2型糖尿病患者IRAK-M变化对胰岛β细胞功能的影响  

Effect of IRAK-M on the functiong of islet βcell in patients with type 2 diabetes mellitus

作　　者：陈胜利 张晓娟[2] 白桂荣 强丹[2] 谢晓敏[2] CHEN Shengli;ZHANG Xiaojuan;BAI Guirong;QIANG Dan;XIE Xiaomin(The Second Affiliated Hospital of Ningxia Medical University,Yinchuan 750001,China;Department of Endocrinology,The First People's Hospital of Yinchuan,Yinchuan 750001,China)

机构地区：[1]宁夏医科大学第二临床医学院,宁夏银川750001 [2]宁夏银川市第一人民医院内分泌科,宁夏银川750001

出　　处：《宁夏医学杂志》2021年第8期697-699,共3页Ningxia Medical Journal

基　　金：宁夏科技厅中央引导地方科技发展专项项目资助基金(201949);宁夏重点研发计划项目(2020BEG03069)。

摘　　要：目的探讨2型糖尿病患者白介素-1受体相关激酶-M(IRAK-M)变化对胰岛β细胞功能的影响。方法选取18~75岁体检者315例,根据空腹血糖分为糖尿病组(DM组)77例、糖尿病前期组2(P2组)80例、糖尿病前期组1(P1组)89例及正常对照组(NC组)79例。检测IRAK-M、空腹血糖(FPG)、空腹胰岛素(FINS)、糖化血红蛋白(HbA 1C)等,计算胰岛素抵抗指数(HOMA-IR)、胰岛β细胞分泌指数(HOMA-β)并对结果进行分析。结果4组间患者IRAK-M、FINS、HOMA-IR、HOMA-β、HbA 1C差异均有统计学意义(P<0.05);DM组分别与P2组、P1组、NC组比较,IRAK-M、FINS、HOMA-IR、HOMA-β、HbA 1C差异均有统计学意义(P<0.05);IRAK-M与FINS、HbA 1C、HOMA-IR呈负相关性(r=-0.463、-0.577、-0.493),与HOMA-β呈正相关性(r=0.535、0.567,P<0.05)。结论IRAK-M可能通过负向调控Toll样受体(TLRs)信号通路,抑制炎症反应,使机体出现胰岛素抵抗和胰岛素分泌缺陷,从而导致2型糖尿病的发生发展。Objective To investigate the effect of changes of interleukin-1 receptor-associated kinase-M(IRAK-M)on the function of islet β cells in type 2 diabetes mellitus.Methods 315 persons aged 18-75 years were selected and divided into diabetes mellitus group(DM group,n=77),pre-diabetes group(PD2 group,n=80),pre-diabetesgroup(PD1 group,n=89)and normal control group(NG group,n=79)according to the fasting blood glucose.IRAK-M,fasting blood glucose(FPG),fasting insulin(FINS),glycated hemoglobin(HbA1c)were detected.The insulin resistance index(HOMA-IR)and islet β cell secretion index(HOMA-β)were calculated and analysed.Results There were significant differences in IRAK-M,FINS,HOMA-IR,HOMA-β and HbA1c among the four groups(P<0.05).IRAK-M,FINS,HOMA-IR,HOMA-β and HbA1C in DM group were significantly higher than those in P2 group,P1 group and NC group(P<0.05).IRAK-M was negatively correlated with FINS,HBAIC,HOMA-IR(r=-0.463,-0.577,-0.493),and positively correlate with HOMA-β(r=0.535,0.567;P<0.05).Conclusion IRAK-M may negatively regulate Toll-like receptor(TLRS)signaling pathway and inhibit inflammatory response,leading to insulin resistance and insulin secretion defect.

关 键 词：2型糖尿病 白细胞介素1受体相关激酶-M 胰岛素抵抗 胰岛Β细胞功能 

分 类 号：R587.1[医药卫生—内分泌]