Glucose inhibits replication of cultured human endothelial cells.
Diabetes is an important risk factor for atherosclerosis but the mechanism of the risk is unknown. As endothelial injury is considered to be an early event in the development of atherosclerosis, the effect of glucose on endothelial cell replication was studied. Concentrations of glucose of 11.2, 16.8 and 22.4 mmol/l inhibited DNA synthesis in cultured human umbilical venous endothelial cells by 8.1 +/- 10.8, 24.3 +/- 8.8 and 30.9 +/- 7.4%, respectively. Glucose also inhibited the proliferative response of endothelial cells to experimental wounds in the cell layer. Sorbitol (22.4 mmol/l) inhibited endothelial cell DNA synthesis by 50 +/- 13.6%, but mannitol (22.4 mmol/l) inhibited DNA synthesis by only 3 +/- 24.3%. It is suggested that in diabetic subjects, high blood glucose levels may cause endothelial injury, or inhibit its repair, and hence allow the exposure of the arterial media to plasma and its constituents.
D002455:Cell Division / Q000187:drug effects*; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D004727:Endothelium / Q000166:cytology* / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D013012:Sorbitol / Q000494:pharmacology; D014470:Umbilical Cord / Q000166:cytology
D013012:Sorbitol; D004247:DNA; D005947:Glucose