Endothelial progenitor cell number and colony-forming capacity in overweight and obese adults.

Objective: To investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity.
Design: Cross-sectional study of normal weight, overweight and obese adult humans.
Participants: Sixty-seven sedentary adults (aged 45-65 years): 25 normal weight (body mass index (BMI) <or=25 kg/m(2); 12 males/13 females); 18 overweight (BMI=25-29.9 kg/m(2); 12 males/6 females); and 24 obese (BMI >or=30 kg/m(2); 18 males/6 females). All participants were non-smokers and free of overt cardiometabolic disease.
Measurements: Peripheral blood samples were collected and circulating EPC number was assessed by flow cytometry. Putative EPCs were defined as CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells. EPC colony-forming capacity was measured in vitro using a colony-forming unit (CFU) assay.
Results: Number of circulating putative EPCs (either CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells) was lower (P<0.05) in obese (0.0007+/-0.0001%; 0.050+/-0.006%) compared with overweight (0.0016+/-0.0004%; 0.089+/-0.019%) and normal weight (0.0015+/-0.0003%; 0.082+/-0.008%) adults. There were no differences in EPC number between the overweight and normal weight groups. EPC colony formation was significantly less in the obese (6+/-1) and overweight (4+/-1) compared with normal weight (9+/-2) adults.
Conclusion: These results indicate that: (1) the number of circulating EPCs is lower in obese compared with overweight and normal weight adults; and (2) EPC colony-forming capacity is blunted in overweight and obese adults compared with normal weight adults. Impairments in EPC number and function may contribute to adiposity-related cardiovascular risk.