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 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 micrograms . 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 microgram . kg-1 . h-1), but neither CCK-octapeptide (0.5 microgram . kg-1 . h-1) nor secretin (1 CU . kg-1 . h-1), elicited a significant rise in gastric vein glucagon levels. It is concluded that 1) 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 language||English (US)|
|Journal||The American journal of physiology|
|Publication status||Published - Feb 1980|
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