Published online May 28, 2019. doi: 10.3748/wjg.v25.i20.2450
Peer-review started: March 28, 2019
First decision: April 11, 2019
Revised: May 7, 2019
Accepted: May 8, 2019
Article in press: May 8, 2019
Published online: May 28, 2019
Processing time: 61 Days and 20.4 Hours
The gut microbial metabolites have been shown to be mediators in the gut-liver axis and play important role in non-alcoholic fatty liver disease. Trimethylamine N-oxide (TMAO) is a gut microbial metabolite derived from dietary choline and L-carnitine and is implied to be involved in the pathogenesis of cardiovascular disease.
Although the gut microbiota has long been found to play important roles in maintaining health, its function and regulation pathways are largely unknown. The gut microbial metabolites are considered to mediate the interaction between the gut commensal bacteria and the host. Exploring the function of gut microbial metabolites may help develop novel therapeutic approaches.
The main objective of the present study was to explore the function of TMAO in the progression of NASH and identify the targets and mechanisms underlying the effect of TMAO.
A rat model of NASH was induced by high-fat high-cholesterol (HFHC) diet feeding for 16 wk. TMAO was orally administrated daily for 8 wk. Histological analysis was performed to evaluate the effect of TMAO on steatohepatitis. Hepatic and serum lipid profiles were measured. Endoplasmic reticulum (ER) stress-related pathways were detected by Western blot and expression levels of intestinal cholesterol transporters were detected by qRT-PCR. 16s rDNA sequencing was preformed to examine the effect of TMAO on gut microbial profile.
Oral TMAO administration significantly improved the histological and serological alterations in HFHC diet-induced steatohepatitis. Hepatic ER stress and cell death were ameliorated by TMAO treatment. Both hepatic and serum levels of cholesterol were decreased by TMAO intervention. The expression levels of intestinal cholesterol transporters were altered by TMAO treatment. And the diversity of gut microbial profile was restored by TMAO treatment.
Under HFHC diet feeding conditions, TMAO inhibits intestinal cholesterol absorption, attenuates hepatic cholesterol overload, and alleviates ER stress mediated liver injury, which leads to the protective role of TMAO in HFHC diet-induced steatohepatitis in rats.
The minimal effective dose of TMAO treatment needs to be defined to avoid the potential harmful effect of TMAO on the cardiovascular system in future studies.