Citation:

Nguyen, H., C. Miller, E. Stewart, P. Phillips, K. OShaughnessy, AND J. Dye. Ozone Exposure during Early Pregnancy Alters Energy Balance and Adipose Morphology in Female Long-Evans Rat Offspring by 6 Months of Age. To be Presented at VIRTUAL-Society for Birth Defects Research & Prevention Meeting, Charleston,SC, June 27 - July 01, 2020.

Impact/Purpose:

The purpose of this study was to longitudinally assess potential metabolic risk in our model of ozone-induced fetal growth restriction. Exposure to air pollutants during implantation can adversely affect fetal development, thereby increasing the risk of obesity and other offspring morbidities.

Description:

Exposure to air pollutants during implantation can adversely affect fetal development, thereby increasing the risk of obesity and other offspring morbidities. 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 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 assessed. Basal metabolic rate (BMR) and respiratory exchange ratios (RER) were assessed by indirect calorimetry at 5 months of age. At 6 months of age, rats were euthanized and retroperitoneal (RP) and inguinal (ING) adipose tissue were fixed, sectioned and stained with H&E to assess adipocyte morphology. Results revealed no significant difference in body weight at weaning. However, FO3 offspring had decreased weight gain over time compared to FA offspring (P<0.05). Despite no difference in food intake, feed efficiency (body weight gain/food consumed) was trending towards a reduction in FO3 compared to FA offspring (P=0.07). During their dark cycle, BMR was increased (P=0.05) and there was a trending RER increase (P=0.06) in FO3 compared to FA offspring, suggesting that carbohydrate was the preferred energy substrate. RP adipocytes from FO3 offspring appeared hyperplastic (decreased cell size and increased cell number averaged over four, 20x fields) compared to FA offspring (P<0.05); whereas, no morphological changes in the ING depot or in total body adiposity were observed. In male offspring, there were no differences in body weight, feed intake, BMR or adiposity. Our study suggests that O3 exposure during implantation alters energy balance in female offspring such that when they are maintained on a low-fat diet, serves to shift RP adipose to a “healthier” hyperplastic phenotype. However, this occurred without accompanying differences in ING fat depots or total adiposity. Thus, peri-implantation O3 exposure not only led to fetal growth restriction, in female offspring, it appeared to program visceral adipocytes and alter basal energy metabolism. Such effects may influence metabolic risk related to additional postnatal stressors, the consequences of which require further investigation. (Abstract does not reflect USEPA policy).

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