首页> 中文期刊> 《中国医学科学院学报》 >2型糖尿病患者T细胞亚群与血糖水平及胰岛素分泌的关系

2型糖尿病患者T细胞亚群与血糖水平及胰岛素分泌的关系

             

摘要

目的 研究2型糖尿病患者T细胞亚群与血糖水平及早相胰岛素分泌之间的关系.方法 以新诊断的78例2型糖尿病(DM)患者、60例葡萄糖耐量异常(IGT)患者和60名健康对照者(NC)为研究对象,分别给予口服葡萄糖耐量试验( OGTT)和胰岛素兴奋试验(IRT),检测糖化血红蛋白(HbAl c)、体重指数(BMI),流式细胞仪监测T细胞亚群(CD4+、CD8+)和自然杀伤(NK)细胞活性,采用葡萄糖负荷后30min的净增胰岛索与净增葡萄糖比值(⊿I30/⊿ G30)评估早相胰岛素分泌功能.结果 与NC组比较,IGT组和DM组患者的CD4+、CD4 +/CD8+、NK细胞活性和⊿I30/⊿G30显著降低,HbA1c和CD8+显著升高(P<0.05或P<0.01);与IGT组相比,DM组患者的CD4+、NK细胞活性、⊿I30/⊿G30显著降低,空腹血糖(FBG)和HbA1c显著升高(P均<0.05),CD8+、CD4+/CD8+差异无统计学意义(P均>0.05).CD4+与FBG(r=-0.213)和HbA1c(r=-0.386)呈显著负相关(P均<0.05),与⊿I30/⊿G30呈显著正相关(r=0.174,P<0.05).逐步回归分析结果显示,CD4+与HbA1c和⊿I30/⊿G30独立相关.结论 2型糖尿病患者细胞免疫存在异常,T细胞亚群的紊乱与血糖升高和胰岛β细胞早相分泌功能缺陷有关.%Objective To explore the relationship between the T cell subsets and glucose level and first-phase insulin secretion function in patients with type 2 diabetes mellitus (T2DM). Methods We determined the oral glucose tolerance ( OGTT) , insulin release test (IRT) , body mass index ( BM1) , glycohemo-globin Al c (HbAl c) , T lymphocyte subsets ( CD4+ , CD8+ ) , and activity of natural kill ( NK) cell and △l30/ △G30 in 78 newly diagnosed T2DM patients, 60 impaired glucose tolerance (IGT) patients, and 60 normal controls. Results DM and IGT patients had significantly lower levels of CD4+ , CD4 VCD8 + ratio, activity of NK cell, and △I30/ A G30 and significantly higher levels of HbAl c and CD8 + compared with normal controls ( all P< 0.05) . Patients in DM group had significantly lower level of CD4 + , △ I30/Zl G30 and significantly higher levels of FBG and HbAlc compared with IGT group. There was no significant difference in terms of CD8 +, CD4+CD8+ ratio, and activity of NK cell between IGT and DM groups, whereas CD4+ T cells were negatively correlated with FBG and HbAlc and positively with △ I30/△C30 . Multipul regression stepwise analysis showed that CD4+ was independently associated with HbAlc and △I30/△G30. Conclusion T2DM patients tends lo have disorders in cellular immunity, which is correlated with blood glucose level and the insulin secretion function.

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