Effects of glucoprivation on gastric motility and pituitary oxytocin secretion in rats

Pharmacological doses of insulin (3-25 U/kg sc) elicited feeding and increased gastric motility in rats. In contrast, the glucose analogue 2-deoxy-D-glucose (2-DG), given ip in doses known to increase food intake, had dose-dependent effects on gastric motility: 100 and 200 mg/kg 2-DG increased gastr...

Full description

Saved in:
Bibliographic Details
Published inThe American journal of physiology Vol. 259; no. 3 Pt 2; p. R447
Main Authors Cato, R K, Flanagan, L M, Verbalis, J G, Stricker, E M
Format Journal Article
LanguageEnglish
Published United States 01.09.1990
Subjects
Animals
Blood Glucose - analysis
Deoxyglucose - pharmacology
Gastrointestinal Motility - drug effects
Glucose - deficiency
Insulin - pharmacology
Male
Naloxone - pharmacology
Oxytocin - blood
Oxytocin - secretion
Pituitary Gland - secretion
Rats
Rats, Inbred Strains
Online AccessGet more information

Cover

More Information
Summary:Pharmacological doses of insulin (3-25 U/kg sc) elicited feeding and increased gastric motility in rats. In contrast, the glucose analogue 2-deoxy-D-glucose (2-DG), given ip in doses known to increase food intake, had dose-dependent effects on gastric motility: 100 and 200 mg/kg 2-DG increased gastric motility, whereas 500 mg/kg 2-DG virtually eliminated gastric contractions. This latter result resembled the known effects on gastric motility of cholecystokinin (CCK) and LiCl. Moreover, like CCK and LiCl, 500 mg/kg 2-DG stimulated pituitary oxytocin (OT) secretion, and its effects on gastric motility and OT secretion were potentiated by pretreatment with the opioid antagonist naloxone. In contrast, OT secretion was not affected by insulin-induced hypoglycemia with or without naloxone pretreatment. These results suggest that there are two components to the effects of 2-DG on gastric motility: an insulin-like excitatory component and a CCK-LiCl-like inhibitory component. The latter inhibitory component may be mediated by the paraventricular nucleus of the hypothalamus, which has already been implicated in the inhibitory control of gastric motility.
ISSN:0002-9513
DOI:10.1152/ajpregu.1990.259.3.R447