The effects of glucose on ascorbic acid uptake in heart endothelial cells: possible pathogenesis of diabetic angiopathies.
Glucose in concentrations of 20 mg% (or greater) significantly inhibited 14C-labelled ascorbic acid (1.25 mg%) uptake in endothelial cells in the presence of insulin (1600 microU/ml). The absence of insulin also significantly reduced ascorbic acid uptake. Furthermore, this reduction could be exacerbated by glucose (40, 160 mg%) but not equimolar concentrations of fructose. Increased ascorbic acid concentrations (two-fold) in the absence of insulin (1) significantly enhanced uptake, and (2) reversed the inhibition of glucose. These findings support earlier reports that ascorbic acid uptake into the cell may be compromised by decreased insulin and/or increased extracellular glucose levels. Since previous animal studies have correlated experimental ascorbic acid deficiencies with atherogenic processes (presumably by altering glycosaminoglycan metabolism), the postulation that the "diabetic condition" (low insulin, hyperglycemia) accelerates the cellular changes leading to atherosclerosis by impairing ascorbic acid uptake into the vascular endothelium, may now be supported.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured; D003925:Diabetic Angiopathies / Q000209:etiology*; D004727:Endothelium / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*
D007328:Insulin; D005947:Glucose; D001205:Ascorbic Acid