Gastric A-Cell Function in Insulin-Deprived Depancreatized Dogs1

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Abstract
To determine if gastric A-cells are a major source of the glucagonemia of insulin-deprived depancreatized dogs and to examine their secretory behavior, immunoreactive glucagon (IRG) was measured simultaneously in plasma from the inferior vena cava (VC) and from a gastric vein (GV) draining the fundus. Basal GV IRG averaged 205 .+-. 35 pg/ml, significantly above the VC level of 71 .+-. 30 (P < 0.001) and rose to 1417 .+-. 498 1.5 min after the start of an arginine infusion, exceeding VC IRG at all points (P < 0.01). Measurement of IRG in gastric, jejunal, and ileal veins and vena cava revealed an IRG gradient only across the stomach. Measurement of glucagon-like immunoreactivity (GLI) revealed no gradient across the stomach, jejunum, or ileum, thus excluding cross-reaction with GLI as the cause of the GV hyperglucagonemia. Intragastric arginine elicited a near doubling of GV IRG within 1.5 min and this persisted for at least 120 min, ranging from 142-623 pg/ml above the VC level. Infusion of insulin at a physiologic rate lowered GV IRG from 665 .+-. 66 to 151 .+-. 49 pg/ml in 20 min and abolished the GV-VC gradient within 60 min, whereas i.v. and intragastric glucose administration without insulin did not alter GV IRG. In the insulin-deprived depancreatized dog, the stomach is a major source of IRG. Gastric IRG secretion is somehow stimulated by i.v. and intragastric arginine administration. It is not influenced by i.v. or intragastric glucose administration. Its release is suppressed by physiologic levels of insulin.

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