Impact of UCP2 polymorphism on long-term exercise-mediated changes in adipocytokines and markers of metabolic syndrome.

BACKGROUND AND AIMS: Variations in genes involved in energy expenditure affect aerobic exercise efficiency, but it remains unclear whether the effect of aerobic exercise on adipocytokines is modified by the obesity-associated genotypes in the uncoupling protein 2 gene (UCP2). The purpose of this study was to assess whether genetic variation in UCP2 may affect exercise-mediated changes in adipocytokines and markers of metabolic syndrome in postmenopausal obese women. METHODS: Forty-two sedentary postmenopausal obese women (age 52.74 ± 6.39 years) participated in this study. Participants were encouraged to train for 3 days a week, for 6 months, for 60 min per session of treadmill walking/running at 60 % [Formula: see text]. Subjects were genotyped for the 45-bp insertion/deletion (I/D) polymorphism in the 3'-untranslated region (UTR) of UCP2. RESULTS: Among the subjects, 23 (57.1 %) and 19 (42.9 %), were deletion homozygotes (DD) and ID heterozygotes, respectively. For DD homozygotes, body weight, body mass index (BMI), % body fat, and waist circumference, and body weight, BMI, and waist circumference of ID heterozygotes, were significantly decreased after the exercise program. There were no significant changes in metabolic markers in individuals with the ID genotype, whereas insulin and HOMA-IR in individuals with the DD genotype were significantly decreased after the exercise program. In DD homozygotes, but not in ID heterozygotes, adiponectin was significantly increased, and leptin, TNF-α, and IL-6 were significantly decreased after exercise training. CONCLUSIONS: Exercise-mediated changes in insulin resistance and adiponectin levels may be affected by genotypes in the 3'UTR I/D polymorphism in UCP2 in postmenopausal obese women.