Citation:

Snow, S., A. Henriquez, W. Cheng, A. Fisher, B. Vallanat, M. Angrish, J. Richards, Mette C. Schladweiler, C. Wood, H. Tong, AND U. Kodavanti. Diets Enriched with Coconut, Fish, and Olive Oil Modify Peripheral Metabolic Effects of Ozone in Rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, 410(1):115337, (2020). https://doi.org/10.1016/j.taap.2020.115337

Impact/Purpose:

Dietary supplements containing fish and olive oil diets have been shown to protect humans from ambient particulate matter-induced vasoconstriction in humans. In this study we examined in rodents receiving coconut oil, fish oil or olive oil-enriched diets would alter systemic metabolic response to ozone. This was a follow up of our prior paper on the influence of same diets on ozone-induced vascular and pulmonary effects. We show that both fish oil and olive oil-rich diets significantly modify metabolic effects of ozone especially in liver and adipose tissue. Olive oil rich diet exacerbate ozone-induced glucose intolerance and affect lipid metabolism. Thus dietary intake can modify ozone-induced metabolic effects.

Description:

Dietary factors may modulate metabolic effects of air pollutant exposures. We hypothesized that diets enriched with coconut oil (CO), fish oil (FO), or olive oil (OO) would alter ozone-induced metabolic responses. Male Wistar-Kyoto rats (1-month-old) were fed normal diet (ND), or CO-, FO-, or OO-enriched diets. After eight weeks, animals were exposed to air or 0.8 ppm ozone, 4 h/day for 2 days. Relative to ND, CO- and OO-enriched diet increased body fat, serum triglycerides, cholesterols, and leptin, while all supplements increased liver lipid staining (OO > FO > CO). FO increased n-3, OO increased n-6/n-9, and all supplements increased saturated fatty-acids. Ozone increased total cholesterol, low-density lipoprotein, branched-chain amino acids (BCAA), induced hyperglycemia, glucose intolerance, and changed gene expression involved in energy metabolism in adipose and muscle tissue in rats fed ND. Ozone-induced glucose intolerance was exacerbated by OO-enriched diet. Ozone increased leptin in CO- and FO-enriched groups; however, BCAA increases were blunted by FO and OO. Ozone-induced inhibition of liver cholesterol biosynthesis genes in ND-fed rats was not evident in enriched dietary groups; however, genes involved in energy metabolism and glucose transport were increased in rats fed FO and OO-enriched diet. FO- and OO-enriched diets blunted ozone-induced inhibition of genes involved in adipose tissue glucose uptake and cholesterol synthesis, but exacerbated genes involved in adipose lipolysis. Ozone-induced decreases in muscle energy metabolism genes were similar in all dietary groups. In conclusion, CO-, FO-, and OO-enriched diets modified ozone-induced metabolic changes in a diet-specific manner, which could contribute to altered peripheral energy homeostasis.

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