To understand how MH regulates the lipid metabolism in the heart, we examined GSK‐3β, which has been previously associated with obese animal models and obese human T2D skeletal muscle insulin resistance.22 Our results showed that the phosphorylation of GSK‐3β was decreased in the T2D‐induced diabetic cardiomyocytes, whereas the MH treatment restored the level of p‐GSK‐3β in T2D‐induced diabetic cardiomyocytes at the 3‐month time point (Figure 4B). Here, GSK3B is linked to Insulin resistance.