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Enhancing effects of anagliptin on myoblast differentiation and the expression of mitochondrial biogenetic factors in C2C12 mouse skeletal muscle cells
Author(s) -
Han Se Eun,
Kim Su Jin,
Kim Young Il,
NamGoong Il Sung,
Jung Hyo Won,
Kim Eun Sook
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13255
Subject(s) - c2c12 , myogenesis , mitochondrial biogenesis , myocyte , skeletal muscle , microbiology and biotechnology , ampk , myosin , chemistry , mitochondrion , biology , endocrinology , phosphorylation , protein kinase a
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, PGC1 α , 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.