Key result
High glucose reduces PGI2 production and inhibits proliferation in cultured aortic endothelial cells.
Why the study?
Does high glucose concentration inhibit prostacyclin production in cultured bovine aortic endothelial cells?
Does high glucose concentration inhibit prostacyclin production in cultured bovine aortic endothelial cells?
High glucose concentrations directly inhibit prostacyclin production and proliferation in cultured aortic endothelial cells, suggesting a potential mechanism for atherosclerosis pathogenesis in diabetes.
No practice change from bovine cell data; hypothesis-generating for endothelial mechanisms in diabetic atherosclerosis.
A reduction in production of prostacyclin (PGI2) by the cells in the vascular wall may play a role in the pathogenesis of atherosclerosis in diabetic patients. The present study was undertaken to evaluate the effect of glucose on PGI2 production by endothelial cells in vitro. It was shown that PGI2 production by cultured bovine aortic endothelial cells was significantly reduced in the presence of a high concentration of glucose (300 mg/dl) compared with physiological concentrations of glucose (100 mg/dl). In contrast, no reduction in PGI2 production was observed in cells cultured with equimolar mannitol, suggesting that glucose itself, rather than the effect of osmolality, inhibited PGI2 production by cultured endothelial cells. In addition, a high concentration of glucose also inhibited the proliferation of cultured endothelial cells.
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Ono et al. (1988) studied Atherosclerosis in diabetic patients. High concentration of glucose vs. Physiological concentrations of glucose (100 mg/dl) and equimolar mannitol was evaluated on Prostacyclin (PGI2) production and cell proliferation. High concentration of glucose (300 mg/dl) significantly reduced prostacyclin (PGI2) production and inhibited proliferation in cultured bovine aortic endothelial cells compared to physiological levels.
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