Effect of visfatin on the function of endothelial progenitor cells in high-fat-fed obese rats and investigation of its mechanism of action.

The aim of this study was to study the quantity change of endothelial progenitor cells (EPCs) in obese rats fed a high-fat-diet and to investigate the correlation of EPC numbers with visfatin. The impact of visfatin on the quantity and function of EPCs were further investigated by cell culture methods. Male Wistar rats were fed on either a standard diet (NC group) or a high-fat diet (HF group) for 16 weeks. Serum visfatin, Lee's index and the protein expression of visfatin in viseral adipose tissue (VAT) were determined. Bone marrow EPCs in 2 groups of rats were isolated, cultured and counted. EPCs primarily cultured from control male Wistar rats were treated with different concentrations of visfatin. The quantity, migration and adhesion capacity of EPCs were evaluated after visfatin treatment. Protein expression of nuclear factor-κB (NF-κB) in the nuclei of EPCs was detected. After 16-week feeding, body weight, serum visfatin, Lee's index and visfatin contents in viseral fat were significantly increased in the HF group compared with NC group (P<0.01 or P<0.05). The quantity of EPCs primarily cultured from rats in HF group was lower than that in NC group. The quantity of EPCs was negatively correlated with serum visfatin levels, visceral fat, fasting blood glucose, HOMA-IR, total cholesterol, triglyceride and body weight (P<0.01). In cultured EPCs, visfatin significantly increased the protein expression of NF-κB in EPC nuclei (P<0.01) in a dose-dependent manner. The migration and adhesion capacity were impaired by visfatin treatment (P<0.01). In conclusion, bone marrow-derived EPCs decrease in number and have impaired migration and adhesion function in high-fat-fed obese rats, along with increased serum visfatin and protein contents in VAT. Visfatin may have an impact on the quantity and function of EPCs through the NF-κB pathway.