Effect of cytochalasin B on the uptake of ascorbic acid and glucose by 3T3 fibroblasts: mechanism of impaired ascorbate transport in diabetes.
Hyperglycemia and/or hypoinsulinemia have been found to inhibit L-ascorbic acid cellular transport. The resultant decrease in intracellular ascorbic acid may de-inhibit aryl sulfatase B and increase degradation of sulfated glycosaminoglycans (sGAG). This could lead to a degeneration of the extracellular matrix and result in increased intimal permeability, the initiating event in atherosclerosis. The present studies show that the glucose transport inhibitor cytochalasin B blocked the uptake of 3H-2-deoxy-D-glucose (2.5 mg%) by mouse 3T3 fibroblasts. Cytochalasin B also blocked the uptake of 14C-L-ascorbic acid (1.25 mg%). The results of these studies further support the hypothesis that glucose and ascorbate share a common transport system. This may have important implications concerning the vascular pathology associated with diabetes mellitus.
Fay
M J
MJ
Department of Pharmacology, School of Pharmacy, University of Mississippi, University 38677.
Bush
M J
MJ
Verlangieri
A J
AJ
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D002460:Cell Line; D003571:Cytochalasin B / Q000494:pharmacology*; D003837:Deoxy Sugars / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts
D003837:Deoxy Sugars; D003571:Cytochalasin B; D003847:Deoxyglucose; D001205:Ascorbic Acid