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Circulating somatostatin‐28 is not a physiologic regulator of gastric acid production in man
Author(s) -
HILDEBRAND P.,
ENSINCK J. W.,
BUETTIKER J.,
DREWE J.,
BURCKHARDT B.,
GYR K.,
BEGLINGER C.
Publication year - 1994
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1994.tb02059.x
Subject(s) - postprandial , gastric acid , medicine , somatostatin , endocrinology , pentagastrin , secretion , basal (medicine) , chemistry , radioimmunoassay , sham feeding , biology , insulin
. Studies were designed to establish the acid inhibitory potency and plasma kinetics of somatostatin‐28 (S‐28) in humans and to determine whether the amount of S‐28 released into the circulation after a meal is sufficient to regulate gastric acid secretion. A liquid meal induced a significant increase of S‐28 ( P < 0·01) whereas S‐14 levels did not change. Postprandial S‐28 concentrations were then mimicked by exogenous infusions and tested on basal and pentagastrin‐stimulated gastric acid secretion. Expressed in terms of circulating plasma concentrations measured by specific radioimmunoassays, S‐14 was 10 times more potent than S‐28 in inhibiting gastric acid production. The plasma half‐life of S‐28 (1·86 min) was longer than that of S‐14 (1·00 min) due to a slower plasma clearance rate. S‐28 did neither affect basal and stimulated gastric acid secretion nor postprandial intragastric acidity. These studies suggest that postprandial plasma concentrations of S‐28 are unlikely to regulate gastric acid secretion in man. They also show that S‐28 is several times less potent than S‐14 with respect to inhibition of gastric acid output.