Inhibition of Meal-stimulated Gastric Acid Secretion in Man by Exogenous and Endogenous Pancreatic Glucagon

F. B. Loud Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

D. Froberg Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

J. Reichardt Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

J. J. Holst Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

J. F. Rehfeld Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

J. Christiansen Dept. of Surgery D, Glostrup Hospital, and Institute of Medical Physiology C, University of Copenhagen, Copenhagen, and Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark

Abstract

The effect of intravenous infusion of glucagon (300 ng X kg⁻¹ X h⁻¹), l-arginine (0.6 g X kg⁻¹ X h⁻¹) and of saline on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Infusion of glucagon and l-arginine enhanced plasma concentrations of pancreatic glucagon to 65-85 pmol/1, a level similar to that seen after a normal protein-rich meal. Both infusions significantly inhibited the acid response to the meal, most pronounced after l-arginine. The difference in acid inhibition could not be ascribed either to differences in plasma glucagon concentrations or to differences in serum gastrin concentrations. The study supports the concept that pancreatic glucagon is a physiological inhibitor of gastric acid secretion.

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Inhibition of Meal-stimulated Gastric Acid Secretion in Man by Exogenous and Endogenous Pancreatic Glucagon

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Inhibition of Meal-stimulated Gastric Acid Secretion in Man by Exogenous and Endogenous Pancreatic Glucagon

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