Prenatal exposure to PM 2.5 disturbs the glucose metabolism of offspring fed with high-fat diet in a gender-dependent manner

Studies have shown that maternal exposure to PM could potentially disrupt glucose and lipid metabolism in offspring supplied with high-fat diet, yet whether this effect is gender-dependent or not and the underlying biological mechanisms are not well understood. In our current research, female ICR mice were exposed to filtered air (FA) or concentrated ambient PM (CAP) before and during pregnancy. The offspring mice were fed with control diet (CD) or high-fat diet (HFD) for 9 weeks, and their metabolic conditions were analyzed. Our findings reveal that maternal exposure to PM induced glucose intolerance and insulin resistance in female offspring fed with HFD but not in males. Specifically, hepatic insulin resistance as indicated by significantly decreased AKT phosphorylation (p-AKT) level, changed liver structure as indicated by increased ballooning and steatosis based on H&E staining images, and impaired liver function as indicated by up-regulated ALT activity were observed in HFD-fed female offspring from CAP-exposed mothers in comparison to those from FA-exposed ones. Further analysis indicated that these impacts of prenatal PM exposure on glucose metabolism in offspring may result from disturbed gluconeogenesis and induced inflammatory response in liver. Our research underscores that prenatal PM exposure induces glucose metabolism abnormalities in offspring fed with HFD in a gender-dependent manner, and the liver potentially serves as a key player in mediating these effects of maternal PM exposure.