Abstract: Objective To investigate the disruptive effects of perinatal exposure to the environmental endocrine disruptor Bisphenol AF (BPAF) on hepatic lipid metabolism in prepubertal (postnatal day 21, PND21) male offspring rats, aiming to provide scientific evidence for assessing the obesogenic effect of BPAF.Methods Sprague-Dawley rats (8 weeks old) were used in this study. Pregnant rats were divided into BPAF dose groups (2, 10, 50 mg·kg^-1) and a vehicle control group (corn oil), with 6 confirmed pregnant females per group. Gavage administration started from gestational day 0 and continued until the end of lactation. On PND21, one male offspring per litter was randomly selected. Serum concentrations of glucose (GLU), triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), leptin (LEP), free fatty acids (FFA), and oxidative stress markers superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. Pathological changes in liver and adipose tissues were observed, and the expression levels of genes related to hepatic lipid metabolism were detected.Results Compared to the vehicle control group, the 50 mg·kg^-1 group showed significantly increased serum LEP and MDA levels in male offspring (P < 0.05), and significant upregulation of hepatic lipoprotein lipase (Lpl), fatty acid synthase (Fas), and peroxisome proliferator-activated receptor γ (Pparg) gene expression (P < 0.05). The 2 mg·kg^-1 group exhibited a significant increase in adipocyte length (P < 0.05), while the 50 mg·kg^-1 group showed significant increases in both adipocyte area and length (P < 0.05). GLU and TG levels showed an increasing trend across all dose groups, but the differences were not statistically significant (P > 0.05). No significant abnormalities were observed in liver histopathological examination.Conclusion Perinatal exposure to 50 mg·kg^-1 BPAF induced adipocyte hypertrophy, elevated leptin levels, upregulation of lipid synthesis gene expression, and enhanced oxidative stress in prepubertal male offspring, suggesting that BPAF may exert environmental obesogenic effects by disrupting lipid metabolism pathways.