Attenuated endothelial function is associated with decreased endothelial progenitor cells and nitric oxide in premenopausal diabetic women.

Abstract

Previous studies have demonstrated that the deleterious effect of diabetes mellitus (DM) on the risk of cardiovascular disease also occurs in premenopausal women, in spite of their relatively high estrogen levels; however, the underlying mechanism remains unclear. The present study aimed to investigate the sex‑related differences in circulating endothelial progenitor cells (EPCs) in a relatively young population with type 2 DM (T2DM) and its underlying mechanism. The number and functional activity of circulating EPCs, and vascular endothelial function assessed using flow‑mediated dilation (FMD), were compared in premenopausal women and age‑matched men with or without T2DM. Nitric oxide (NO) in the plasma or NO secreted by EPCs was also measured. The number and activity of circulating EPCs, and NO levels in the plasma or culture medium, were lower in premenopausal women with T2DM compared with those without T2DM. In addition, the number and activity of circulating EPCs and NO levels were decreased in men with T2DM compared with in age‑matched premenopausal women with T2DM. FMD was positively correlated with the number and activity of circulating EPCs, and NO levels. In conclusion, DM in premenopausal women may significantly impair the repair capability of EPCs and lead to endothelial dysfunction, which may be associated with reduced NO production. In patients with both DM and normal glucose tolerance, sex‑related differences of EPCs are presented in a young population.