Abstract
Increasing concentrations of insulin were found to increase transport of radioactive ascorbic acid into fetal bovine heart endothelial cells (FBHE). A linear relationship was found between the log of the insulin concentration (range 0 μU/ml to 400 μU/ml) and the uptake of ascorbic acid quantified as dpm/μg protein. Evidence has accrued which relates ascorbic acid to atherogenesis by its possible effect on preventing the breakdown of the glycosaminoglycan matrix of the intimal layer of the artery. Since insulin was found to increase ascorbic acid uptake, any compound, like glucose, that competes for the carrier mechanism may, if present in high enough concentrations, competitively inhibit ascorbic acid transport into the cell. The hyperglycemia and inadequate insulin production associated with diabetes mellitus may cause an ascorbic acid deficiency within the cell. This deficiency would lead to intimal matrix breakdown with subsequent increase in atherogenesis. The microangiopathies associated with diabetes and with the aging process itself may be related to this mechanism.
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