TY - JOUR
T1 - Gastric glucagon release during gastric and intestinal phase of a meal in dogs
AU - Schusdziarra, V.
AU - Rouiller, D.
AU - Unger, Roger H
PY - 1980
Y1 - 1980
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpgi.1980.238.2.g109
DO - 10.1152/ajpgi.1980.238.2.g109
M3 - Article
C2 - 7361897
AN - SCOPUS:0018979274
SN - 0193-1857
VL - 1
SP - G109-G113
JO - American Journal of Physiology - Gastrointestinal and Liver Physiology
JF - American Journal of Physiology - Gastrointestinal and Liver Physiology
IS - 2
ER -