Research
Hormonal
Gut microbiota-derived Trimethylamine-N-oxide (TMAO) and secondary bile acids modulate NAFLD progression through regulation of bile acid metabolism, insulin resistance, and hepatic inflammation.
The conversion of dietary nutrients (choline, carnitine) by gut bacteria into TMA, and subsequently TMAO in the liver, influences bile acid metabolism and insulin resistance. Managing dietary intake of these precursors and supporting healthy bile acid signaling (via secondary bile acids) may help manage NAFLD.
ModerateQualifiesMEDIUM confidence
Gut microbiota-mediated TMA/FMO3/TMAO pathway modulates insulin resistance, glycolipid metabolism, cholesterol homeostasis, and hepatic inflammation, thereby affecting hepatic triglyceride accumulation and liver steatosis.
Why this rating
Review of mechanistic studies; clinical biomarker status is noted but causal intervention data is limited.
Source
Gut Microbiota-Derived Components and Metabolites in the Progression of Non-Alcoholic Fatty Liver Disease (NAFLD)
Yun Ji et al. · Nutrients · 2019
DOI 10.3390/nu11081712
narrative_reviewCited 225×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Gut microbiota-derived lipopolysaccharides (LPS) and peptidoglycan (PGN) promote NAFLD progression by activating hepatic Toll-like receptors (TLR4, TLR2, NOD1/2), triggering inflammatory cytokine release and steatosis.Moderate
- Gut microbiota-derived metabolites, specifically Short-Chain Fatty Acids (SCFAs) like butyrate, acetate, and propionate, ameliorate NAFLD by inhibiting histone deacetylases (HDACs) and activating G-protein coupled receptors (GPR41, GPR43).Moderate
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