Gastric glucagon release during gastric and intestinal phase of a meal in dogs

V. Schusdziarra, D. Rouiller, Roger H Unger

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

The intragastric instillation of a liver meal at pH 7 elicited a prompt and significant rise in gastric vein glucagon levels in anesthetized dogs. This was reduced by truncal vagotomy and by atropine. The liver meal at pH 2 elicited a significantly smaller rise in gastric vein glucagon levels that was not reduced by truncal vagotomy, but was abolished by atropine. Infusion of gastrin-17 (0.1 μg/kg-1/h-1) failed to increase gastric vein glucagon levels above the control group. Gastric glucagon release was significantly increased by intestinal instillation of the liver meal at pH 7. This was reduced by truncal vagotomy and atropine infusion. Gastric inhibitory peptide (GIP) (1 μg/kg-1/h-1), but neither CCK-octapeptide (0.5μg/kg-1/h-1) nor secretion (1 CU/kg-1/h-1), elicited a significant rise in gastric vein glucagon levels. It is concluded that I) gastric glucagon release is stimulated during the gastric and intestinal phase of a meal, 2) gastric glucagon release is stimulated by GIP, and 3) gastric glucagon release is modified by vagal and muscarinic cholinergic mechanisms, suggesting a neuroendocrine influence on its release.

Original languageEnglish (US)
Pages (from-to)G109-G113
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume1
Issue number2
DOIs
StatePublished - Jan 1 1980

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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