Stimulatory effect of isoferulic acid on α1A-adrenoceptor to increase glucose uptake into cultured myoblast C2C12 cell of mice

In an attempt to elucidate the effect of isoferulic acid on α1-adrenoceptor (AR), the myoblast C2C12 cells of mice were employed to investigate the change of glucose uptake in the present study. Isoferulic acid enhanced the uptake of radioactive glucose into C2C12 cells in a concentration-dependent manner, which were abolished by pretreatment with prazosin. Effect of isoferulic acid on α1-AR was further characterized using the displacement of [3H]YM617 binding in C2C12 cells. The radioactive glucose uptake increasing action of isoferulic acid was abolished by tamsulosin or WB 4101 at concentration sufficient to block α1A-adrenoceptor (α1A-AR) but it was not modified by chlorethylclonidine (CEC) at the concentration sufficient to abolish α1B-AR. An activation of α1A-AR by isoferulic acid in C2C12 cells can thus be considered. Pharmacological inhibition of phospholipase C (PLC) by U73312 resulted in a concentration-dependent reduction of isoferulic acid-stimulated glucose uptake in C2C12 cells. This inhibition by U73122 was specific because the inactive congener, U73343, failed to modify the action of isoferulic acid. Also, chelerythrine and GF 109203X diminished the action of isoferulic acid at concentration sufficient to inhibit the activity of protein kinase C (PKC). The obtained data suggest that an activation of α1A-AR by isoferulic acid may increase the glucose uptake via PLC–PKC pathway in C2C12 cells.