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Research Article Free access | 10.1172/JCI108940
Departments of Internal Medicine, Veterans Administration Hospital, Dallas, Texas 75216
University of California at Los Angeles Health Science Center, Los Angeles, California 90093
University of Texas Southwestern Medical School, Dallas, Texas 75235
Find articles by Feldman, M. in: JCI | PubMed | Google Scholar
Departments of Internal Medicine, Veterans Administration Hospital, Dallas, Texas 75216
University of California at Los Angeles Health Science Center, Los Angeles, California 90093
University of Texas Southwestern Medical School, Dallas, Texas 75235
Find articles by Walsh, J. in: JCI | PubMed | Google Scholar
Departments of Internal Medicine, Veterans Administration Hospital, Dallas, Texas 75216
University of California at Los Angeles Health Science Center, Los Angeles, California 90093
University of Texas Southwestern Medical School, Dallas, Texas 75235
Find articles by Wong, H. in: JCI | PubMed | Google Scholar
Departments of Internal Medicine, Veterans Administration Hospital, Dallas, Texas 75216
University of California at Los Angeles Health Science Center, Los Angeles, California 90093
University of Texas Southwestern Medical School, Dallas, Texas 75235
Find articles by Richardson, C. in: JCI | PubMed | Google Scholar
Published February 1, 1978 - More info
Amino acids and peptides release gastrin and stimulate gastric acid secretion. However, the relation between gastrin release and acid secretory response is unclear. An isotonic mixed amino acid solution (casein hydrolysate) was continuously infused into the stomach of eight healthy human subjects. Acid secretion, measured by in vivo intragastric titration, increased 12.8 meq/h over the response to intragastric infusion of isotonic saline. Plasma gastrin heptadecapeptide (G-17) concentration, measured by specific radioimmunoassay, increased 13 pmol/liter during intragastric amino acid infusion.
To determine whether this rise in plasma G-17 concentration could account for some or all of the acid secretory response, several doses of synthetic human G-17-I were infused intravenously into the same subjects. During i.v. G-17-I infusion, the stomach was continuously infused with isotonic saline. By graphically relating plasma G-17 concentration during i.v. G-17 infusion to concomitant acid secretion, it was determined that a 13-pmol/liter rise in plasma G-17 concentration could increase acid secretion 14.8 meq/h. Therefore, the rise in plasma G-17 concentration during intragastric amino acid infusion could have produced all of the observed acid secretory response. This suggests that gastrin heptadecapeptide is the major physiologic mediator of the human acid secretory response to meals containing mixed amino acids.