• • Intrauterine BaP exposure at 800 and 1600 μg·kg−1 induced dose-dependent pancreatic damage in offspring, characterized by disrupted islet morphology and reduced islet area, which persisted from postnatal day 2 to week 12, indicating irreversible developmental toxicity.
• • PDX-1 and TFAM protein and mRNA expression were significantly downregulated in a dose-dependent manner in both 2-day and 12-week offspring, suggesting molecular mechanisms linking BaP exposure to impaired pancreatic development and mitochondrial dysfunction.
• • At week 12, the 1600 μg·kg−1 BaP group showed pre-diabetic symptoms, with significantly elevated blood glucose at 120 min post-glucose challenge (P<0.01) and slower glucose clearance during IPITT (P<0.05 at 30, 60, 120 min), indicating impaired glucose tolerance and insulin resistance.
• • The area under the curve (AUC) for IPGTT and IPITT in the 1600 μg·kg−1 group was significantly higher than control (P<0.01), confirming functional impairment of pancreatic β-cells and systemic insulin resistance, which may increase long-term risk of type 2 diabetes.