肾移植术后糖尿病的发病机制

Pathogenesis of Post-transplantation Diabetes Mellitus in 40 Renal Transplantation Recipients

目的研究肾移植受者移植术后糖尿病(PTDM)的发病机制。方法根据葡萄糖耐量试验结果将40例肾移植受者分为正常糖耐量(NGT)组(n=10)、糖代谢失常(IFG+IGT)组(n=16)和PTDM组(n=14),采用稳态模型评估法(HOMA)评估β细胞功能和胰岛素抵抗。结果3组间的钙离子神经蛋白抑制剂血药谷浓度和前1个月糖皮质激素总用量差异均无统计学意义(P>0.05);IGT+IFG组和PTDM组的胰岛素分泌曲线下面积和HOMA胰岛素抵抗指数均明显高于NGT组(P均<0.05),PTDM组的胰岛素初期分泌指数和HOMAβ细胞功能指数均明显低于NGT组和IGT+IFG组(P均<0.05)。结论胰岛素抵抗和胰岛β细胞功能减低可能是PTDM发病的关键,胰岛素抵抗贯穿于PTDM发生发展的全过程。

Objective To explore pathogenesis of post-transplantation diabetes mellitus （PTDM） in renal transplantation recipients. Methods A total of 40 renal transplantation recipients were divided into three groups based on oral glucose tolerance test results： normal glucose tolerance （NGT） group （n = 10 ）, impaired fasting glycaemia ＋ impaired glucose tolerance （ IFG ＋ IGT） group （ n = 16 ）, and FrDM group （ n = 14）. Insulin resistance （IR） and β cell function were assessed by homeostasis model. Results The differences of the immunosuppressive agents used in these groups were not statistically significant （ P 〉 0.05 ） . Compared with NGT group, insulin area under curve and homeostasis model assessment-insulin resistance index were significantly higher in IGT ＋ IFG group and PTDM group （ P 〈 0.05 ）. Compared with NGT group and IGT ＋ IPG group, insulin secretion index at 30 min and homeostasis model assessment-insulin secretion index were significantly lower in PTDM group （P 〈 0.05 ）. Conclusion Insulin resistance and β-cell dysfunction may play a key role in the pathogenesis of PTDM.