Abstract
Over the last 30 years the combination of both a sedentary lifestyle and excessive food availability has led to a significant increase in the prevalence of obesity and aggravation of rates of metabolic syndrome and type 2 diabetes mellitus (T2DM). Several lines of scientific evidence have been demonstrating that a low level of physical activity and decreased daily energy expenditure leads to the accumulation of visceral fat and, consequently, the activation of the oxidative stress/inflammation cascade, which underlies the development of insulin resistant T2DM and evolution of micro, and macrovascular complications. This paper focuses on the pathophysiological pathways associated with the involvement of oxidative stress and inflammation in the development of T2DM and the impact of regular physical exercise (training) as a natural antioxidant and anti-inflammatory strategy to prevent evolution of T2DM and its serious complications.
Highlights
Oxidation is viewed in general as a chemical process whereby electrons are removed from molecules, generating highly reactive free radicals, which include reactive oxygen species (ROS), such as superoxide and hydroperoxyl, and reactive nitrogen species (RNS) [1]
Several lines of scientific evidence have been demonstrating that a low level of physical activity and decreased daily energy expenditure leads to the accumulation of visceral fat and, the activation of the oxidative stress/inflammation cascade, which underlies the development of insulin resistant type 2 diabetes mellitus (T2DM) and evolution of micro, and macrovascular complications
This paper focuses on the pathophysiological pathways associated with the involvement of oxidative stress and inflammation in the development of T2DM and the impact of regular physical exercise as a natural antioxidant and anti-inflammatory strategy to prevent evolution of T2DM and its serious complications
Summary
Oxidation is viewed in general as a chemical process whereby electrons are removed from molecules, generating highly reactive free radicals, which include reactive oxygen species (ROS), such as superoxide and hydroperoxyl, and reactive nitrogen species (RNS) [1]. Data from the literature suggest that acute exercise increases oxidative stress, in contrast to chronic exercise, in which adaptation to the stimulus decreases oxidative stress It appears that acute exercise induces the generation of ROS whereas exercise training maintains redox homeostasis [22,23,24]. Based on the current literature, as well as on our knowledge concerning the effects of exercise training in an obese animal model of T2DM, the Zucker Diabetic Fatty (ZDF) rats, this paper will briefly review, firstly, the key pathophysiological aspects of the disease, focusing on the involvement of oxidative stress and inflammation and the use of regular physical exercise of moderate intensity (training) as a strategy to improve antioxidant and anti-inflammatory status in T2DM
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