Abstract
Anti-inflammatory cytokine interleukin-4 (IL-4) promotes glucose tolerance and insulin sensitivity while reduces lipid deposits. However, the effects of IL-4 on energy metabolism in muscle, the largest insulin-targeting organ, remain obscure. The study aimed at addressing the roles of IL-4 in myocyte differentiation (myogenesis) and energy metabolism of muscle cells. Effects of IL-4 on myogenesis, and interaction between IL-4 and insulin on glucose metabolism of C2C12 myoblasts and the terminal differentiated myocytes were analyzed. IL-4 improved GLUT4 translocation and tended to elevate glucose uptake by boosting insulin signaling. In diabetic mice, transient and long-term IL-4 showed differential effects on insulin signaling and efficacy. The study provides evidence to address the roles of IL-4 in mediating whole-body muscle reservoir and glucose metabolism, as well as the interaction between immune responses and energy homeostasis. IL-4 has dual potential to act as an adjuvant therapeutic target for sarcopenia to preserve muscle mass and insulin resistance to improve insulin sensitivity, which implicates the regulation of immune system to the muscle differentiation and exercise performance.
Highlights
Type 2 diabetes mellitus (T2DM) is a common endocrine disease characterized by hyperglycemia and insulin resistance [1]
Following the initial fusion of myoblasts to form myotubes, IL-4 treatment leads to further nuclear addition and increased myotube size
In support of the conclusion that IL-4 promotes muscle differentiation and regeneration [19, 20], this study demonstrates that IL-4-treated mature myotubes contain more nuclei with longer diameter (Figure 2(b))
Summary
Type 2 diabetes mellitus (T2DM) is a common endocrine disease characterized by hyperglycemia and insulin resistance [1]. Hotamisligil et al first demonstrated that expression of tumor necrosis factor-α (TNF-α) in adipose tissue of obese animals is markedly increased [2]. Accumulating studies proved that T2DM is an inflammatory condition with elevated acute phase inflammatory reactants [3,4,5,6]. Excess glucose and nutrient intake leads to oxidative stress which induces elevated levels of pro-inflammatory cytokines. These increased cytokines, such as interleukin-6 (IL-6), result in impaired insulin action on peripheral glucose metabolism [7, 8]. Cytokines are involved in the development of insulin resistance.
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