Abstract: Objective To determine levels of nuclear factor (NF)-κB, interleukin (IL)-10, and visfatin in adipocytes treated by different degrees of intermittent hypoxia (IH), and to investigate the mechanism of IH leading to insulin resistance (IR). Methods The cell model of intermittent hypoxia/re-oxygenation (IH/ROX) in obstructive sleep apnea (OSA) was established. Differentiation mature 3T3- L1 adipocytes, were randomly divided into 10 groups including four differentfrequency intermittent hypoxia groups（IH1-4, fixed intermittent hypoxia scheme for 1.5% O2 45 s and then re-oxygen 21% O2 for 2 min 15 s, 4 min 15 s, 5 min 45 s and 8 min 45 s, 60 times circulation), and their normal oxygen control groups (SC 1-4, instead each IH group 1.5% O2 to 21% O2, the rest groups were treated as same as IH group), continuous hypoxia group (CH, 10% O2 for 6 h) and normal oxygen control group (CC, 21%O2 for 6 h). ELISA method was used to determine the levels of IL- 10 and visfatin in the supematant of adipocytes. Western blot method was used to determine the protein levels of NF-κB p65 and visfatin. Real-time PCR method was used to determine the mRNA levels of IL-10 and visfatin. Results The protein and mRNA expressions of IL-10 were significantly lower in IH group and CH group than those of control groups (P＜ 0.01). The levels of NF-κB p65 protein were significantly increased in IH group and CH group than those of control group. The protein and mRNA expressions of visfatin were significantly higher in IH1, IH2 and CH groups than those of control group (P＜ 0.01). Conclusion As a prominent feature of OSA pathophysiology, IH may take part in insulin resistance of OSA patients by abnormally secreting NF-κB, IL-10 and visfatin in adipocytes.

Key words: sleep apnea, obstructive, intermittent hypoxia, insulin resistance, NF-kappa B, nicotinamide phosphoribo syltransferase, interleukin-10, visfatin