An explanation may be that long-term muscle disuse can lead to muscle atrophy or fibrotic alterations, thereby aggravating muscle insulin resistance[26–28]; TG: long-term abnormal TG levels can compete with glucose, culminating in glucose oxidase utilization disorders, and can release large amounts of free fatty acids to interfere with insulin binding to its receptors, hence abating insulin biological efficacy and aggravating insulin resistance.[29,30] These factors may contribute to T2DM pathogenesis through different mechanisms. This evidence concerns the gene INS and Insulin resistance.