Incretin secretion stimulated by ursodeoxycholic acid in healthy subjects

Murakami, Masanori; Une, Naoko; Nishizawa, Maiko; Suzuki, Sayaka; Ito, Hideki; Horiuchi, Toshiyuki

doi:10.1186/2193-1801-2-20

Cited by 40 publications

(28 citation statements)

References 24 publications

(28 reference statements)

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“…Already in the 1980s, there were reports of bileinduced secretion of GIP (54,55) and glucagon-like reactive materials in dogs (46,57,58,59) and insulin (60). Since then, various groups have reported similar findings (13, 61,62,63,64).…”

Section: Glp1 Secretionsupporting

confidence: 66%

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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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Section: Glp1 Secretionsupporting

confidence: 66%

“…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: 99%

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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“…In our study, the postprandial concentration of GLP-1 was significantly lower at 60 min in women with ICP; however, we observed that treatment with UDCA partially reversed this deficit. In support of this, a recent longitudinal study reported an increased GLP-1 release and a fall in plasma glucose levels following initiation of UDCA therapy (39).…”

Section: Bile Acids and Glucose And Lipid Homeostasissupporting

confidence: 54%

The Metabolic Profile of Intrahepatic Cholestasis of Pregnancy Is Associated With Impaired Glucose Tolerance, Dyslipidemia, and Increased Fetal Growth

et al. 2014

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OBJECTIVEQuantification of changes in glucose and lipid concentrations in women with intrahepatic cholestasis of pregnancy (ICP) and uncomplicated pregnancy and study of their influence on fetal growth. RESEARCH DESIGN AND METHODSA prospective study comparing metabolic outcomes in cholestastic and uncomplicated singleton pregnancies was undertaken at two university hospitals in the U.K. and U.S. from 2011-2014. A total of 26 women with ICP and 27 control pregnancies with no prior history of gestational diabetes mellitus were recruited from outpatient antenatal services and followed until delivery. Alterations in glucose, incretins, cholesterol, and triglycerides were studied using a continuous glucose monitoring (CGM) system and/or a standard glucose tolerance test (GTT) in conjunction with GLP-1 and a fasting lipid profile. Fetal growth was quantified using adjusted birth centiles. RESULTSMaternal blood glucose concentrations were significantly increased in ICP during ambulatory CGM (P < 0.005) and following a GTT (P < 0.005). ICP is characterized by increased fasting triglycerides (P < 0.005) and reduced HDL cholesterol (P < 0.005), similar to changes observed in metabolic syndrome. The offspring of mothers with ICP had significantly larger customized birth weight centiles, adjusted for ethnicity, sex, and gestational age (P < 0.005). CONCLUSIONSICP is associated with impaired glucose tolerance, dyslipidemia, and increased fetal growth. These findings may have implications regarding the future health of affected offspring.

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“…The potential mechanism for this increase in GLP-1 may be explained by an increase in bile acids, which may specifically increase GLP-1 concentration. Experimental administration of bile acids was shown to stimulate GLP-1 secretion via L-cells and consequently increase GLP-1 concentration during fasting and postprandial states in healthy humans (Meyer-Gerspach et al 2013;Murakami et al 2013;Wu et al 2013); however, the effect of D r a f t bile acids on GIP concentration remains unclear. Moreover, the intake of high-fat diet elevates fecal concentration of bile acids (Cummings et al 1978), suggesting a perfusion of a high concentration of bile acids into L-cells localized in the intestine after the intake of high-fat diet.…”

Section: Discussionmentioning

confidence: 99%

Short-term high-fat diet alters postprandial glucose metabolism and circulating vascular cell adhesion molecule-1 in healthy males

Numao

Kawano

Endo

et al. 2016

Appl. Physiol. Nutr. Metab.

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Short-term intake of a high-fat diet aggravates postprandial glucose metabolism; however, the dose-response relationship has not been investigated. We hypothesized that short-term intake of a eucaloric low-carbohydrate/high-fat diet (LCHF) would aggravate postprandial glucose metabolism and circulating adhesion molecules in healthy males. Seven healthy young males (mean ± SE; age: 26 ± 1 years) consumed either a eucaloric control diet (C, approximately 25% fats), a eucaloric intermediate-carbohydrate/intermediate-fat diet (ICIF, approximately 50% fats), or an LCHF (approximately 70% fats) for 3 days. An oral meal tolerance test (MTT) was performed after the 3-day dietary intervention. The concentrations of plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 (VCAM-1) were determined at rest and during MTT. The incremental area under the curve (iAUC) of plasma glucose concentration during MTT was significantly higher in LCHF than in C (P = 0.009). The first-phase insulin secretion indexes were significantly lower in LCHF than in C (P = 0.04). Moreover, the iAUC of GLP-1 and VCAM-1 concentrations was significantly higher in LCHF than in C (P = 0.014 and P = 0.04, respectively). The metabolites from ICIF and C were not significantly different. In conclusion, short-term intake of eucaloric diet containing a high percentage of fats in healthy males excessively increased postprandial glucose and VCAM-1 concentrations and attenuated first-phase insulin release.

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Incretin secretion stimulated by ursodeoxycholic acid in healthy subjects

Cited by 40 publications

References 24 publications

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

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

The Metabolic Profile of Intrahepatic Cholestasis of Pregnancy Is Associated With Impaired Glucose Tolerance, Dyslipidemia, and Increased Fetal Growth

Short-term high-fat diet alters postprandial glucose metabolism and circulating vascular cell adhesion molecule-1 in healthy males

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