Document Detail

Cholecystokinin type A receptors mediate intestinal fat-induced inhibition of acid secretion through somatostatin-14 in dogs.
MedLine Citation:
PMID:  7910794     Owner:  NLM     Status:  MEDLINE    
This study was designed to examine whether one or both principle molecular forms of somatostatin (SLI), somatostatin-28 (S-28) and somatostatin-14 (S-14), mediate inhibition of stimulated gastric acid by intestinal fat and to determine whether the mode of action includes activation of type A cholecystokinin (CCK) receptors in conscious dogs. SLI molecular forms were separated by gel filtration chromatography after extraction of acidified plasma on octadecyl silyl cartridges and quantified by RIA. Basal plasma levels of S-28 and S-14 were 4.1 +/- 0.6 and 3.6 +/- 0.3 fmol/ml, respectively. Intraduodenal perfusion with a 10% fat emulsion increased plasma S-28 by 6.3 +/- 1.2 fmol/ml (P < 0.01) and S-14 by 17.8 +/- 2.6 fmol/ml (P < 0.001), and suppressed by 76 +/- 3% (P < 0.001) gastrin (150 pmol/kg.h)-stimulated gastric acid. Blockade of type A CCK receptors with MK-329 (75 micrograms/kg, i.v.) abolished S-28 and S-14 responses (both P < 0.001) and completely reversed the inhibitory effect of gastric acid produced by intraduodenal fat. Intravenous infusions of S-14 dose-dependently inhibited gastrin-stimulated secretion with an estimated 50% inhibitory dose of 125 pmol/kg.h that achieved an incremental plasma S-14 rise of 40 +/- 2 fmol/ml; infusions of S-28 at 30 pmol/kg.h increased plasma S-28 by 47 +/- 3 fmol/ml without altering acid output. The SLI antagonist cyclo-[7-aminoheptanoly-Phe-D-Trp-Lys-Thr(BZL)] (CyCam) reversed by 89 +/- 4% (P < 0.001) exogenous S-14-induced inhibition of gastrin-stimulated acid secretion, but did not influence gastric acid output after the infusion of S-28. CyCam also reversed by 139 +/- 9% (P < 0.001) the early phase of fat-induced acid inhibition; in the late phase, CyCam treatment was associated with a further 2-fold elevation of plasma peptide-YY (PYY) to 102 +/- 6 fmol/ml (P < 0.001) and a 75 +/- 5% suppression of gastric acid. Simulation of this plasma PYY increment with infusions of PYY at 50 pmol/kg.h inhibited by 44 +/- 5% gastrin-stimulated acid secretion. These results indicate that in conscious dogs, endogenous CCK mediation of intraintestinal fat-induced inhibition of stimulated acid secretion occurs in part through CCK type A receptor activation of S-14 secretion. Modulation of gastric acid by S-14 includes both inhibition and attenuation of further suppression via counterregulation of PYY secretion.
L Fung; S Pokol-Daniel; G R Greenberg
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Endocrinology     Volume:  134     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1994 Jun 
Date Detail:
Created Date:  1994-06-28     Completed Date:  1994-06-28     Revised Date:  2008-08-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2376-82     Citation Subset:  AIM; IM    
Department of Medicine, University of Toronto, Ontario, Canada.
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MeSH Terms
Amino Acid Sequence
Duodenum / drug effects
Fats / pharmacology*
Gastric Acid / secretion*
Intestines / drug effects*
Molecular Sequence Data
Peptide YY
Peptides / antagonists & inhibitors,  blood
Receptors, Cholecystokinin / physiology*
Somatostatin / analogs & derivatives,  pharmacology*
Reg. No./Substance:
0/Fats; 0/Peptides; 0/Receptors, Cholecystokinin; 0/somatostatin-like peptides; 106388-42-5/Peptide YY; 51110-01-1/Somatostatin; 75037-27-3/Somatostatin-28; 84211-54-1/cyclo(7-aminoheptanoylphenylalanyl-tryptophyl-lysyl-benzylthreonyl)

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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