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)

In previous studies, 1,5-anhydro-D-glucitol (1-DG), an endogenous glucose analog, was found to significantly influence physiological feeding behavior. The relationships between the hydroxyl group positions on the pyranose ring carbons and the anorectic action induced by 1-DG and its analogs are discussed. To investigate the effects of these glucose analogs on ingestive behavior, 24 mumole of test solution was injected into the rat third cerebral ventricle immediately before normal eating time, which starts at the beginning of the dark. After initial transient hyperphagia, 1-DG suppressed feeding during the first 12-hr dark period. It prolonged postprandial intermeal interval beginning shortly after injection, but eating rate was not affected and meal size did not decrease until near the end of the normal feeding period. The incidence of drinking episodes decreased concomitant with feeding suppression. Feeding and drinking suppression were also produced by 1,2-dideoxy-D-glucose, 1,3-dideoxy-D-glucose, and 1,4-dideoxy-D-glucose, although they were less potent than 1-DG. They suppressed feeding by prolonging the postprandial intermeal interval, but did not change meal size or eating rate. The anorectic effects of 1-DG were abolished by removal of the hydroxyl group at carbon 6 and by epimerization at carbons 2, 3, and 4. These findings indicate that feeding suppression induced by 1-DG and its analogs is induced mainly by prolongation of the postprandial intermeal interval, and the presence or absence of a hydroxyl group on each carbon of 1-DG is important for its feeding suppression.
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PMID:Structural evaluation of anorectic action induced by 1,5-anhydro-D-glucitol. 398 30

1,5-Anhydroglucitol (1-DG) has been known as an antimetabolic glucose analogue. Using gas chromatography, 1-DG was found to be physiologically present in rat serum. In order to investigate its direct and long-term effects on feeding, 1-DG was infused during the light period into the rat third ventricle in doses of 3.0, 6.0 and 12.0 mumol/rat. Its effects were then compared to those of similarly applied 2-deoxy-D-glucose (2-DG). Following initial hyperphagia, both of these glucose-analogues produced suppressive effects on feeding during the subsequent day throughout the light and dark periods. On the third day after 2-DG injection reduction of feeding did not recover completely to the pretreatment baseline levels, but it did recover after 1-DG. Both 1-DG and 2-DG caused linear dose-related hypophagia, with the slope for 1-DG being about half of that for 2-DG. It is suggested that the delayed hypophagia which followed the initial hyperphagia produced by deoxyglucose was a result of sustained inactivation of the Na-pump due to intracellular ATP deficiency caused by accumulation of deoxy-glucose-6-phosphate.
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PMID:Feeding suppression induced by intra-ventricle III infusion of 1,5-anhydroglucitol. 631 43