The results highlighted that the lipidome of the rats was modified by the luseogliflozin’s treatment with decreased intramuscular fatty acid metabolism markers (such as Scd1, Fasn, and Elovl6) and genetic muscle atrophy-related transcripts (such as Mstn, Trim63, Fbxo32, and Foxo1) expression that has not only decreased the mice’s visceral fat accumulation but also increased the soleus muscles weight of the treated mice. The gene discussed is FOXO1; the disease is muscle atrophy.