MicroRNA-29a Compromises Hepatic Adiposis and Gut Dysbiosis in High Fat Diet-Fed Mice via Downregulating Inflammation

Mol Nutr Food Res. 2023 Jul;67(13):e2200348. doi: 10.1002/mnfr.202200348. Epub 2023 May 15.

Abstract

Scope: miR-29a expression patterns influence numerous physiological phenomena. Of note, upregulation of miR-29a ameliorates high-fat diet (HFD)-induced liver dysfunctions in mice. However, the miR-29a effect on gut microbiome composition and HFD-induced gut microbiota changes during metabolic disturbances remains unclear. The study provides compelling evidence for the protective role of miR-29a in gut barrier dysfunction and steatohepatitis.

Methods and results: miR-29a overexpressed mice (miR-29aTg) are bred to characterize intestinal, serum biochemical, and fecal microbiota profiling features compared to wild-type mice (WT). Mice are fed an HFD for 8 months to induce steatohepatitis, and intestinal dysfunction is determined via histopathological analysis. miR-29aTg has better lipid metabolism capability that decreases total cholesterol and triglyceride levels in serum than WT of the same age. The study further demonstrates that miR-29aTg contributes to intestinal integrity by maintaining periodic acid Schiff positive cell numbers and diversity of fecal microorganisms. HFD-induced bacterial community disturbance and steatohepatitis result in more severe WT than miR-29aTg. Gut microorganism profiling reveals Lactobacillus, Ruminiclostridium_9, and Lachnoclostridium enrichment in miR-29aTg and significantly decreases interleukin-6 expression in the liver and intestinal tract.

Conclusion: This study provides new evidence that sheds light on the host genetic background of miR-29a, which protects against steatohepatitis and other intestinal disorders.

Keywords: gut microbiota; high-fat diet; inflammation; miR-29a; steatohepatitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects
  • Dysbiosis
  • Fatty Liver* / genetics
  • Fatty Liver* / metabolism
  • Inflammation
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Non-alcoholic Fatty Liver Disease / etiology
  • Non-alcoholic Fatty Liver Disease / metabolism

Substances

  • MicroRNAs
  • MIRN29a microRNA, mouse