Peri-implantation ozone exposure alters adipose morphology in female Long-Evans rat offspring
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Exposure to air pollutants during critical periods of development can alter fetal growth and program cardiometabolic disease risk in offspring. Hence, the purpose of this study was to longitudinally assess potential metabolic risk in our model of ozone-induced fetal growth restriction. Pregnant Long-Evans rats were exposed to either 0.8 ppm ozone (O3) or air (A) for 4 hours during implantation receptivity on gestation days 5-6. The heaviest male (M) and female (F) offspring from each litter were weaned at postnatal day 19 and fed a 10% low-fat diet ad libitum. Food intake, body weight and body composition were sequentially monitored. At 3 months of age, glucose tolerance tests (GTT) were performed to assess glucose homeostasis. At 5 months of age, indirect calorimetry was performed to assess basal metabolic rate (BMR) and respiratory exchange ratios (RER). At 6 months of age, rats were euthanized and retroperitoneal (RP) and inguinal (ING) adipose tissues were stained with H&E to assess adipocyte morphology. Results revealed no difference in body weight at weaning, however, FO3 offspring had decreased weight gain over time compared to FA offspring (p<0.05). Feed efficiency (body weight gain/food intake) was trending downward in FO3 offspring compared to FA offspring (p=0.07). During the dark cycle, FO3 offspring had an elevated BMR (p=0.05) and an upward trending RER (p=0.06), suggesting that carbohydrates were the preferred energy substrate. RP adipocytes from FO3 offspring appeared hyperplastic (decreased cell size and increased cell count averaged over four 20x fields) compared to FA offspring (p<0.05); whereas no changes in ING morphology, total adiposity, serum leptin concentration or GTT were observed. Male offspring had no differences in these endpoints. Our study suggests that peri-implantation O3 exposure programs continued postnatal growth restriction in female offspring with altered energy balance and hyperplastic adipocytes in the RP depot. This occurred, however, without accompanying differences in the ING depot or in total adiposity. (This abstract does not reflect U.S. EPA policy.)