Inhibition of Hepatic Bile Acid Uptake by Myrcludex B Promotes Glucagon-Like Peptide-1 Release and Reduces Obesity

Cell Mol Gastroenterol Hepatol. 2020;10(3):451-466. doi: 10.1016/j.jcmgh.2020.04.009. Epub 2020 Apr 21.

Abstract

Background & aims: Bile acids are important metabolic signaling molecules. Bile acid receptor activation promotes body weight loss and improves glycemic control. The incretin hormone GLP-1 and thyroid hormone activation of T4 to T3 have been suggested as important contributors. Here, we identify the hepatic bile acid uptake transporter Na+ taurocholate co-transporting polypeptide (NTCP) as target to prolong postprandial bile acid signaling.

Methods: Organic anion transporting polypeptide (OATP)1a/1b KO mice with or without reconstitution with human OATP1B1 in the liver were treated with the NTCP inhibitor Myrcludex B for 3.5 weeks after the onset of obesity induced by high fat diet-feeding. Furthermore, radiolabeled T4 was injected to determine the role of NTCP and OATPs in thyroid hormone clearance from plasma.

Results: Inhibition of NTCP by Myrcludex B in obese Oatp1a/1b KO mice inhibited hepatic clearance of bile acids from portal and systemic blood, stimulated GLP-1 secretion, reduced body weight, and decreased (hepatic) adiposity. NTCP inhibition did not affect hepatic T4 uptake nor lead to increased thyroid hormone activation. Myrcludex B treatment increased fecal energy output, explaining body weight reductions amongst unaltered food intake and energy expenditure.

Conclusions: Pharmacologically targeting hepatic bile acid uptake to increase bile acid signaling is a novel approach to treat obesity and induce GLP1- secretion.

Keywords: Myrcludex B; NTCP; OATP; Obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bile Acids and Salts / metabolism*
  • Diet, High-Fat / adverse effects
  • Disease Models, Animal
  • Female
  • Glucagon-Like Peptide 1 / metabolism*
  • Humans
  • Lipopeptides / pharmacology*
  • Lipopeptides / therapeutic use
  • Liver / drug effects
  • Liver / metabolism
  • Liver-Specific Organic Anion Transporter 1 / genetics
  • Male
  • Mice
  • Mice, Transgenic
  • Obesity / drug therapy*
  • Obesity / etiology
  • Organic Anion Transporters, Sodium-Dependent / antagonists & inhibitors*
  • Organic Cation Transport Proteins / genetics
  • Symporters / antagonists & inhibitors*

Substances

  • Bile Acids and Salts
  • Lipopeptides
  • Liver-Specific Organic Anion Transporter 1
  • Oatp1a1 protein, mouse
  • Organic Anion Transporters, Sodium-Dependent
  • Organic Cation Transport Proteins
  • SLCO1B1 protein, human
  • Symporters
  • myrcludex-B
  • sodium-bile acid cotransporter
  • Glucagon-Like Peptide 1