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.