Obesity and type 2 diabetes mellitus are multifactorial health threats caused by a complex interplay between genetic predisposition and the environment with dramatically increasing worldwide prevalence. The role of heritability in their etiology is well recognized, however, the numerous attempts made in order certain genetic variants determining individual susceptibility to be identified have had limited success, until recently. At present the advancements in human genetics and the utilization of the genome-wide association approach have led to the identification of over 20 genetic loci associated with, respectively obesity and type 2 diabetes. Most of the genes identified to date, however, have modest effect on disease risk suggesting that both diseases are unlikely to develop without the individual being exposed to obesity- and/or type 2 diabetes-promoting environment. Indeed, unhealthy lifestyle, characterized by physical inactivity and food overconsumption is an unequivocally established risk factor for obesity and type 2 diabetes. Numerous epidemiological studies and randomized controlled trials, on the other hand, have demonstrated that lifestyle modification is effective in obesity and type 2 diabetes prevention. Furthermore, gene-lifestyle interaction studies suggest that genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future. By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.

Chemerin is an adipokine that may mediate the link between obesity, inflammation, insulin resistance, type 2 diabetes mellitus, and cardiovascular disease. In this study, we examined the association between chemerin and various cardiometabolic risk factors in cross-sectional setting and tested the hypothesis that a 6-month combined exercise program decreases serum chemerin in overweight or obese, non-diabetic individuals. Serum chemerin concentration was measured in a cross-sectional analysis including 98 individuals with a wide range of age and body mass index (BMI). In addition, chemerin was measured in 79 sedentary, overweight or obese, non-diabetic individuals who completed a 6-month combined endurance and resistance exercise program (CEP, n = 51) or served as controls (C, n = 28). Chemerin was significantly associated with total cholesterol (p = 0.04), triglycerides (p < 0.001), fasting insulin (p < 0.001), homeostasis model assessment of insulin resistance (HOMA-IR, p < 0.001), systolic blood pressure (p = 0.04), highly sensitive C-reactive protein (p = 0.03), leucocytes count (p = 0.047), and leptin (p = 0.008) independently of age and BMI. In multiple regression analysis, chemerin was an independent determinant of HOMA-IR. As a result of the 6-month training program, serum chemerin decreased significantly in CEP group (-13.8 ± 13.2 ng/ml, p < 0.001). A significant association between the changes in chemerin and improved HOMA-IR were found even after adjustment for changes in waist circumference. Among non-diabetic individuals serum chemerin was associated with various cardiometabolic risk factors independently of BMI. In addition, the 6-month combined strength and endurance training program led to a significant reduction in circulating chemerin levels in overweight or obese individuals.

SUMMARYObjective: We examined the effect of a 6-month combined aerobic and resistance training programme on cardiometabolic risk factors in nondiabetic subjects and compared its effectiveness when executed under strict professional supervision or without direct supervision.Methods: Eighty-five sedentary, non-diabetic subjects (27 men and 58 women), mean age 47.5±0.6 years, mean body mass index (BMI, 33.8±0.6 kg/m 2 ) participated in a combined exercise programme assigned to supervised (S, n=31), non-supervised (NS, n=24) or control group (C, n=30). Cardiometabolic risk parameters were assessed at baseline and after the 6-month training.Results: In both the S and NS group there was a significant decrease in BMI (−1.6±0.3, p<0.001 and −1.0±0.3 kg/m 2 , p=0.004), waist circumference (−10.1±1.1 cm, p<0.001 and −7.8±0.8 cm, p<0.001), fat mass (−1.8±0.4%, p<0.001 and −2.1±0.6%, p=0.003), and a significant increase in fat-free mass (+1.7±0.4%, p<0.001 and +2.0±0.7%, p=0.008), and aerobic capacity (+6.9±1.1, p<0.001 and +6.9±0.8 ml/kg per min, p=0.008). Fasting glucose did not change in S and NS, but increased in C (p=0.048). In the S group a significant decrease in fasting insulin (p<0.001), homeostasis model assessment of insulin resistance (p<0.001), highly sensitive C-reactive protein (p=0.004), leucocytes count (p=0.04), systolic high (p<0.001) and diastolic (p=0.009) blood pressure was found. Comparable significant decreases in total and low-density lipoprotein cholesterol were observed in all study groups.Conclusions: A 6-month combined exercise programme led to substantial improvement of various cardiometabolic risk factors. This programme was effective even when executed without direct supervision, although the effects were more pronounced in the supervised group. Our findings suggest that non-supervised exercise programmes may be a valuable, cost-effective tool to translate the current physical activity guidelines in a real-life setting.

We found a strong inverse relationship between the level of PA during leisure time (including sport), BMI, and the prevalence of T2DM. Uncontrolled eating behaviour was also found to have a significant effect on BMI.

Objective: To investigate the association of physical activity with insulin resistance and biomarkers of inflammation, coagulation, and fibrinolysis in a population at high risk for type 2 diabetes. Patients and Methods: A total of 778 subjects from the Risk factors in Impaired Glucose Tolerance for Atherosclerosis and Diabetes (RIAD) study aged 40-70 years were included in the present cross-sectional analysis. Results: Participants classified as having low physical activity (PA) were more insulin resistant in comparison to participants with medium (P = 0.042) and high PA (P = 0.015). Individuals with high physical activity had a significantly lower leucocytes count than individuals with low PA (P = 0.027) and significantly lower hs-CRP and fibrinogen concentrations than individuals with medium (P = 0.011 and P = 0.021) and low physical activity (P = 0.04 and P = 0.007). Although a trend towards a decrease in plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) levels with increasing physical activity was present, significant differences were observed only between subjects with high and medium physical activity (P = 0.045 and P = 0.033). In multivariate regression analyses physical activity was an independent determinant of insulin resistance, leucocytes count, hs-CRP, and fibrinogen concentrations. Conclusions: Physical activity was independently associated with insulin resistance and biomarkers of inflammation, whereas only a tendency towards decreased concentrations of coagulation and fibrinolytic biomarkers with increasing physical activity was observed.