Hepatic mRNA expression studies highlighted three potential mechanisms by which feeding with L-EF can lead to increased hepatic steatosis: there was no increase in β-oxidation of fatty acids (e.g., Ppar-a and Cpt1α) compared to control, despite of fat ingestion; increased de novo lipogenesis (e.g., Acc2); and reduced Irs-1 and -2 expression. Here, ACACB is linked to Hepatic steatosis.