The Black Box Orchestra of Gut Bacteria and Bile Acids: Who Is the Conductor?

Int J Mol Sci. 2023 Jan 17;24(3):1816. doi: 10.3390/ijms24031816.

Abstract

Over the past decades the potential role of the gut microbiome and bile acids in type 2 diabetes mellitus (T2DM) has been revealed, with a special reference to low bacterial alpha diversity. Certain bile acid effects on gut bacteria concern cytotoxicity, or in the case of the microbiome, bacteriotoxicity. Reciprocally, the gut microbiome plays a key role in regulating the bile acid pool by influencing the conversion and (de)conjugation of primary bile acids into secondary bile acids. Three main groups of bacterial enzymes responsible for the conversion of bile acids are bile salt hydrolases (BSHs), hydroxysteroid dehydrogenases (HSDHs) and enzymes encoded in the bile acid inducible (Bai) operon genes. Interventions such as probiotics, antibiotics and fecal microbiome transplantation can impact bile acids levels. Further evidence of the reciprocal interaction between gut microbiota and bile acids comes from a multitude of nutritional interventions including macronutrients, fibers, prebiotics, specific individual products or diets. Finally, anatomical changes after bariatric surgery are important because of their metabolic effects. The heterogeneity of studies, diseases, bacterial species and (epi)genetic influences such as nutrition may challenge establishing specific and detailed interventions that aim to tackle the gut microbiome and bile acids.

Keywords: bile acids; enterohepatic circulation; gut microbiome; nutrition; prebiotics; probiotics; type 2 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • Bacteria / metabolism
  • Bile Acids and Salts / metabolism
  • Diabetes Mellitus, Type 2*
  • Gastrointestinal Microbiome* / physiology
  • Humans
  • Microbiota*

Substances

  • Bile Acids and Salts

Grants and funding

M.N. is supported by a personal ZONMW VICI grant 2020 (09150182010020). M.S. is funded by the ZonMW and Dutch Diabetes foundation (Grant No. 95105011).