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  • 1
    Abstract: INTRODUCTION: Maintenance of normal weight and higher levels of physical activity are associated with a reduced risk of several types of cancer. As genomic instability is regarded as a hallmark of cancer development, one proposed mechanism is improvement of DNA repair function. We investigated links between dietary weight loss, exercise, and strand break rejoining in an ancillary study to a randomized-controlled trial. METHODS: Overweight/obese postmenopausal women (n=439) were randomized to: a) reduced-calorie weight-loss diet ("diet" n=118); b) moderate-to-vigorous intensity aerobic exercise ("exercise" n=117); c) a combination ("diet+exercise" n=117); or d) control (n=87). The reduced-calorie diet had a 10% weight-loss goal. The exercise intervention consisted of 45 minutes of moderate-to-vigorous aerobic activity 5 days/week for 12 months. DNA repair capacity was measured in a subset of 226 women at baseline and 12 months, from cryopreserved peripheral mononuclear cells using the Comet assay. Anthropometric and body composition measures were performed at baseline and 12 months. RESULTS: DNA repair capacity did not change significantly with any of the 12 month interventions compared to control; there were also no significant changes when stratified by changes in body composition or aerobic fitness (VO2max). At baseline, DNA repair capacity was positively associated with weight, BMI, and fat mass (r=0.20, p=0.003; r=0.19, p=0.004; r=0.13, p=0.04, respectively) and inversely with lean body mass (r=-0.14, p=0.04). CONCLUSION: In conclusion, DNA repair capacity did not change with dietary weight loss or exercise interventions in postmenopausal women within a period of 12 months. Other assays that capture different facets of DNA repair function may be needed.
    Type of Publication: Journal article published
    PubMed ID: 25160845
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  • 2
    Abstract: BackgroundExcess body weight and a sedentary lifestyle are associated with the development of several diseases, including cardiovascular disease, diabetes and cancer in women. One proposed mechanism linking obesity to chronic diseases is an alteration in adipose-derived adiponectin and leptin levels. We investigated the effects of 12-month reduced calorie, weight loss and exercise interventions on adiponectin and leptin concentrations. MethodsOverweight/obese postmenopausal women (n=439) were randomized as follows: (i) a reduced calorie, weight-loss diet (diet; N=118), (ii) moderate-to-vigorous intensity aerobic exercise (exercise; N=117), (iii) a combination of a reduced calorie, weight-loss diet and moderate-to-vigorous intensity aerobic exercise (diet+exercise; N=117), and (iv) control (N=87). The reduced calorie diet had a 10% weight-loss goal. The exercise intervention consisted of 45min of moderate-to-vigorous aerobic activity 5days per week. Adiponectin and leptin levels were measured at baseline and after 12months of intervention using a radioimmunoassay. ResultsAdiponectin increased by 9.5% in the diet group and 6.6% in the diet+exercise group (both P0.0001 vs. control). Compared with controls, leptin decreased with all interventions (diet+exercise, -40.1%, P〈0.0001; diet, -27.1%, P〈0.0001; exercise, -12.7%, P=0.005). The results were not influenced by the baseline body mass index (BMI). The degree of weight loss was inversely associated with concentrations of adiponectin (diet, P-trend=0.0002; diet+exercise, P-trend=0.0005) and directly associated with leptin (diet, P-trend〈0.0001; diet+exercise, P-trend〈0.0001). ConclusionWeight loss through diet or diet+exercise increased adiponectin concentrations. Leptin concentrations decreased in all of the intervention groups, but the greatest reduction occurred with diet+exercise. Weight loss and exercise exerted some beneficial effects on chronic diseases via effects on adiponectin and leptin.
    Type of Publication: Journal article published
    PubMed ID: 23432360
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