Effects of PM_2.5 exposure on glucose and lipid metabolism in offspring mice

Objective To explore the effect of prenatal PM_2.5 exposure on the glucolipotoxicity of male and female mice under post weaning high fat diet.

Methods Twelve four-week-old clean grade female C57BL/6J mice were randomly divided into PM_2.5 exposure group and filter air (FA) control group. After real-time exposure for 7 weeks(6 h/d, 5 d/week), female mice in each group were caged with male mice (female∶male=2∶1), and continued to be exposed until the pups were born. The offspring were fed a high-fat diet (total energy 4.67 kcal/g: 37.0% carbohydrate, 20.00% protein and 45.0% fat) after weaning. Glucose tolerance was measured by the intraperitoneal glucose tolerance test. Pathological changes were observed with hematoxylin-eosin staining. Real-time PCR was used to measure the mRNA expression of estrogen receptor alpha (ERα) and peroxisome proliferator-activated receptor gamma (PPARγ).

Results Prenatal exposure to PM_2.5 significantly decreased the birth weight of offspring, and significantly increased the body weight and reduced the glucose intolerance of the adult male offspring, but with no significant changes in the adult female offspring. Compared with those in the control group, the adult male offspring with prenatal PM_2.5 exposure had significantly increased energy efficiency and significantly reduced gene expression of ERα and PPARγ in the adipose tissue.

Conclusion Prenatal exposure to PM_2.5 may regulate the gene expression of ERα and PPARγ in the adipose tissue in a programmed way, to induce disturbances in glucose and lipid metabolism in adult male offspring, but have no significant implications for adult female offspring.