Enhancing effects of anagliptin on myoblast differentiation and the expression of mitochondrial biogenetic factors in C2C12 mouse skeletal muscle cells.
Se Eun HanSu Jin KimYoung Il KimIl Sung Nam-GoongHyo Won JungEun Sook KimPublished in: Clinical and experimental pharmacology & physiology (2020)
To investigate the regulatory effects of anagliptin, a DPP-IV inhibitor used to treat type 2 diabetes mellitus (T2DM), on myoblast differentiation and mitochondrial biogenesis in C2C12 mouse skeletal muscle cells. C2C12 myoblasts were differentiated into myotubes and then treated with anagliptin (10, 25, and 50 μmol/L) for 24 hours. In C2C12 myotubes, anagliptin treatment was significantly increased the expression of MHC, PGC1α, Sirt-1, NRF-1, and TFAM and the phosphorylation of AMPK and ACC in a concentration-dependent manner. Anagliptin also significantly increased the total ATP levels in the myotubes. These results suggest that anagliptin can help prevent skeletal muscle dysfunction in T2DM by promotion of myoblast differentiation and enhancement of energy production via upregulation of mitochondrial biogenetic factors and activation of the AMPK/ACC signalling pathway.
Keyphrases
- skeletal muscle
- oxidative stress
- induced apoptosis
- poor prognosis
- insulin resistance
- cell cycle arrest
- signaling pathway
- glycemic control
- ischemia reperfusion injury
- endoplasmic reticulum stress
- transcription factor
- type diabetes
- cell death
- binding protein
- cell proliferation
- long non coding rna
- cardiovascular disease
- protein kinase
- pi k akt