Myristic acid selectively augments β‐tubulin levels in C2C12 myotubes via diacylglycerol kinase δ

Effective amelioration of type II diabetes requires therapies that increase both glucose uptake activity per cell and skeletal muscle mass. Myristic acid (14:0) increases diacylglycerol kinase (DGK) δ protein levels and enhances glucose uptake in myotubes in a DGKδ‐dependent manner. However, it is still unclear whether myristic acid treatment affects skeletal muscle mass. In this study, we found that myristic acid treatment increased the protein level of β‐tubulin, which constitutes microtubules and is closely related to muscle mass, in C2C12 myotubes but not in the proliferation stage in C2C12 myoblasts. However, lauric (12:0), palmitic (16:0) and oleic (18:1) acids failed to affect DGKδ and β‐tubulin protein levels in C2C12 myotubes. Moreover, knockdown of DGKδ by siRNA significantly inhibited the increased protein level of β‐tubulin in the presence of myristic acid, suggesting that the increase in β‐tubulin protein by myristic acid depends on DGKδ. These results indicate that myristic acid selectively affects β‐tubulin protein levels in C2C12 myotubes via DGKδ, suggesting that this fatty acid improves skeletal muscle mass in addition to increasing glucose uptake activity per cell. Myristic acid (14:0, MA) increases diacylglycerol kinase (DGK) δ protein levels and enhances glucose uptake in myotubes in a DGKδ‐dependent manner. In this study, we found that MA also augments β‐tubulin protein levels through DGKδ in C2C12 myotubes. Because β‐tubulin is closely related to muscle mass, MA may improve both glucose uptake per cell and skeletal muscle mass.