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Trimethylamine-N-Oxide Pathway: A Potential Target for the Treatment of MAFLD

Xun Li1, Jia Hong2, Yao Wang1

  • 1Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, China.

Frontiers in Molecular Biosciences
|October 18, 2021
PubMed

Insights

Trimethylamine-N-oxide (TMAO), a gut microbe metabolite, is linked to metabolic dysfunction-associated fatty liver disease (MAFLD). Dietary changes targeting TMAO may offer new strategies for MAFLD prevention and treatment.

Area of Science:

  • Metabolomics
  • Gastroenterology
  • Hepatology

Background:

  • Trimethylamine-N-oxide (TMAO) is a metabolite produced by gut microbiota.
  • TMAO is increasingly recognized as a potential risk factor for metabolic dysfunction-associated fatty liver disease (MAFLD).

Purpose of the Study:

  • To review the relationship between TMAO and MAFLD.
  • To summarize strategies for reducing TMAO levels for MAFLD prevention and treatment.

Main Methods:

  • Literature review focusing on TMAO metabolism and its role in MAFLD pathogenesis.
  • Analysis of dietary influences on TMAO production and circulation.
  • Examination of TMAO's impact on liver metabolic pathways.

Main Results:

  • High-nutrient diets rich in TMA precursors (red meat, eggs, fish) increase plasma TMAO.
  • Elevated TMAO promotes MAFLD development by affecting bile acid metabolism, unfolded protein response, and oxidative stress.
  • TMAO is synthesized in the liver from gut-derived trimethylamine (TMA) via hepatic flavin monooxygenases (FMOs).

Conclusions:

  • Circulating TMAO levels are associated with MAFLD development.
  • Intervention strategies aimed at reducing TMAO warrant further investigation for MAFLD management.
  • Targeting gut microbiota and dietary precursors may be beneficial for preventing and treating MAFLD.
Keywords:
FMO3MAFLD (metabolic associated fatty liver disease)TMA precursorTMAO (trimethylamine oxide)oxidative stresstrimethylamineunfolded protein response

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