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  • Aerobic exercise plays an important

    2024-04-01

    Aerobic exercise plays an important role in the regulation of death associated protein kinase metabolism in the skeletal muscle. It is also associated with increases in AMPK and GLUT4 levels, resulting in the improvement of the glucose uptake signaling pathway [17,18]. Recently, it has been shown that exercise markedly increases AMPK activity and glucose transports in diabetes [19,20], strongly suggesting that exercise is a potent regulator of glucose metabolism. Additionally, Michelle et al. [21] previously showed that 8 weeks of aerobic exercise was able to significantly increase AMPK, FNDC5, PGC-1α, and UCP levels in HFD-induced obese rats. Taken together, aerobic exercise may provide the stimulus to increase AMPK, GLUT4, FNDC5, PGC-1α, and UCP levels and subsequently improve glucose metabolism in the skeletal muscles. However, the effect of aerobic exercise training on glucose metabolism through decreasing CRBN levels and increasing AMPK levels has not been evaluated in the skeletal muscle in T1DM.
    Materials and methods
    Results
    Discussion T1DM is associated with a state of hyperglycemia, which contributes to the dysfunction of basal metabolic conditions and the accumulation of cholesterol [29]. Sustained accumulation of blood glucose leads to reduced insulin sensitivity, impairing the regulation of normal glucose metabolism, and resulting in diminished glucose uptake [30]. In the present study, we explored influences on the glucose metabolism in the blood of a STZ-induced diabetic rats. We found that STZ-induced diabetic rat had increased blood glucose, HOMA-IR, TG, and T-C (Fig. 1); these results have been previously reported [31]. These findings also suggest that STZ causes progressive body weight loss, insulin insufficiency, dyslipidemia and chronic hyperglycemia, all of which contribute to the pathogenesis of diabetes complications. Consistent with the results of a previous study, we also observed that aerobic exercise training reduced these parameters, accompanied by a significant increase in HDL-C (Fig. 1) [32]. Laaksonen et al. [33] also suggest that aerobic exercise training decreased TG and increased HDL-C levels in young patients with type 1 diabetes. Taken together, these results indicate that aerobic exercise training has excellent therapeutic potential for the management of type 1 diabetes. CRBN acts as multifunctional protein in various organelles including the cytoplasm, nucleus, mitochondria, and endoplasmic reticulum [34]. It directly binds to AMPK, a potent metabolic sensor that plays an important role in the regulation of metabolic pathways [35]. Indeed, ablation of CRBN in mice increased hepatic AMPK, suggesting that these signaling pathways act as key modulators of obesity and diabetes [36]. Activation of AMPK and Akt increases GLUT4-mediated glucose uptake in vitro [37]. Moreover, exercise training causes increased glucose uptake via the AMPK/Akt/GLUT4 signaling pathway and activates PGC-1α and FNDC5, resulting in improved glucose metabolism in the skeletal muscle [38]. However, whether exercise training had similar effects in the skeletal muscle of individuals with T1DM was unknown. In this study, we show that CRBN is reduced and AMPK, Akt, and GLUT4 protein levels are increased in the skeletal muscle of exercise-trained diabetic rats. In addition, PGC-1α and FNDC5 protein levels were also significantly increased, indicating that, similar to the results of a previous study, aerobic exercise training plays a critical role in glucose homeostasis [39]. Moreover, we found that aerobic exercise training in diabetic rats increased SOD1 and UCP3 levels, indicating increased scavenging of free superoxide radicals and enhanced fatty acid oxidation, respectively. Our findings from this study indicate that aerobic exercise training induced AMPK activation via increasing levels of Akt, GLUT4, PGC-1α and FNDC5, as well as those of SOD1 and UCP3, suggesting that together these proteins function to improve glucose homeostasis in the skeletal muscle of rats with T1DM.