Indole-3-propionic acid inhibits gut dysbiosis and endotoxin leakage to attenuate steatohepatitis in rats

Exp Mol Med. 2019 Sep 10;51(9):1-14. doi: 10.1038/s12276-019-0304-5.

Abstract

Microbial metabolites have emerged as critical components that mediate the metabolic effects of the gut microbiota. Here, we show that indole-3-propionic acid (IPA), a tryptophan metabolite produced by gut bacteria, is a potent anti-non-alcoholic steatohepatitis (NASH) microbial metabolite. Here, we demonstrate that administration of IPA modulates the microbiota composition in the gut and inhibits microbial dysbiosis in rats fed a high-fat diet. IPA induces the expression of tight junction proteins, such as ZO-1 and Occludin, and maintains intestinal epithelium homeostasis, leading to a reduction in plasma endotoxin levels. Interestingly, IPA inhibits NF-κB signaling and reduces the levels of proinflammatory cytokines, such as TNFα, IL-1β, and IL-6, in response to endotoxin in macrophages to repress hepatic inflammation and liver injury. Moreover, IPA is sufficient to inhibit the expression of fibrogenic and collagen genes and attenuate diet-induced NASH phenotypes. The beneficial effects of IPA on the liver are likely mediated through inhibiting the production of endotoxin in the gut. These findings suggest a protective role of IPA in the control of metabolism and uncover the gut microbiome and liver cross-talk in regulating the intestinal microenvironment and liver pathology via a novel dietary nutrient metabolite. IPA may provide a new therapeutic strategy for treating NASH.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diet, High-Fat
  • Disease Models, Animal
  • Dysbiosis / drug therapy
  • Dysbiosis / genetics
  • Dysbiosis / metabolism
  • Dysbiosis / microbiology
  • Endotoxins / metabolism
  • Gastrointestinal Microbiome / drug effects*
  • Gastrointestinal Microbiome / genetics
  • Gene Expression Regulation / drug effects
  • Humans
  • Indoles / pharmacology
  • Interleukin-1beta
  • Interleukin-6 / genetics
  • Liver / drug effects
  • Liver / injuries
  • Liver / pathology
  • Macrophages / drug effects
  • NF-kappa B / genetics
  • Non-alcoholic Fatty Liver Disease / drug therapy*
  • Non-alcoholic Fatty Liver Disease / genetics
  • Non-alcoholic Fatty Liver Disease / metabolism
  • Non-alcoholic Fatty Liver Disease / microbiology
  • Occludin / genetics*
  • Propionates / pharmacology*
  • Rats
  • Tryptophan / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Zonula Occludens-1 Protein / genetics*

Substances

  • Endotoxins
  • Indoles
  • Interleukin-1beta
  • Interleukin-6
  • NF-kappa B
  • Occludin
  • Ocln protein, rat
  • Propionates
  • Tjp1 protein, rat
  • Tumor Necrosis Factor-alpha
  • Zonula Occludens-1 Protein
  • Tryptophan
  • propionic acid