Objective : By observing the changes of interleukin-22 ( IL-22) ，signal transduction and transcriptional activator 3 (STAT3) ，fasting blood glucose ( FBG) and fasting insulin ( FINS) of rats under the circumstance of chronic intermittent hypoxia and reoxygenation，to explore the role of IL-22 / STAT3 pathway in insulin resistance in- duced by chronic intermittent hypoxia． Methods : 4 SD rats were randomly divided into control group (NC group) and intermittent hypoxia group ( CIH group) ，with 12 rats in each group．NC group was placed in normoxia environment for 12 weeks，while CIH group was first given intermittent hypoxia for 8 weeks and then resumed normoxia feeding until 12 weeks．FBG，FINS，IL-22 and p-STAT3 / STAT3 levels were measured at baseline，week 8 and week 12 in both groups，and insulin resistance index (HOMA-IR) was calculated．The differences between the two groups were compared. Results : ① There was no significant difference of the observation indexes between the two groups at baseline (P＞0. 05) ．At 8 weeks，the levels of FBG，FINS and HOMA-IR in CIH group were higher than those in NC group (P＜0. 05) ，and the levels of IL-22 were lower than those in NC group (P ＜0. 05) ．p-STAT3 / STAT3 showed a decreasing trend，but not statistically significant．At 4 weeks of reoxygenation，there were no significant differences in FBG，FINS，HOMA-IR and IL-22 levels between the two groups (P ＞0. 05 ) ．p-STAT3 / STAT3 in CIH group was significantly higher than that in NC group ( P ＜0. 05 ) . ② Spearman rank correlation analysis showed that HOMA-IR was negatively correlated with IL-22 and p-STAT3 / STAT3 ( all P ＜0. 05) ． Conclusion Chronic intermittent hypoxia can inhibit the expression of IL-22 / STAT3 signaling pathway，IL-22 / STAT3 signaling pathway may mediate insulin resistance induced by chronic intermittent hypoxia.

Objective : To investigate the role of endoplasmic reticulum stress in hepatic insulin resistance induced by intermittent hypoxia in rats． Methods : Twenty-four SD rats were randomly divided into control group ( NC group) and intermittent hypoxia group ( CIH group) ．The NC group was placed in a normoxia environment for 12 weeks，and the CIH group was given intermittent hypoxia for 8 weeks，and then returned to normoxia until the 12th week．In both groups，fasting blood glucose (FBG) ，fasting insulin (FINS) ，and liver inositol-requiring enzyme- 1 α(IRE1 α) ，X-box binding protein 1s(XBP1s) ，forkhead box transcription factor O1 (FoxO1) ，activating transcription factor-6(ATF6) ，cAMP-response element binding protein( CREB) ，CREB-regulated transcription coacti- vator-2( CRTC2) ，double-stranded RNA-dependent protein kinase-like ER kinase ( PERK) ，eukaryotic initiation factor 2 α(eIF2 α) ，protein kinase B ( AKT) ，phosphoenolpyruvate carboxykinase ( PEPCK) ，glucose-6-phosphat- ase( G6Pase) mRNA were measured at baseline，week 8，and week 12 . Results : There was no significant differ- ence in each observation index between the two groups at baseline ; at 8 weeks，the levels of FBG，FINS and the mRNA levels of IRE1α , XBP1s，ATF6，PERK，eIF2 α , PEPCK and G6Pase in the CIH group were higher than those in the NC group (P＜0. 05) ，while the mRNA levels of CREB，CRTC2 and AKT were lower than those in the NC group (P＜0. 05) ; at 12 weeks，there was no significant difference in each observation index between the two groups．Pearson correlation analysis showed(8th week of intermittent hypoxia group) : homeostasis model as- sessment-insulin resistance(HOMA-IR) was positively correlated with FoxO1，CREB，CRTC2 and PERK，eIF2 α mRNA levels (r = 0. 172，0. 595，0. 183，0. 702，0. 608 ; P＜0. 05) while it was negatively correlated with IRE1α , XBP1s，ATF6，AKT mRNA levels (r = －0. 422 ，－0. 327 ，－0. 309 ，－0. 399 ; P＜0. 05) ． Conclusion Intermittent hypoxia can lead to insulin resistance，and endoplasmic reticulum stress may mediate this effect.