Effects of biliary and pancreatic juice diversion into the ileum on gastrointestinal motility and gut hormone secretion in conscious dogs

Sato, Manabu; Shibata, Chikashi; Kikuchi, Daisuke; Ikezawa, Fumie; Imoto, Hirofumi; Sasaki, Iwao

doi:10.1016/j.surg.2010.03.007

Cited by 13 publications

(9 citation statements)

References 19 publications

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“…The elevated GLP‐2 concentrations observed after duodenal transposition in rats are therefore likely to reflect the increased delivery of bile acids to the distal ileum, where L‐cells both occur at a higher density and express greater levels of the bile acid receptor. This is also in agreement with a recent paper that showed elevated PYY levels following biliary diversion to the ileum in dogs (Sato et al ., 2010). Indeed, the improvement of glucose tolerance and elevated GLP‐1 levels that have been observed to follow gastric bypass surgery in obese patients, along with the recently reported increased crypt cell proliferation and elevated GLP‐2 levels in rat models of gastric bypass (le Roux et al ., 2010), may be linked to the increased delivery of bile acids to distal gut regions, as well as to the conversion by colonic bacteria of primary to secondary bile acids which have increased potency on GPBA (Kawamata et al ., 2003).…”

Section: Discussionsupporting

confidence: 94%

Molecular mechanisms underlying bile acid‐stimulated glucagon‐like peptide‐1 secretion

Parker

Wallis

Roux

et al. 2011

British J Pharmacology

201

172

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BACKGROUND AND PURPOSEThe glucagon-like peptides GLP-1 and GLP-2 are secreted from enteroendocrine L-cells following nutrient ingestion. Drugs that increase activity of the GLP-1 axis are highly successful therapies for type 2 diabetes, and boosting L-cell secretion is a potential strategy for future diabetes treatment. The aim of the present study was to further our understanding of the bile acid receptor GPBA (TGR5), an L-cell target currently under therapeutic exploration. EXPERIMENTAL APPROACHGLUTag cells and mixed primary murine intestinal cultures were exposed to bile acids and a specific agonist, GPBAR-A. Secretion was measured using hormone assays and intracellular calcium and cAMP responses were monitored using real-time imaging techniques. KEY RESULTSBile acid-triggered GLP-1 secretion from GLUTag cells was GPBA-dependent, as demonstrated by its abolition following tgr5 siRNA transfection. Bile acids and GPBAR-A increased GLP-1 secretion from intestinal cultures, with evidence for synergy between the effects of glucose and GPBA activation. Elevation of cAMP was observed following GPBA activation in individual GLUTag cells. Direct calcium responses to GPBAR-A were small, but in the presence of the agonist, a subpopulation of cells that was previously poorly glucose-responsive exhibited robust glucose responses. In vivo, increased delivery of bile to more distal regions of the ileum augmented L-cell stimulation. CONCLUSIONS AND IMPLICATIONSGPBA signalling in L-cells involves rapid elevation of cAMP, and enhanced calcium and secretory responses to glucose. Modulation of this receptor therapeutically may be an attractive strategy to enhance GLP-1 secretion and achieve better glycaemic control in diabetic patients. AbbreviationsCDCA, chenodeoxycholic acid; CFP, cyan fluorescent protein; DCA, deoxycholic acid; Epac, cAMP-guanine nucleotide exchange factors; fsk/IBMX, forskolin plus 3-isobutyl-1-methylxanthine; GLP-1, -2, glucagon-like peptide-1, -2; KATP, ATP-sensitive potassium channel; LCA, lithocholic acid; PYY, peptide YY; TLCA, taurolithocholic acid; YFP, yellow fluorescent protein BJP British Journal of Pharmacology

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Section: Discussionsupporting

confidence: 94%

Molecular mechanisms underlying bile acid‐stimulated glucagon‐like peptide‐1 secretion

Parker

Wallis

Roux

et al. 2011

British J Pharmacology

201

172

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“…In the same study, it was also highlighted that delivery of bile acids to the colon, where L cells are believed to be present at a higher density (204,205,206) and express greater levels of TGR5, results in enhanced L cell secretion (105,197,198,203). Indeed, Sato et al (207) has recently demonstrated, in a study in dogs, that biliary diversion to the ileum increases the secretion of the L cell product PYY. Recently, the results from several human studies have supported a role for bile-induced secretion of GLP1 (13, 61,62,63,64).…”

Section: Tgr5-dependent Mechanismsmentioning

confidence: 92%

MECHANISMS IN ENDOCRINOLOGY: Bile acid sequestrants in type 2 diabetes: potential effects on GLP1 secretion

Sonne

Hansen

Knop

2014

European Journal of Endocrinology

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Bile acid sequestrants have been used for decades for the treatment of hypercholesterolaemia. Sequestering of bile acids in the intestinal lumen interrupts enterohepatic recirculation of bile acids, which initiate feedback mechanisms on the conversion of cholesterol into bile acids in the liver, thereby lowering cholesterol concentrations in the circulation. In the early 1990s, it was observed that bile acid sequestrants improved glycaemic control in patients with type 2 diabetes. Subsequently, several studies confirmed the finding and recently -despite elusive mechanisms of action -bile acid sequestrants have been approved in the USA for the treatment of type 2 diabetes. Nowadays, bile acids are no longer labelled as simple detergents necessary for lipid digestion and absorption, but are increasingly recognised as metabolic regulators. They are potent hormones, work as signalling molecules on nuclear receptors and G protein-coupled receptors and trigger a myriad of signalling pathways in many target organs. The most described and well-known receptors activated by bile acids are the farnesoid X receptor (nuclear receptor) and the G protein-coupled cell membrane receptor TGR5. Besides controlling bile acid metabolism, these receptors are implicated in lipid, glucose and energy metabolism. Interestingly, activation of TGR5 on enteroendocrine L cells has been suggested to affect secretion of incretin hormones, particularly glucagon-like peptide 1 (GLP1 (GCG)). This review discusses the role of bile acid sequestrants in the treatment of type 2 diabetes, the possible mechanism of action and the role of bile acid-induced secretion of GLP1 via activation of TGR5.

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“…Sato et al . reported that cholecystoileostomy with a ligated common bile duct seemed to inhibit inter‐digestive and postprandial upper gut contractions in association with an increase in levels of plasma Peptide YY (PYY) . That report did not indicate a correlation between cholecystoileostomy and increased GLP‐1.…”

Section: Discussionmentioning

confidence: 99%

Duodenal–jejunal bypass improves diabetes and liver steatosis via enhanced glucagon‐like peptide‐1 elicited by bile acids

Kashihara

Shimada

Kurita

et al. 2015

J of Gastro and Hepatol

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Effects of biliary and pancreatic juice diversion into the ileum on gastrointestinal motility and gut hormone secretion in conscious dogs

Cited by 13 publications

References 19 publications

Molecular mechanisms underlying bile acid‐stimulated glucagon‐like peptide‐1 secretion

Molecular mechanisms underlying bile acid‐stimulated glucagon‐like peptide‐1 secretion

MECHANISMS IN ENDOCRINOLOGY: Bile acid sequestrants in type 2 diabetes: potential effects on GLP1 secretion

Duodenal–jejunal bypass improves diabetes and liver steatosis via enhanced glucagon‐like peptide‐1 elicited by bile acids

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