RESUMO
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.
RESUMO
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.