Abstract
This study compares the effects of a single bout of exercise (acute extenuating) with those promoted by an exercise training program (chronic), focusing on low-grade chronic inflammation profile and on oxidative stress status, using the obese ZDF rats as a model of type 2 diabetes mellitus (T2DM). Animals were sacrificed after 12 weeks of a swimming training program and after a single bout of acute extenuating exercise. Glycaemic, insulinemic, and lipidic profile (triglycerides, total-cholesterol) were evaluated, as well as inflammatory (serum CRPhs, TNF-α, adiponectin) and oxidative (lipidic peroxidation and uric acid) status. When compared to obese diabetic sedentary rats, the animals submitted to acute exercise presented significantly lower values of glycaemia and insulinaemia, with inflammatory profile and oxidative stress significantly aggravated. The trained animals showed amelioration of glycaemic and lipidic dysmetabolism, accompanied by remarkable reduction of inflammatory and oxidative markers. In conclusion, the results presented herein suggessted that exercise pathogenesis-oriented interventions should not exacerbate underlying inflammatory stress associated with T2DM.
Highlights
Diabetes is an increasing health problem worldwide
This study compares the effects of a single bout of exercise with those promoted by an exercise training program, focusing on low-grade chronic inflammation profile and on oxidative stress status, using the obese Zucker Diabetic Fatty (ZDF) rats as a model of type 2 diabetes mellitus (T2DM)
The purpose of this study is to compare the effects of a single bout of exercise with those promoted by an exercise training program, focusing on glycaemic and lipid metabolism, but on low-grade chronic inflammation profile and on oxidative stress status, using the obese ZDF rats as model of T2DM
Summary
Diabetes is an increasing health problem worldwide. The core pathophysiology of type 2 diabetes (T2DM) has been attributed to the classic triad of decreased insulin secretion, increased insulin resistance, and elevated hepatic glucose production. Hyperglycaemia and hyperlipidaemia are key promoters of diabetes dysmetabolism, namely, through the formation of reactive oxygen species (ROS) and advanced glycation end products (AGEs), which causes cell damage and insulin resistance [3, 4]. Both of them stimulate proinflammatory cytokines, contributing to β-cell degradation, due to apoptosis pathways [5]. Exercise has been shown to promote beneficial effects on insulin resistance, both in humans and in rodent models of T2DM [7, 8]. Prospective studies assessing the physiological and biochemical effects of physical training in human populations are complex and, a suitable animal
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