The significant increase and reduction of these gene expressions of the liver and morphological changes of the liver cells in the HFD group and HFD plus PSE-treated group (Figure 3) indicate that the lipogenesis-inhibiting effects of PSE may be mediated by repressing fatty acid uptake via inhibition of SREBP-1c, FAS, SCD-1, and CD36, and PSE significantly affects nonalcoholic fatty liver disease. Here, FAS is linked to metabolic dysfunction-associated steatotic liver disease.