Chambers ES, et al. - In adults with non-alcoholic fatty liver disease (NAFLD), researchers examined the impact of raising colonic propionate production on hepatic steatosis. The findings demonstrated that the predominant short chain fatty acid from colonic fermentation of inulin was acetate, which in an environment of NAFLD and a hepatic metabolic profile that promotes fat accretion, might provide surplus lipogenic substrate to the liver. Results of this study suggested that the increased colonic delivery of propionate from inulin-propionate ester seems to lessen this acetate-mediated increase in intrahepatocellular lipid.