Postprandial gut microbiota-driven choline metabolism links dietary cues to adipose tissue dysfunction

Adipocyte. 2018 Jan 2;7(1):49-56. doi: 10.1080/21623945.2017.1398295. Epub 2017 Nov 27.

Abstract

The human body is an integrated circuit between microbial symbionts and our Homo sapien genome, which communicate bi-directionally to maintain homeostasis within the human meta-organism. There is now strong evidence that microbes resident in the human intestine can directly contribute to the pathogenesis of obesity and associated cardiometabolic disorders. In fact, gut microbes represent a filter of our greatest environmental exposure - the foods we consume. It is now clear that we each experience a given meal differently, based on our unique gut microbial communities. Biologically active gut microbe-derived metabolites, such as short chain fatty acids, secondary bile acids, and trimethylamine-N-oxide (TMAO), are now uniquely recognized as contributors to obesity and related cardiometabolic disorders. However, mechanistic insights into how microbe-derived metabolites promote obesity are largely unknown. Recent work has demonstrated that the meta-organismal production of the bacterial co-metabolite TMAO is linked to suppression of beiging of white adipose tissue in mice and humans. Furthermore, the TMAO pathway is becoming an increasingly attractive therapeutic target in obesity-associated diseases such as type 2 diabetes, kidney failure, and cardiovascular disease. In this commentary we discuss recent findings linking the TMAO pathway to obesity-associated disorders, and provide additional insights into potential mechanisms driving this microbe-host interaction.

Keywords: adipose; diabetes; microbiome; microbiota; nutrition; obesity; trimethylamine N-oxide.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology*
  • Animals
  • Choline / metabolism*
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / microbiology
  • Gastrointestinal Microbiome / physiology*
  • Humans
  • Postprandial Period

Substances

  • Choline