Enhancing effects of anagliptin on myoblast differentiation and the expression of mitochondrial biogenetic factors in C2C12 mouse skeletal muscle cells. (4th February 2020)

• Record Type: Journal Article
• Authors: Han, Se Eun; Kim, Su Jin; Kim, Young Il; Nam‐Goong, Il Sung; Jung, Hyo Won; Kim, Eun Sook
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 47:Number 5(2020)
• Page Start: 903
• Page End: 906
• Publication Date: 2020-02-04
• Subjects: anagliptin -- C2C12 myoblast -- mitochondrial biogenesis -- myotube differentiation -- skeletal muscle; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.13255
• Languages: English
• ISSNs: 0305-1870

Abstract

Abstract: 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.