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10.1053/j.gastro.2012.09.055 http://scihub22266oqcxt.onion/10.1053/j.gastro.2012.09.055 C6054127!6054127!23041323     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23041323&cmd=llinks): Failed to open stream: HTTP request failed! 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THE RECEPTOR TGR5 MEDIATES THE PROKINETIC ACTIONS OF INTESTINAL BILE ACIDS AND IS REQUIRED FOR NORMAL DEFECATION IN MICE |pdf=|usr=}}{{23041323}} gab.com Text THE RECEPTOR TGR5 MEDIATES THE PROKINETIC ACTIONS OF INTESTINAL BILE ACIDS AND IS REQUIRED FOR NORMAL DEFECATION IN MICE JO: Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=23041323 #FOAvip Background & Aims:: Abnormal delivery of bile acids (BAs) to the colon, due to disease or therapy, causes constipation or diarrhea by unknown mechanisms. The G protein-coupled BA receptor TGR5 (or GPBAR1) is expressed by enteric neurons and endocrine cells, which regulate motility and secretion. Methods:: We analyzed gastrointestinal and colon transit, and defecation frequency and water content, in wild-type, knockout and transgenic mice (trg5-wt, tgr5-ko and tgr5-tg, respectively). We analyzed colon tissues for contractility, peristalsis, and transmitter release. Results:: Deoxycholic acid inhibited contractility of colonic longitudinal muscle from tgr5-wt but not tgr5-ko mice. Application of deoxycholic acid, lithocholic acid, or oleanolic acid (a selective agonist of TGR5) to the mucosa of tgr5-wt mice caused oral contraction and caudal relaxation, indicating peristalsis. BAs stimulated release of the peristaltic transmitters 5-hydroxytryptamine and calcitonin gene-related peptide; antagonists of these transmitters suppressed BA-induced peristalsis, consistent with TGR5 localization to enterochromaffin cells and intrinsic primary afferent neurons. tgr5-ko mice did not undergo peristalsis or transmitter release in response to BAs. Mechanically induced peristalsis and transmitter release were not affected by deletion of tgr5. Whole-gut transit was 1.4-fold slower in tgr5-ko than tgr5-wt or tgr5-tg mice, whereas colonic transit was 2.2-fold faster in tgr5-tg mice. Defecation frequency was reduced 2.6-fold in tgr5-ko and increased 1.4-fold in tgr5-tg mice, compared to tgr5-wt mice. Water content in stool was lower (37%) in tgr5-ko than tgr5-tg (58%) or tgr5-wt mice (62%). Conclusions:: The receptor TGR5 mediates the effects of BAs on colonic motility; TGR5 deficiency causes constipation in mice. These findings might mediate the long-known laxative properties of BAs; TGR5 might be a therapeutic target for digestive diseases. Twit Text FOAVip THE RECEPTOR TGR5 MEDIATES THE PROKINETIC ACTIONS OF INTESTINAL BILE ACIDS AND IS REQUIRED FOR NORMAL DEFECATION IN MICE ????Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=23041323 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23041323 #FOAvip English Wikipedia <ref>{{Cite pmid|23041323}}</ref> THE RECEPTOR TGR5 MEDIATES THE PROKINETIC ACTIONS OF INTESTINAL BILE ACIDS AND IS REQUIRED FOR NORMAL DEFECATION IN MICE #MMPMID23041323 Alemi F; Poole DP; Chiu J; Schoonjans K; Cattaruzza F; Grider JR; Bunnett NW; Corvera CU Gastroenterology 2013[Jan]; 144 (1): 145-54 PMID23041323show ga Background & Aims:: Abnormal delivery of bile acids (BAs) to the colon, due to disease or therapy, causes constipation or diarrhea by unknown mechanisms. The G protein-coupled BA receptor TGR5 (or GPBAR1) is expressed by enteric neurons and endocrine cells, which regulate motility and secretion. Methods:: We analyzed gastrointestinal and colon transit, and defecation frequency and water content, in wild-type, knockout and transgenic mice (trg5-wt, tgr5-ko and tgr5-tg, respectively). We analyzed colon tissues for contractility, peristalsis, and transmitter release. Results:: Deoxycholic acid inhibited contractility of colonic longitudinal muscle from tgr5-wt but not tgr5-ko mice. Application of deoxycholic acid, lithocholic acid, or oleanolic acid (a selective agonist of TGR5) to the mucosa of tgr5-wt mice caused oral contraction and caudal relaxation, indicating peristalsis. BAs stimulated release of the peristaltic transmitters 5-hydroxytryptamine and calcitonin gene-related peptide; antagonists of these transmitters suppressed BA-induced peristalsis, consistent with TGR5 localization to enterochromaffin cells and intrinsic primary afferent neurons. tgr5-ko mice did not undergo peristalsis or transmitter release in response to BAs. Mechanically induced peristalsis and transmitter release were not affected by deletion of tgr5. Whole-gut transit was 1.4-fold slower in tgr5-ko than tgr5-wt or tgr5-tg mice, whereas colonic transit was 2.2-fold faster in tgr5-tg mice. Defecation frequency was reduced 2.6-fold in tgr5-ko and increased 1.4-fold in tgr5-tg mice, compared to tgr5-wt mice. Water content in stool was lower (37%) in tgr5-ko than tgr5-tg (58%) or tgr5-wt mice (62%). Conclusions:: The receptor TGR5 mediates the effects of BAs on colonic motility; TGR5 deficiency causes constipation in mice. These findings might mediate the long-known laxative properties of BAs; TGR5 might be a therapeutic target for digestive diseases. äTHE RECEPTOR TGR5 MEDIATES THE PROKINETIC ACTIONS OF INTESTINAL BILE A(epmc).pdf DeepDyve Pubget Overpricing