Non alcoholic fatty liver disease (NAFLD) is a metabolic disease. The worldwide prevalence of NAFLD has been increasing in parallel with the increase in the obese population. Recently, NAFLD been known as Metabolic dysfunction-associated steatotic liver disease (MASLD), reflecting its association with metabolic dysfunction. A condition in which lipid accumulation is > 5% of the liver weight is diagnosed as MASLD is progression. This study examined the effects of MPG-2 on lipid accumulation in FL83B liver cells. Oleic Acid (OA) treatment induced lipid accumulation in FL83B cells via the following mechanism: FL83B cells were treated with 0.5 mM OA for 48 h, and MPG-2 was treated for 24 h. This study analyzed the reduction in lipid accumulation and confirmed the effects of MPG-2 on lipid accumulation. In FL83B cells, treatment with 0.5 mM OA induced lipid accumulation, whereas that with MPG-2 resulted in increased phosphorylation of Adenosine monophosphate-activated kinase and suppressed Sterol regulatory element binding protein-1c (SREBP-1c). The suppression of SREBP-1c leads to a reduced expression of fatty acid synthase. In addition, treatment with MPG-2 increased in the expression of Adipose triglyceride lipase, a lipase that catalyzes the hydrolysis of triglycerides into diglycerides. As a result, MPG-2 inhibited lipid accumulation in OA-induced FL83B cells and it has the potential to be used as a postbiotic material for MASLD.