Skeletal muscle is the tissue directly involved in insulin-stimulated glucose uptake. Glucose is the primary energy substrate for contracting muscles, and proper metabolism of glucose is essential for health. Contractile activity and the associated Ca²⁺signaling regulate functional capacity and muscle mass. A high concentration of Ca²⁺and the presence of calmodulin (CaM) leads to the activation of calcineurin (CaN), a protein with serine-threonine phosphatase activity. The signaling pathway linked with CaN and transcription factors like the nuclear factor of activated T cells (NFAT) is essential for skeletal muscle development and reprogramming of fast-twitch to slow-twitch fibers. CaN activation may promote metabolic adaptations in muscle cells, resulting in better insulin-stimulated glucose transport. The molecular mechanisms underlying the altered insulin response remain unclear. The role of the CaN/NFAT pathway in regulating skeletal muscle hypertrophy is better described than its involvement in the pathogenesis of insulin resistance. Thus, there are opportunities for future research in that field. This review presents the role of CaN/NFAT signaling and suggests the relationship with insulin-resistant muscles.

骨骼肌是直接参与胰岛素刺激的葡萄糖摄取的组织。葡萄糖是收缩肌肉的主要能量底物，葡萄糖的适当代谢对于健康至关重要。收缩活动和相关的 Ca ²⁺信号传导调节功能能力和肌肉质量。高浓度的 Ca ²⁺和钙调蛋白 (CaM) 的存在会导致钙调神经磷酸酶 (CaN) 的激活，钙调磷酸酶是一种具有丝氨酸-苏氨酸磷酸酶活性的蛋白质。与 CaN 和激活 T 细胞核因子 (NFAT) 等转录因子相关的信号通路对于骨骼肌发育和快肌纤维重编程为慢肌纤维至关重要。CaN 激活可能会促进肌肉细胞的代谢适应，从而更好地促进胰岛素刺激的葡萄糖转运。胰岛素反应改变的分子机制仍不清楚。CaN/NFAT 通路在调节骨骼肌肥大中的作用比它在胰岛素抵抗发病机制中的作用更容易描述。因此，该领域的未来研究有机会。这篇综述介绍了 CaN/NFAT 信号传导的作用，并表明其与胰岛素抵抗肌肉的关系。