Abstract 1010: Impaired Number and Function of Circulating Endothelial Progenitor Cells in Patients with Morbid Obesity
Aims: Morbid Obesity (MO) is an increasing global health problem associated with high CVD morbidity & mortality. Traditional CVD risk factors can only partly explain why life expectancy is diminished by 12 years in MO patients (pts). Since reduced endothelial progenitor cells (EPC) were recently found to predict CVD death & events, low EPC in MO pts may contribute to the increased CVD mortality. We studied EPC in MO pts before & after weight loss.
Methods: 35 pts with MO (BMI: 46±7 kg/m2) were studied before weight loss surgery in comparison with 35 controls (CO) (BMI: 23±3 kg/m2) & 35 pts with massive weight loss 2 years after bariatric surgery (BMI: 31±7 kg/m2). Circulating progenitor cells (CPC, CD34+/133+), endothelial progenitor cells (EPC, CD34+/133+/309+) and activated EPC (actEPC, CD34+/133+/309+/31+) were enumerated by FACS. EPC/CPC ratio, actEPC/EPC ratio and concentrations of fasting MCP-1, IL-18, hsCRP & OPG were determined.
Results: CPC, EPC and actEPC were drastically reduced in MO pts compared to CO. CPC, EPC and actEPC were significantly higher in pts presenting with a mean weight loss of 34±17 kg, but did not reach the numbers of CO. The reduction of EPC and actEPC was significantly associated with BMI, insulin resistance (fasting insulin & glucose, 2-hour insulin & glucose, HOMA-IR), and markers of inflammation (hsCRP, MCP-1 & IL-18). CPC were most strongly related to BMI (R=−0.465, p<0.001) in univariate fashion, EPC to HOMA-IR (R=−0.635, p<0.001) and actEPC to IL-18 (R=−0.465, p<0.001).
Conclusion: The novel finding of this study is a significant impairment of EPC in MO pts. Marked weight loss induced by bariatric surgery resulted in a significant increase of CPC, EPC, actEPC and the respective ratios. In addition, the reported reduced CVD mortality of MO pts after weight loss could also be explained - at least in part - by the increase of EPC and especially the four-fold increase in activated EPC, both assumed to have a critical role in vascular repair mechanism.