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  • Title: Exercise training is associated with improved levels of C-reactive protein and adiponectin in ZDF (type 2) diabetic rats.
    Author: de Lemos ET, Reis F, Baptista S, Pinto R, Sepodes B, Vala H, Rocha-Pereira P, Silva AS, Teixeira F.
    Journal: Med Sci Monit; 2007 Aug; 13(8):BR168-74. PubMed ID: 17660720.
    Abstract:
    BACKGROUND: Chronic low-grade systemic inflammation is a feature of such chronic diseases as cardiovascular disease and type 2 diabetes (T2D). There is evidence that regular exercise is effective as a treatment in these situations. This study intended to assess the levels of two inflammatory mediators, C-reactive protein (CRP) and adiponectin, in Zucker Diabetic Fatty (ZDF, fa/fa) rats, an experimental model of T2D, and to determine whether exercise-induced changes in insulin resistance could be explained by modifications in these inflammation markers. MATERIAL/METHODS: Male ZDF (Gmi fa/fa) rats and their littermates (Gmi +/+), aged 8 weeks, were randomly assigned in two groups: an exercise trained and a sedentary one. Swimming was conducted 1 h/day 3 days/week for 12 weeks. The rats were sacrificed 48 h after the last round of exercise. Rats had their body weight, insulin, adiponectin, CRP, as well as glucose, total cholesterol, triglycerides, MDA, and SOD measured and HOMA-IR calculated before and after the 12-week swimming training. RESULTS: In the ZDF (fa/fa) rats underwent swimming exercise, all the metabolic abnormalities were totally or partially prevented (p<0.001), namely the hyperglycemic, hyperinsulinemic, and dyslipidemic pattern observed in their sedentary counterparts. Furthermore, even without body weight change, a plasma adiponectin increase (28.0%) and a CRP decrease (12.7%) were also observed. CONCLUSIONS: A 12-week thrice-weekly swimming training was associated with improved measures of chronic inflammation markers as measured by adiponectin and CRP. Moreover, improvements in insulin sensitivity resulting from swimming exercise appeared to be related to changes in these inflammatory mediators.
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