Endothelial progenitor cell number and colony-forming capacity in overweight and obese adults.
Endothelial progenitor cell number and colony-forming capacity in overweight and obese adults.
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DOI：
10.1038/ijo.2008.262
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发表时间：
2009-02
影响因子：
4.9
通讯作者：
DeSouza, C. A.
中科院分区：
文献类型：
--
作者：
MacEneaney, O. J.;Kushner, E. J.;Van Guilder, G. P.;Greiner, J. J.;Stauffer, B. L.;DeSouza, C. A.
探讨肥胖是否影响内皮祖细胞(EPC)数量和集落形成能力。正常体重、超重和肥胖成年人的横断面研究。67名久坐不动的成年人(年龄45-65岁)：25名正常体重(体重指数≤=25公斤/平方米；12名男性/13名女性)；18名超重(体重指数=25-29.9公斤/平方米；12名男性/6名女性)；24名肥胖(体重指数≥=30公斤/平方米；18名男性/6名女性)。所有受试者均为非吸烟者，且无明显的心脏代谢疾病。采集外周血标本，用流式细胞仪检测外周血中EPC的数量。CD45EPC定义为CD45EPC/−/CD34+/VEGFR-2+/CD133+或CD45EPC/CD34+细胞。采用集落形成单位法测定EPC的体外集落形成能力。肥胖组外周血中−/CD34+/VEGFR-2+/CD133+或CD45−/CD34+细胞数(0.0007±0.0001%；0.050±0.006%)低于超重(0.0016±0.0004%；0.089±0.019%)和正常体重(0.0015±0.0003%；0.082±0.008%)。超重和正常体重组间EPC数无差异。肥胖组(6±1)和超重组(4±1)的EPC集落形成率明显低于正常体重组(9±2)。这些结果表明：1)肥胖者的循环内皮祖细胞数量低于超重和正常体重的成年人；2)超重和肥胖的成年人与正常体重的成年人相比，EPC的集落形成能力减弱。内皮祖细胞数量和功能的受损可能导致肥胖相关的心血管风险。
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 (age 45–65y): 25 normal weight (BMI ≤ 25 kg/m2; 12 males/13 females); 18 overweight (BMI = 25–29.9 kg/m2; 12 males/6 females); and 24 obese (BMI ≥ 30 kg/m2; 18 males/6 females). All subjects 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 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.
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