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. SUBJECTS: Sixty-seven sedentary adults (age 45–65y): 25 normal weight (BMI ≤ 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 ≥ 30 kg/m(2); 18 males/6 females). All subjects 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 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.