Endothelial plasma membrane is a glucocorticoid-regulated barrier for the uptake of glucose into the cell.
The effect of glucose concentrations and hormones on glucose consumption, lactate, pyruvate, sorbitol and fructose formation of porcine aortic endothelial cells and human umbilical vein endothelial cells has been investigated. Endothelial cells have a high glycolytic activity which is saturated far below physiologic blood glucose levels (KM apparent less than 1 mmol/l). Glucocorticoids reduce glucose catabolism as a function of their concentration. Insulin, adrenaline, triiodothyronine and glucagon do not influence glucose consumption. Studies with the non-metabolizable analogue 3-O-methyl-D-glucose revealed that glucocorticoids slow down glucose transport into the endothelial cell. The passage of glucose through the cell membrane is the rate-limiting step of glucose utilization. Consequently, the intracellular glucose level is independent of the ambient glucose concentration and endothelial cells do not accumulate sorbitol under hyperglycaemic conditions since the affinity of aldose reductase for glucose is low.
D019325:3-O-Methylglucose; D000818:Animals; D001011:Aorta / Q000166:cytology*; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004727:Endothelium / Q000166:cytology; D005934:Glucagon / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D008757:Methylglucosides / Q000494:pharmacology; D013012:Sorbitol / Q000032:analysis / Q000378:metabolism; D013552:Swine; D014471:Umbilical Veins / Q000166:cytology*
D007328:Insulin; D008757:Methylglucosides; D019325:3-O-Methylglucose; D013012:Sorbitol; D003907:Dexamethasone; D005934:Glucagon; D005947:Glucose