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Am J Physiol Gastrointest Liver Physiol 258: G358-G364, 1990;
0193-1857/90 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 258, Issue 3 358-G364, Copyright © 1990 by American Physiological Society


ARTICLES

Somatostatin regulates duodenal cholecystokinin and somatostatin messenger RNA

S. Kanayama and R. A. Liddle
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.

The gastrointestinal peptides, cholecystokinin (CCK) and somatostatin, are produced by discrete endocrine cells in the mucosa of the small intestine. Although somatostatin may inhibit CCK secretion, the mechanism by which this occurs is unknown. The present study was designed to determine the effect of somatostatin on intestinal CCK and somatostatin mRNA levels. Rats, prepared with indwelling intraduodenal and jugular cannulas, were first fed an elemental diet that did not stimulate CCK release. Next, as a means of stimulating CCK secretion, soybean trypsin inhibitor was added to the diet and perfused intraduodenally at 50 mg/h for 24 h. Trypsin inhibitor caused an 11-fold increase in plasma CCK levels and a 2.4-fold increase in duodenal CCK mRNA levels. Simultaneous intravenous infusion of somatostatin-14 (1-100 micrograms.kg-1.h-1) reduced trypsin inhibitor-stimulated CCK levels by 50% and lowered trypsin inhibitor-stimulated CCK mRNA levels by 58%. Somatostatin infusion also reduced intestinal somatostatin mRNA levels stimulated by trypsin inhibitor but did not affect basal somatostatin mRNA levels. Duodenal CCK and somatostatin peptide concentrations did not change under any of the experimental conditions. These studies demonstrate that somatostatin reduces duodenal CCK mRNA levels stimulated by diet and suggest that somatostatin itself inhibits duodenal somatostatin gene expression.


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Am. J. Physiol. Gastrointest. Liver Physiol.Home page
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Diazepam-binding inhibitor33-50 elicits Ca2+ oscillation and CCK secretion in STC-1 cells via L-type Ca2+ channels
Am J Physiol Gastrointest Liver Physiol, March 1, 1999; 276(3): G694 - G702.
[Abstract] [Full Text] [PDF]




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