High glucose concentrations stimulate human monocyte sodium/hydrogen exchanger activity and modulate atherosclerosis-related functions.

In the present study, the effect of high (20 mM) glucose concentrations on human monocyte sodium/hydrogen exchanger (NHE1) activity, scavenger receptor CD36 expression, cell adhesion, and cell migration have been investigated. Incubation with high glucose concentrations caused an increase in NHE1 activity, as estimated by internal pH and sodium-uptake measurements. This effect was specific for glucose, since it was not observed when monocytes were incubated in the presence of 20 mM of galactose, fructose, or mannitol. In addition, the activation of sodium uptake was inhibited by ethylisopropyl amiloride (EIPA), phloretine and cytochalasine B, and calphostin C. High glucose concentrations also increased the expression of CD36 receptors on the surface of monocytes and positively influenced monocyte migration and adhesion to laminin. EIPA added together with glucose counteracted these effects. The data of the present study suggest that a high glucose concentration can influence atherosclerosis-related monocyte functions via NHE1 activation.