Exercise-mediated increase in PGC1α and MEF2 expression in type 2 diabetes mellitus

Sedentarism accounts for exacerbated fat storage in skeletal muscle that can impair mitochondrial biogenesis and progress to Type 2 Diabetes (T2D). A signaling pathway coordinated by coactivators and transcription factors such as myocyte stimulating factor 2 (MEF2), peroxisome proliferator-activated receptor 1-alpha (PGC1α), and mitochondrial transcription factor (TFAM) is essential to preserve mitochondrial function. So, we tested the effect of chronic physical exercise on the expression of MEF2, PGC1α, and TFAM, in gastrocnemius. Were analyzed lipidic profile, fasting glucose, and gene expressions (PGC1 α, TFAM, MEF2) in muscle obtained from Wistar rats divided into four groups: Control (fed with balanced chow and sedentary), Exercised (fed with balanced chow and exercised), T2D (fed with high-fat chow + a low dose of streptozotocin and sedentary) and T2D-exercised (fed with high-fat diet + a low dose of streptozotocin and exercised). Exercised group exhibited increased expression of PGC1α and MEF2 compared to the Control and T2D groups (sedentary or exercised). PGC1α was higher in Exercised by 143 % compared to Control, and by 220 % compared to T2D groups. MEF2 was 39 % higher in Exercised group when compared to the T2D group and 300 % higher than the exercised T2D group. High-Density Lipoprotein was positively associated with PGC1α expression, probably associated with the improvement in mitochondrial function in exercised animals, and fasting glucose was negatively associated with MEF2, probably related to impaired mitochondrial functioning in animals with T2D. We conclude that physical could improve some T2D harming effects by enhancing mitochondrial biogenesis and homeostasis.