APMCG-1 normalizes muscle capacity in T2DM zebrafish
The main causes of insulin resistance include abnormal fat metabolism, abnormal fat distribution and excessive accumulation. The body weight of APMCG-1-treated zebrafish was significantly decreased compared with that of the model group (Fig. 5A). According to the determination of swimming endurance, it was found that APMCG-1 enhanced swimming endurance compared with the model group (Fig. 5B). The FBG, INS, T-CHO, TG, FFA and MG of zebrafish in the APMCG-1-treated group significantly decreased, and MG was significantly increased, indicating that APMCG-1 improved the symptoms of insulin resistance in type 2 diabetic zebrafish (Fig. 5C). Meanwhile, the levels of SOD, GSH-PX and CAT levels increased, and that of MDA, TNF-ɑ and IL-6 decreased in the APMCG-1 group, demonstrating that APMCG-1 improved the oxidant-induced muscle injury (Fig. 5D). In the control group, the heart and skeletal muscle structure were complete and the muscle fibers were arranged neatly. In the model group, muscle fibers were disordered and broken. Compared with the model group, APMCG-1 alleviated the pathological damage of heart and skeletal muscle and muscle fiber breakage in type 2 diabetic zebrafish (Fig. 5E, 5F). The results of IHC showed that APMCG-1 could also increase the expression of AKT in skeletal muscle tissue (Fig. 5G). The cells of zebrafish in the control group showed normal size, high density and less apoptosis. In the model group, the number of apoptotic cells were increased and showed sparse. Whereas, the apoptosis of cells in zebrafish treated with APMCG-1 were gradually decreased (Fig. 5H, 5I). Altogether, in vivo results confirmed that APMCG-1 treatment significantly protects cardiomyocytes and skeletal myoblasts in type 2 diabetes.