MacEneaney O J, Kushner E J, Van Guilder G P, Greiner J J, Stauffer B L, DeSouza C A
Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, USA.
Int J Obes (Lond). 2009 Feb;33(2):219-25. doi: 10.1038/ijo.2008.262. Epub 2008 Dec 16.
To investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity.
Cross-sectional study of normal weight, overweight and obese adult humans.
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.
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.
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.
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.
研究肥胖是否会影响内皮祖细胞（EPC）数量及集落形成能力。
对正常体重、超重和肥胖成年人群进行横断面研究。
67名久坐不动的成年人（年龄45 - 65岁）：25名正常体重者（体重指数（BMI）≤25 kg/m²；12名男性/13名女性）；18名超重者（BMI = 25 - 29.9 kg/m²；12名男性/6名女性）；24名肥胖者（BMI≥30 kg/m²；18名男性/6名女性）。所有参与者均不吸烟且无明显的心脏代谢疾病。
采集外周血样本，通过流式细胞术评估循环EPC数量。假定的EPC定义为CD45(-)/CD34(+)/VEGFR - 2(+)/CD133(+)或CD45(-)/CD34(+)细胞。使用集落形成单位（CFU）测定法在体外测量EPC集落形成能力。
与超重（0.0016±0.0004%；0.089±0.019%）和正常体重（0.0015±0.0003%；0.082±0.008%）的成年人相比，肥胖成年人中循环假定EPC数量（CD45(-)/CD34(+)/VEGFR - 2(+)/CD133(+)或CD45(-)/CD34(+)细胞）更低（P<0.05）。超重和正常体重组之间的EPC数量无差异。与正常体重（9±2）的成年人相比，肥胖（6±1）和超重（4±1）成年人的EPC集落形成明显减少。
这些结果表明：（1）与超重和正常体重成年人相比，肥胖成年人中循环EPC数量更低；（2）与正常体重成年人相比，超重和肥胖成年人的EPC集落形成能力减弱。EPC数量和功能的损害可能导致与肥胖相关的心血管风险。
