Abstract
Background/Aims. Sexual differences exist in endothelial progenitor cells (EPCs), and various cardiovascular risk factors are associated with the preservation of endothelial function in premenopausal women. However, it is unclear whether differences in endothelial function and circulating EPCs exist between overweight premenopausal women and age-matched men. Methods. We compared EPC counting and functions in normal-weight and overweight premenopausal women and men, evaluated endothelial function in each group, and detected the expression of the guanosine triphosphate cyclohydrolase I (GTPCH I) pathway. Results. The number of EPCs was lower in the male group than in the female group, regardless of normal-weight or overweight status, and there was no significant difference between the different weight groups among females or males. Endothelial function and EPC migration and proliferation were preserved in overweight premenopausal women compared with overweight men as were nitric oxide (NO) levels in plasma and secreted by EPCs. Endothelial function, the circulating EPC population, and NO levels were not different between normal-weight and overweight premenopausal women. Flow-mediated dilatation was significantly correlated with EPC function, plasma NO levels, and EPC-secreted NO. Conclusions. This investigation provides the first evidence for sex-based differences in EPC activity and endothelial function in overweight middle-aged individuals; these differences are associated with alterations in NO production and may partly occur through downregulation of the GTPCH I pathway. The present results provide new insights into the mechanism underlying the preserved endothelial function in overweight premenopausal women and may uncover a potential therapeutic target for endothelial repair in overweight population.
Highlights
Epidemiological studies have shown an increasing prevalence of overweight and obesity in adults worldwide, resulting in a high incidence of cardiovascular disease (CVD), such as coronary heart disease and peripheral arteriosclerosis, and constituting a major health threat [1, 2].Body mass index (BMI, calculated as weight in kilograms/2), a reasonable and practical estimate of general adiposity, is used routinely in the diagnosis of Cardiology Research and Practice overweight and obesity
flow-mediated endothelium-dependent vasodilatation (FMD) was preserved in normal-weight and overweight premenopausal women compared with normalweight and overweight men (P < 0.05 and P < 0.05, respectively) but was decreased in overweight men compared with normal-weight men (P < 0.05); there was no difference in FMD between normal-weight and overweight premenopausal women in our study (P > 0.05). ere were no differences in blood pressure or in fasting plasma glucose (FPG), low-density lipoprotein (LDL), total cholesterol (TC), triglycerides (TG), or high-density lipoprotein (HDL) levels among the four groups (P > 0.05)
Discussion e results of this study showed that Endothelial progenitor cells (EPCs) migratory activity and proliferative potential were preserved in overweight premenopausal women compared with overweight men, consistent with the alterations in endothelial function
Summary
Shaohong Wu ,1 Hao He ,2 Ge-Xiu Liu ,3 Xiao-Peng Li ,4 Shun Yao ,5 Huan-Xing Su, Xiang Li ,7 Zi Ren, Haitao Zeng ,8 and Jinli Liao 9. Sexual differences exist in endothelial progenitor cells (EPCs), and various cardiovascular risk factors are associated with the preservation of endothelial function in premenopausal women. It is unclear whether differences in endothelial function and circulating EPCs exist between overweight premenopausal women and age-matched men. We compared EPC counting and functions in normal-weight and overweight premenopausal women and men, evaluated endothelial function in each group, and detected the expression of the guanosine triphosphate cyclohydrolase I (GTPCH I) pathway. Endothelial function and EPC migration and proliferation were preserved in overweight premenopausal women compared with overweight men as were nitric oxide (NO) levels in plasma and secreted by EPCs. Endothelial function, the circulating EPC population, and NO levels were not different between normal-weight and overweight premenopausal women. Is investigation provides the first evidence for sex-based differences in EPC activity and endothelial function in overweight middle-aged individuals; these differences are associated with alterations in NO production and may partly occur through downregulation of the GTPCH I pathway. e present results provide new insights into the mechanism underlying the preserved endothelial function in overweight premenopausal women and may uncover a potential therapeutic target for endothelial repair in overweight population
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