论文部分内容阅读
目的了解优降糖继发失效的２型糖尿病患者对不同胰岛素刺激物的反应，探讨线粒体基因第３２４３位点Ａ→Ｇ突变在优降糖继发失效病因学的作用。方法对２８例优降糖继发失效患者进行胰升糖素刺激试验及标准馒头餐试验，并筛查线粒体ＤＮＡ第３２４３位点Ａ→Ｇ的突变。结果失效组与有效组比较，空腹及胰升糖素刺激后６分钟血清Ｃ肽水平没有显著差别，但餐后１、２、３小时胰岛素、Ｃ肽值明显降低（Ｐ均＜０．０１），高峰值在餐后２小时（胰岛素１３８６±７０２ｐｍｏｌ／Ｌ对２５２７±１２５３ｐｍｏｌ／Ｌ，Ｃ肽１５９８±４５４ｐｍｏｌ／Ｌ对２７０６±９４３ｐｍｏｌ／Ｌ，Ｐ均＜０．０１）。聚合酶链反应（ＰＣＲ）结合ＡｐａＩ酶切的方法未在２８例继发失效患者中检出外周血线粒体ＤＮＡ第３２４３位点Ａ→Ｇ的突变。结论在优降糖继发失效的２型糖尿病患者，以胰升糖素刺激试验评估的胰岛素分泌功能无明显减退，但胰岛β细胞选择性对葡萄糖刺激胰岛素分泌的反应下降；线粒体基因３２４３位点Ａ→Ｇ突变不是优降糖继发失效的常见原因。
Objective To investigate the response of type 2 diabetic patients with glyburide secondary failure to different insulin stimuli and to explore the role of the A → G mutation at position 3243 of mitochondrial DNA in secondary etiology of glyburide. Methods 28 cases of patients with secondary hypoglycemic failure were treated with glucagon stimulation test and standard steamed bread meal test, and the mitochondrial DNA at the 3243 A → G mutation was screened. Results Compared with the effective group, there was no significant difference in the level of serum C-peptide 6 minutes after fasting and glucagon stimulation, but the levels of insulin and C-peptide decreased significantly after 1, 2 and 3 hours after meal (all P <0.01) , With a peak at 2 hours postprandial (insulin 1386 ± 702 pmol / L vs. 2527 ± 1253 pmol / L, C peptide 1598 ± 454 pmol / L vs 2706 ± 943 pmol / L, P both <0.01). Polymerase chain reaction (PCR) combined with ApaI digestion method was not detected in 28 cases of secondary failure of mitochondrial DNA in peripheral blood, the first 3243 A → G mutations. Conclusions In type 2 diabetic patients with secondary hypoglycemic failure, insulin secretion assessed by glucagon stimulating test showed no significant decrease, but selective response of pancreatic β cells decreased glucose-stimulated insulin secretion. Mitochondrial gene 3243 A → G mutation is not a common cause of secondary failure of glyburide.