| Literature DB >> 27803047 |
Catherine Duggan1, Jean de Dieu Tapsoba2, Ching-Yun Wang2,3, Kristin L Campbell4, Karen Foster-Schubert5, Myron D Gross6, Anne McTiernan2,3.
Abstract
Oxidative stress, a potential mechanism linking obesity and cancer, results from an imbalance between activation/inactivation of reactive oxygen species, byproducts of cellular metabolism. In a randomized controlled trial, we investigated effects of diet and/or exercise on biomarkers of oxidative stress. A total of 439 overweight/obese [body mass index (BMI) > 25 kg/m2] postmenopausal women, ages 50 of 75 years, were randomized to 12 months of (i) reduced-calorie weight loss diet ("diet"; n = 118); (ii) moderate-to-vigorous intensity aerobic exercise ("exercise"; n = 117); (iii) combined diet and exercise intervention ("diet + exercise"; n = 117); or (iv) control (n = 87). Outcomes were circulating markers of oxidative stress, including fluorescent oxidation products (FOP), F2-isoprostanes, and oxidized low-density lipoprotein (LDL). On average, participants were 57.9 years, with a BMI of 30.9 kg/m2 F2-isprostanes were significantly reduced in the diet (-22.7%, P = 0.0002) and diet + exercise (-23.5%, P < 0.0001) arms versus controls (-2.99%) and nonsignificantly reduced in the exercise arm (-14.5%, P = 0.01). Participants randomized to the diet and diet + exercise arms had significant increases in levels of FOP [control -5.81%; diet +14.77% (P = 0.0001); diet + exercise +17.45%, (P = 0.0001)]. In secondary analyses, increasing weight loss was statistically significantly associated with linear trends of greater reductions in oxidized LDL and in F2-isoprostanes and increases in FOP. Compared with controls, exercise participants whose maximal oxygen consumption increased had significant decreases in levels of F2-isoprostanes and in oxidized LDL and increases in FOP. Dietary weight loss, with or without exercise, significantly reduced some markers of oxidative stress in postmenopausal women. Cancer Prev Res; 9(11); 835-43. ©2016 AACR. ©2016 American Association for Cancer Research.Entities:
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Year: 2016 PMID: 27803047 PMCID: PMC5117666 DOI: 10.1158/1940-6207.CAPR-16-0163
Source DB: PubMed Journal: Cancer Prev Res (Phila) ISSN: 1940-6215