These results suggest that OJ alleviates obesity-induced muscle atrophy by activating the PI3K-AKT-mTOR/FoxO3a pathway, upregulating CPT1b, and downregulating SREBP-1c, thereby enhancing protein synthesis pathways, suppressing proteolysis, and improving lipid metabolism in skeletal muscle. The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.