Yourlocation: Home > News > Investigate whether the infusion of chenodeoxycholic acid (CDCA) in the duodenum can stimulate the secretion of FGF and intestinal peptide
Bile acids (BAs) are activated by TGR5 and subsequently released by intestinal peptide, as well as Fannahil X receptor activation and secondary fibroblast growth factor release (FGFs), involved in glycemic control. In order to investigate whether the infusion of chenodeoxycholic acid (CDCA) in the duodenum can stimulate the secretion of FGF and intestinal peptide, it has a positive effect on blood glucose homeostasis. Professor Christoph Beglinger and his team from the University Hospital in Basel, Switzerland, conducted a study that found that BAs play a role in glycemic control. The results of the study were published online at the journal end of the journal endoscopy on June 20, 2013.
The study was a randomized, double-blind, placebo-controlled, cross-trial, including 12 patients receiving saline, CDCA (5 or 15 mmol / l) and fatty acids (sodium oleate) (alone or with 5 mmol / l CDCA) Infants who are infused with both ends of the intestine. Oral glucose tolerance test (OGTT) was performed after 60 minutes. (GLP-1), casein, cholecystokinin (CCK), total Bas, FGF19, FGF21, C-peptide, insulin, blood glucose and glucagon.
The results of this study show that high concentrations of CDCA induce a significant increase in GLP-1 and CCK secretion (P = 0.016 and P = 0.011) in the first 60 minutes, however, for plasma C-peptide, insulin and blood glucose influences. A decrease in C-peptide and insulin release (P = 0.013 and P = 0.011) was observed after OGTT in 15 mmol / l CDCA group. Plasma BA and FGF19 levels were significantly increased after transfusion of CDCA (P = 0.001 and P <0.001).
The study found that chenodeoxycholic acid(CDCA) regulates GLP-1 and CCK secretion; the effect is weak and does not affect blood glucose levels. Significant increase in plasma BAs and a decrease in insulin release after OGTT suggest that BAs play a role in glycemic control and are independent of the insulin bolus axis and suggest that it involves the Fenixia X receptor activation pathway.

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