Document Detail

Short-chain fatty acid sensing in rat duodenum.
MedLine Citation:
PMID:  25433076     Owner:  NLM     Status:  Publisher    
Intraduodenal fatty acids (FA), or bacterial overgrowth, which generate short-chain FAs (SCFAs), have been implicated in the generation of functional dyspepsia symptoms. We thus studied the mechanisms by which luminal SCFA perfusion affects duodenal HCO3 (-) secretion (DBS), a measure of mucosal neurohumoral activation. The free fatty acid receptor (FFAR) 1 (FFA1), which binds long-chain FA (LCFA), and SCFA receptors FFA2 and FFA3 were immunolocalised to duodenal enteroendocrine cells. FFA3 colocalised with glucagon-like peptide (GLP)-1, whereas FFA2 colocalised with 5-hydroxytryptamine (5-HT). Luminal perfusion of the SCFA acetate or propionate increased DBS, enhanced by dipeptidyl peptidase (DPP) IV inhibition, while increasing GLP-2 portal blood concentrations. Acetate-induced DBS was partially inhibited by monocarboxylate/HCO3 (-) exchanger inhibition without affecting GLP-2 release, implicating acetate absorption in the partial mediation of DBS. A selective FFA2 agonist dose-dependently increased DBS, unaffected by DPPIV inhibition or by cholecystokinin or 5-HT3 receptor antagonists, but was inhibited by atropine and a 5-HT4 antagonist. In contrast, a selective FFA1 agonist increased DBS accompanied by GLP-2 release, enhanced by DPPIV inhibition and inhibited by a GLP-2 receptor antagonist. Activation by of FFA1 by LCFA and presumably FFA3 by SCFA increased DBS via GLP-2 release, whereas FFA2 activation stimulated DBS via muscarinic and 5-HT4 receptor activation. SCFA/HCO3 (-) exchange also appears to be present in the duodenum. The presence of duodenal fatty acid sensing receptors that signal hormone release and possibly signal neural activation may be implicated in the pathogenesis of functional dyspepsia. This article is protected by copyright. All rights reserved.
Yasutada Akiba; Takuya Inoue; Izumi Kaji; Masaaki Higashiyama; Kazuyuki Narimatsu; Ken-Ichi Iwamoto; Masahiko Watanabe; Paul H Guth; Eli Engel; Atsukazu Kuwahara; Jonathan D Kaunitz
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-28
Journal Detail:
Title:  The Journal of physiology     Volume:  -     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-29     Completed Date:  -     Revised Date:  2014-11-30    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
This article is protected by copyright. All rights reserved.
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