Myo-inositol enhances the proliferation of human endothelial cells in culture but fails to prevent the delay induced by high glucose

Metabolism: Clinical and Experimental
M Lorenzi, S Toledo

Abstract

Evidence is accumulating, indicating that the abnormal metabolic milieu of diabetes might interfere with orderly replication of some cellular systems and in vitro studies point to a causal contribution of elevated glucose. We had previously shown that human umbilical vein endothelial cells cultured in 20 mmol/L glucose are delayed in achieving saturation density primarily as a consequence of decreased cellular proliferation. We have now addressed whether depletion of myo-inositol--a prevailing consequence of hyperglycemia in other tissues and overcome by provision of supplemental inositol--might play a role in the observed replicative abnormality. Control cultures (5 mmol/L glucose) displayed a dose-dependent response to myo-inositol supplementation that was maximal at concentrations (40 mumol/L) matching physiologic serum levels. The increment in cell number was (mean +/- SD) 141 +/- 20% of control (P less than 0.001), and saturation density was achieved at a cell number 160% higher than in nonsupplemented cultures. Thymidine incorporation and cell cycle studies documented that myo-inositol increased the number of cells cycle studies documented that myo-inositol increased the number of cells engaged in DNA synthesis. These eff...Continue Reading

References

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