Research

Hormonal

Flavin Monooxygenase 3 (FMO3) activity promotes dyslipidemia and atherosclerosis by regulating hepatic lipogenesis, gluconeogenesis, and impairing transintestinal cholesterol export (TICE).

FMO3 is an enzyme that not only processes nutrients into TMAO but also directly regulates how your liver handles fats and sugars. High FMO3 activity is linked to worse lipid profiles and increased atherosclerosis risk. This regulation happens through complex gene signaling (FXR, LXR, PPARa) that controls cholesterol export and fat storage.

GoodSupportsHIGH confidence
Furthermore, FMO3 may promote dyslipidemia by regulating multiple genes involved in hepatic lipogenesis and gluconeogenesis. FMO3 also impairs multiple aspects of cholesterol homeostasis, including transintestinal cholesterol export and macrophage-specific RCT.
Marina Canyelles et al. · International Journal of Molecular Sciences · 2018

Why this rating

Strong evidence from mouse models (knockdown studies) showing reduced atherosclerosis and improved lipid profiles when FMO3 is inhibited.

Source

Trimethylamine N-Oxide: A Link among Diet, Gut Microbiota, Gene Regulation of Liver and Intestine Cholesterol Homeostasis and HDL Function

Marina Canyelles et al. · International Journal of Molecular Sciences · 2018

DOI 10.3390/ijms19103228

narrative_reviewCited 188×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →