According to the findings of a retrospective cross-sectional study, plasma short-chain fatty acids (SCFAs) levels were elevated in people with non-alcoholic fatty liver disease (NAFLD) compared with those in healthy control, and plasma SCFAs were diminished in non-alcoholic steatohepatitis (NASH) and NAFLD-cirrhosis people compared with those in NAFLD people. Researchers aimed to determine the plasma levels of general SCFAs in both healthy subjects and patients with various stages of NAFLD.

By using gas chromatography, three major SCFAs—butyrate, propionate, and acetate —were examined. By using ELISA, the plasma TNF-alpha (TNF-α) concentration was calculated. In order to calculate the correlations between SCFAs, TNF-α, and disease development, one-way ANOVA, Spearman's correlation, and Pearson's correlation assessment were used. To investigate the predictive variables of circulated TNF-α, computation of multiple linear stepwise regression was done.

Nine healthy control (HC) subjects were included in the analysis along with 71 patients with NAFLD [including 27 people with NAFL, 20 people with non-alcoholic steatohepatitis (NASH), and 24 people with NAFLD-associated cirrhosis (NAFLD-cirrhosis)]. Plasma SCFAs were higher in NAFL people when compared to HC people, albeit this difference was not clinically meaningful.

Compared to HC people, plasma SCFAs were higher in NAFL people, albeit this difference was not statistically significant.

In contrast, most SCFAs were statistically lower in NASH or NAFLD-cirrhosis people than in NAFL people. In comparison to HC participants, the plasma SCFAs in people with NASH or NAFLD-cirrhosis were not considerably different. Significantly unfavorable associations between TNF-α and SCFAs were witnessed. Multiple linear stepwise regression model identified NAFLD advancement (regression coefficient [β] = 0.849) and fall of 3 SCFA concentrations (β = -0.189) as independent risk factors connected to higher peripheral TNF-α.

SCFAs in circulation may contribute to NAFLD pathophysiology by acting as inflammatory mediators and inhibitors. The concentrations of plasma SCFA may change as a result of the onset of NAFLD and may be related to TNF- α and disease's development, perhaps acting as a preventative measure. It is necessary to do additional mechanistic research, including examinations of the gastrointestinal microecology, signalling pathways, and TNF-α  related functions. Further investigation and validation are also required for the therapeutic addition of SCFAs for NASH and NAFLD-cirrhosis.