Obesity-induced oxidative stress and inflammation are involved in the pathogenesis of cardiovascular disease. We investigated whether diet-induced, long-term, mild weight loss improved proinflammatory cytokine levels, leukocyte count, and oxidative stress. Overweight/obese participants (25 ≤ body mass index < 34 kg/m2, N = 122, 30-59 years) joined a 3-year-long clinical intervention involving daily 100-kcal calorie deficits. Successful weight loss was defined as a reduction in initial body weight equal to 2 kg after the clinical intervention period. Body weight in the successful mild weight loss group (SWL, n = 50) changed 5.4% (-4.16 ± 0.31 kg) compared to 0.05 ± 0.14 kg in the unsuccessful weight loss group (n = 49). After 3 years, SWL participants exhibited significantly reduced insulin, triglycerides, total and low-density lipoprotein cholesterol, free fatty acids, and leukocyte count (P = .030). Furthermore, in the SWL group, serum interleukin (IL)-1β, IL-6, and urinary 8-epi-prostaglandin (PG)F2α were significantly reduced (45%, 30%, and 14%, respectively). In contrast, the unsuccessful weight loss group exhibited significant increases in percentage of body fat, waist circumference, oxidized low-density lipoprotein, and tumor necrosis factor-α, as well as a significant decrease in high-density lipoprotein cholesterol. After adjusting for baseline values, the 2 groups demonstrated significantly different percentage of body fat, waist circumference, leukocyte count (P = .018), insulin, IL-6 (P = .031), IL-1β (P < .001), and tumor necrosis factor-α (P < .001), as well as urinary 8-epi-PGF2α (P = .036). A positive correlation existed between IL-1β and urinary 8-epi-PGF2α (r = 0.435, P < .001) and between changes in IL-6 and urinary 8-epi-PGF2α (r = 0.393, P < .001). Long-term mild weight loss reduces inflammatory cytokine levels, leukocyte counts, and oxidative stress and may reverse the elevated oxidative stress induced by inflammatory mediators in the overweight and obese.
Bibliographical noteFunding Information:
This work was supported by the National Research Foundation, Ministry of Education, Science and Technology (Mid-career Researcher Program: 2011-0016444 , M10642120002-06N4212-00210 , and 2011-0000068 ), Republic of Korea.
All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics