Figure 2.

TRPV1 activation increases PGC-1α expression and mitochondrial biogenesis in a Ca²⁺-dependent manner. (A) Immunoblot of PGC-1α in C2C12 myotubes treated with capsaicin (100 nM) in the presence or absence of the TRPV1 inhibitor iRTX (1 μM) or the intracellular Ca²⁺ chelator BAPTA (10 μM). (B, C) Protein expression of genes involved in fatty acid oxidation, glycolysis (B) and mitochondrial respiration (C) in myotubes treated with capsaicin (100 nM) in the presence or absence of iRTX (1 μM). (D, E) Mitochondrial content (D) and ATP production (E) in myotubes. C2C12 cells were treated with capsaicin (100 nM) in the presence or absence of iRTX (1 μM) or BAPTA (10 μM) for 24 h. Data are means ± S.E.M. for three independent experiments. Con, control; Cap, capsaicin. ^*P < 0.05, ^**P < 0.01 vs Con. ^#P < 0.05, ^##P < 0.01 vs Cap.