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Influence of high carbohydrate versus high fat diet in ozone induced pulmonary injury and systemic metabolic impairment in a Brown Norway (BN) rat model of healthy aging
Kodavanti, U., B. Virginia, M. Schladweiler, C. Gordon, K. Jarema, P. Phillips, A. Ledbetter, D. Miller, S. Snow, AND J. Richards. Influence of high carbohydrate versus high fat diet in ozone induced pulmonary injury and systemic metabolic impairment in a Brown Norway (BN) rat model of healthy aging. Presented at American Thoracic Society, San Diego, CA, May 16 - 21, 2014.
Diet induced obesity can influence ones susceptibility to air pollution health effects. This study shows that in a rat model of healthy aging, high fat or high fructose diet did not increase obesity but produced systemic metabolic changes. The ozone induced systemic and pulmonary effects are slightly exacerbated in rats on a high fat diet.
Rationale: Air pollution has been recently linked to the increased prevalence of metabolic syndrome. It has been postulated that dietary risk factors might exacerbate air pollution-induced metabolic impairment. We have recently reported that ozone exposure induces acute systemic metabolic changes, likely via neurohormonal stimulation. In this study, we hypothesized that 1) a three month high carbohydrate or high fat dietary regimen will induce metabolic alterations causing obesity in male Brown Norway (BN) rats (a model of healthy aging), and 2) the pulmonary injury and systemic metabolic effects of acute ozone exposure will be modified by diet. Methods: Male BN rats began dietary regimen at 1 month of age (control normal chow, high fructose or high fat). At 4 months of age, these rats were exposed to air or ozone (0.8 ppm), 5 hours/day, 1 day/week, for either 1 week or 4 consecutive weeks. Body fat composition and glucose tolerance were examined during the dietary regimen. Glucose tolerance was also examined immediately after weekly episodic ozone exposures. Pulmonary toxicity and systemic inflammation were examined by the analysis of BALF immediately following the 1 or 4 week exposures (n=10). Results: The high fat diet did not increase body weight relative to normal diet and rats on high fructose diet actually showed a decrease in body weight as compared to rats fed a normal diet. However, lipidemia was observed in rats on the high fructose diet. High fat but not high fructose diet induced a small degree of glucose intolerance after 3 months on the diet. A single ozone exposure was associated with glucose intolerance in rats maintained on all three dietary regimens. At week 2 and 3, ozone effect on glucose tolerance was minimal in normal diet rats, but glucose intolerance was observed in rats on high fat and high fructose diets. A single ozone exposure caused a small degree of protein leakage as analyzed immediately following exposure in rats on the high fat but not high fructose or normal diet. There were no differences in BALF neutrophils in any of the dietary or exposure groups. However, ozone exposure decreased circulating lymphocytes in all rats regardless of diet. Conclusion: These data show that a high fructose or high fat diet might not increase body weight but can result in lipidemia and likely metabolic impairment. Ozone toxicity might be exacerbated in those on a high fat diet. (Does not reflect US EPA policy).