The bile acid-sequestering resin sevelamer eliminates the acute GLP-1 stimulatory effect of endogenously released bile acids in patients with type 2 diabetes

Diabetes Obes Metab. 2018 Feb;20(2):362-369. doi: 10.1111/dom.13080. Epub 2017 Sep 24.

Abstract

Aims: Discovery of the specific bile acid receptors farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) in enteroendocrine L cells has prompted research focusing on the impact of bile acids on glucagon-like peptide-1 (GLP-1) secretion and glucose metabolism. The aim of the present study was to assess the GLP-1 secretory and gluco-metabolic effects of endogenously released bile, with and without concomitant administration of the bile acid-sequestering resin, sevelamer, in patients with type 2 diabetes.

Materials and methods: We performed a randomized, placebo-controlled, double-blinded cross-over study including 15 metformin-treated patients with type 2 diabetes. During 4 experimental study days, either sevelamer 3200 mg or placebo in combination with intravenous infusion of cholecystokinin (CCK) (0.4 pmol sulfated CCK-8/kg/min) or saline was administered in randomized order. The primary endpoint was plasma GLP-1 excursions as measured by incremental area under the curve. Secondary endpoints included plasma responses of glucose, triglycerides, insulin, CCK, fibroblast growth factor-19 and 7α-hydroxy-4-cholesten-3-one (C4). In addition, gallbladder dynamics, gastric emptying, resting energy expenditure, appetite and ad libitum food intake were assessed.

Results: CCK-mediated gallbladder emptying was demonstrated to elicit a significant induction of GLP-1 secretion compared to saline, whereas concomitant single-dose administration of the bile acid sequestrant sevelamer was shown to eliminate the acute bile acid-induced increase in plasma GLP-1 excursions.

Conclusions: Single-dose administration of sevelamer eliminated bile acid-mediated GLP-1 secretion in patients with type 2 diabetes, which could be explained by reduced bile acid stimulation of the basolaterally localized TGR5 on enteroendocrine L cells.

Keywords: bile acid sequestrant; bile acids; cholecystokinin; glucagon-like peptide-1; sevelamer.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Bile Acids and Salts / antagonists & inhibitors*
  • Bile Acids and Salts / metabolism
  • Chelating Agents / therapeutic use*
  • Cholagogues and Choleretics / administration & dosage
  • Cholagogues and Choleretics / pharmacology
  • Cross-Over Studies
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / metabolism
  • Double-Blind Method
  • Drug Therapy, Combination
  • Enteroendocrine Cells / drug effects*
  • Enteroendocrine Cells / metabolism
  • Female
  • Gallbladder Emptying / drug effects
  • Gastric Emptying / drug effects
  • Gastrointestinal Agents / therapeutic use*
  • Glucagon-Like Peptide 1 / antagonists & inhibitors*
  • Glucagon-Like Peptide 1 / blood
  • Glucagon-Like Peptide 1 / metabolism
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Infusions, Intravenous
  • Male
  • Metformin / therapeutic use
  • Middle Aged
  • Sevelamer / therapeutic use*
  • Sincalide / administration & dosage
  • Sincalide / pharmacology

Substances

  • Bile Acids and Salts
  • Chelating Agents
  • Cholagogues and Choleretics
  • Gastrointestinal Agents
  • Hypoglycemic Agents
  • Glucagon-Like Peptide 1
  • Metformin
  • Sevelamer
  • Sincalide