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Effects of maternal high-fat diet and sedentary lifestyle on susceptibility of adult offspring to ozone exposure in rats
Citation:
Gordon, C., P. Phillips, A. Johnstone, Judy Schmid, M. Schladweiler, A. Ledbetter, S. Snow, AND U. Kodavanti. Effects of maternal high-fat diet and sedentary lifestyle on susceptibility of adult offspring to ozone exposure in rats. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 29(6):239-254, (2017).
Impact/Purpose:
Maternal sedentary lifestyle combined with consuming a predominantly calorically rich diet has well known negative impacts on the offspring, including increased susceptibility to diabetes, obesity, and other diseases related to the metabolic syndrome. This study questioned if similar maternal exercise and dietary treatments would alter the susceptibility of the adult offspring to an air pollutant. It was shown that the pulmonary inflammatory responses to ozone was exacerbated in adult offspring whose mothers had been pre-treated with a high fat diet. In addition, maternal exercise led, in some cases, to an attenuation in some of the inflammatory responses to ozone. While the results of this study should be considered as exploratory and will be followed up by another thorough assessment, this is the first study to show the deleterious impact of a maternal sedentary lifestyle and high fat diet on susceptibility of adult offspring to an air pollutant.
Description:
Epidemiological and experimental data suggest that obesity exacerbates the health effects of air pollutants such as ozone (O3). Maternal inactivity and calorically rich diets lead to offspring that show signs of obesity. Exacerbated O3 susceptibility of offspring could thus be manifested by maternal obesity. Thirty-day old female Long-Evans rats were fed a control (CD) or high fat (HF) (60% calories) diet for 6 wks and then bred. GD1 rats were then housed with a running wheel (RW) or without a wheel (SED) until parturition, creating 4 groups of offspring: CD-SED, CD-RW, HF-SED, and HF-RW. HF diet was terminated at PND 35 and all offspring were placed on CD. Body weight and %fat of dams were greatest in order; HF-SED>HF-RW>CD-SED>CD-RW. Adult offspring were exposed to O3 for 2 consecutive days (0.8 ppm, 4 hr/day). Glucose tolerance tests (GTT), ventilatory parameters (plethysmography), and bronchoalveolar fluid (BALF) cell counts and protein biomarkers were performed to assess response to O3. Exercise and diet altered body weight and %fat of young offspring. GTT, ventilation, and BALF cell counts were exacerbated by O3 with responses markedly exacerbated in males. HF diet and O3 led to significant exacerbation of several BALF parameters: Total cell count, neutrophils, and lymphocytes were increased in male HF-SED vs. CD-SED. Males were hyperglycemic after O3 exposure and exhibited exacerbated GTT responses. Ventilatory dysfunction was also exacerbated in males. Maternal exercise had minimal effects on O3 response. The results of this exploratory study suggest a link between maternal obesity and susceptibility to O3 in their adult offspring in a sex-specific manner.
