Insulin resistance is a significant contributor to the development of type 2 diabetes (T2D) and is associated with obesity, physical inactivity, and low maximal oxygen uptake. While intense and prolonged exercise may have negative effects, physical activity can have a positive influence on cellular metabolism and the immune system. Moderate exercise has been shown to reduce oxidative stress and improve antioxidant status, whereas intense exercise can increase oxidative stress in the short term. The impact of exercise on pro-inflammatory cytokine production is complex and varies depending on intensity and duration. Exercise can also counteract the harmful effects of ageing and inflamm-ageing. This review aims to examine the molecular pathways altered by exercise in non-obese individuals at higher risk of developing T2D, including glucose utilization, lipid metabolism, mitochondrial function, inflammation and oxidative stress, with the potential to improve insulin sensitivity. The focus is on understanding the potential benefits of exercise for improving insulin sensitivity and providing insights for future targeted interventions before onset of disease.
Keywords: creatine kinase (CK); glutathione (GSH); hepatic insulin-sensitizing substance (HISS); high-intensity interval (HIT); malondialdehyde (MDA); peroxisome proliferator-activated receptor alpha-stimulated lipid mediators (PAHSAs); short-chain fatty acids (SCFAs); superoxide dismutase (SOD); thiobarbituric acid reactive substances (TBARS); total antioxidant status (TAS); type 2 diabetes mellitus (T2DM).
© 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.