title: Stimulatory effect of isoferulic acid on alpha1A-adrenoceptor to increase glucose uptake into cultured myoblast C2C12 cell of mice.
abstract: In an attempt to elucidate the effect of isoferulic acid on alpha1-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 alpha1-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 alpha1A-adrenoceptor (alpha1A-AR) but it was not modified by chlorethylclonidine (CEC) at the concentration sufficient to abolish alpha1B-AR. An activation of alpha1A-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 U73112 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 alpha1A-AR by isoferulic acid may increase the glucose uptake via PLC-PKC pathway in C2C12 cells.
authors.affiliation: Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
authors.forename: I M
authors.initials: IM
authors.lastname: Liu
authors.forename: C C
authors.initials: CC
authors.lastname: Tsai
authors.forename: T Y
authors.initials: TY
authors.lastname: Lai
authors.forename: J T
authors.initials: JT
authors.lastname: Cheng
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D002934:Cinnamates / Q000494:pharmacology*; D003847:Deoxyglucose / Q000037:antagonists & inhibitors / Q000493:pharmacokinetics; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D051379:Mice; D018482:Muscle, Skeletal / Q000166:cytology / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects* / Q000502:physiology*; D013449:Sulfonamides / Q000378:metabolism; D000077409:Tamsulosin; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors
chemical_list: D000317:Adrenergic alpha-Antagonists; D002934:Cinnamates; D004791:Enzyme Inhibitors; D011942:Receptors, Adrenergic, alpha; D013449:Sulfonamides; D003847:Deoxyglucose; D011493:Protein Kinase C; D010738:Type C Phospholipases; D000077409:Tamsulosin; D005947:Glucose; C008180:isoferulic acid