetate, propionate and distension of the rumen did not significantly affect hay intakes. However, in each case the linear relationship between intake depression and level of treatment suggested that these factors could contribute to the control of feed intake.
 ...
PMID:Responses in the voluntary intake of hay or silage by lactating cows to intraruminal infusions of sodium acetate or sodium propionate, the tonicity of rumen fluid or rumen distension. 832 46

Short-bowel syndrome is a state of severe malabsorption secondary to extensive bowel resection. The most common reasons for extensive bowel resection are Crohn's disease and mesenteric infarction. The pathophysiological consequences depend on extent and site of resection, integrity and adaptation of the remaining bowel, and secondary effects on other organs. Most extensively bowel resected patients can be adequately nourished by mouth, especially since they develop compensatory hyperphagia. For patients with colon in function a high-carbohydrate low-fat diet is beneficial compared to a diet with a normal fat content, because it results in decreased diarrhoea, decreased faecal mineral losses, and increased energy assimilation. The relative amount of dietary fat does not influence stool mass or energy assimilation in jejunostomy patients. Patients with jejunostomy have a high faecal output of water, sodium, and divalent cations, and they often need permanent parenteral supply of saline as well as calcium and magnesium if their small intestinal remnant is < 200 cm and parenteral nutritional support if they retain < 100 cm small bowel. In contrast, 50 cm of the jejunum often suffices for adequate oral nutrition if most of the colon is preserved. The majority of patients needing long-term intravenous supply are trained to administer parenteral nutrition at home (HPN). Most patients on HPN obtain a good or fair quality of life with hospital readmissions corresponding to an average of 10% of the HPN duration and an overall HPN related mortality of about 4%.
 ...
PMID:Nutrition in short-bowel syndrome. 872 85

The role of beta-adrenoreceptors in modulating feeding in glucoprivation- and lipoprivation-induced hyperphagias was studied in rats by measuring the efficacy of the selective beta2-adrenoreceptor agonist salbutamol to antagonize the hyperphagic response induced by injection of 2-deoxy-D-glucose (2-DG), insulin, or sodium mercaptoacetate (MA). 2-DG and insulin are blockers of glucose utilization, and their administration stimulates receptor cells that are selectively sensitive to central glucose availability. MA stimulates feeding in rats maintained on a fat-supplemented diet, by blocking fatty acid oxidation at different levels in the metabolic pathway. We found that salbutamol dose-dependently antagonized both the insulin- and MA-induced hyperphagia, with reductions in food intake up to 100% compared with rats treated with insulin or MA alone. On the contrary, salbutamol, even at the highest dose (15 mg/kg, IP), was completely ineffective against 2-DG-induced hyperphagia. The present results support the previously proposed notion that there are different neuronal or humoral circuits underlying the hyperphagic responses to the metabolic stimuli induced by glucoprivation (i.e., 2-DG and insulin administration), and they extend our knowledge on the effects of salbutamol on glucoprivic and lipoprivic control of feeding.
 ...
PMID:Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia. 874 3

1. The effect of chronic saccharin (benzosulphimide) consumption on glucose homeostasis was examined in normal lean +/+ mice and genetically obese hyperglycaemic insulin-resistant ob/ob mice. 2. Consumption of a 5% (w/v) sodium saccharin solution for 7 weeks prevented the development of hyperglycaemia, improved glucose tolerance (area under curve decreased by 51%), reduced the extent of hyperinsulinaemia (by 21%), and reduced excessive weight gain (by 18%) in ob/ob mice. 3. Consumption of 5% (w/v) sodium saccharin temporarily decreased hyperphagia at the beginning of treatment, decreased hepatic glycogen content (by 47%), increased abdominal muscle glycogen content (by 82%), but did not significantly alter the hypoglycaemic response to exogenous insulin in ob/ob mice. 4. Consumption of a 1% (w/v) sodium saccharin solution did not prevent the development of hyperglycaemia in ob/ob mice. 5. Normal lean +/+ mice consuming 5% (w/v) sodium saccharin solution showed a marginal decrease (by 8%) in glycaemia, and glucose tolerance was improved (area under curve decreased by 30%) without a significant change in the insulin response to glucose or the hypoglycaemic effect of exogenous insulin. 6. These results suggest that chronic consumption of saccharin can defer the development of hyperglycaemia and improve glucose homeostasis in insulin-resistant ob/ob mice through a mechanism that is independent of insulin.
 ...
PMID:Antihyperglycaemic effect of saccharin in diabetic ob/ob mice. 911 2

The effects of 1 day of streptozotocin-induced diabetes in rats on glucose transport across the brush border membrane (BBM) and basolateral membrane (BLM) prepared from jejunal enterocytes has been studied. The effects on glucose transport of treatment of diabetic animals with insulin to reduce to normal the elevated blood glucose levels has also been assessed. The maximum capacity (Vmax) for SGLT1-mediated glucose uptake by BBM vesicles was unaffected by diabetes or insulin treatment of diabetic rats. In contrast, Vmax for BLM glucose uptake was increased by 206% in diabetes, a response that could not be reversed by treatment with insulin. Western blotting of BBM for SGLT1 protein revealed a single band with a molecular weight of 73 kDa and the intensity of this band was unaffected by diabetes. However, an increased level of GLUT2 was noted in diabetic BLM and this was not a consequence of changes in glycaemic or insulin status. Diabetes hyperpolarised the BBM, implying an increased driving force for Na(+)-sugar co-transport but insulin treatment only partially reversed this enhanced potential difference. Benzamil (2 microns), an epithelial Na+ channel blocker, hyperpolarised the BBM of control but not diabetic enterocytes, implying that a reduced Na+ permeability was responsible for the diabetic hyperpolarisation. It was concluded that in early diabetes, before the onset of hyperphagia, a greater driving force for Na(+)-dependent BBM sugar transport together with increased GLUT2 activity at the BLM promotes sugar movement across the enterocyte. Possible triggers for the transport responses are discussed.
 ...
PMID:Early diabetes-induced changes in rat jejunal glucose transport and the response to insulin. 924 34


<< Previous 1 2 3 4 5 6 7 Next >>