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目的探讨血管紧张素转换酶（ＡＣＥ）基因插入／缺失（Ｉ／Ｄ）多态性与Ⅱ型糖尿病（ＮＩＤＤＭ）及其肾脏合并症发病的关系。方法应用聚合酶链反应（ＰＣＲ）扩增技术检测了１０９例ＮＩＤＤＭ患者及１５５例健康对照者的ＡＣＥ基因Ｉ／Ｄ多态性。结果位于ＡＣＥ基因第１６内含子的Ｉ／Ｄ多态性经ＰＣＲ技术扩增后分为三种基因型：纯合子缺失型（ＤＤ），纯合子插入型（Ｉ）及杂合子插入／缺失型（ＩＤ）。１０９例ＮＩＤＤＭ患者与１５５例正常对照组之间基因型及等位基因频率差异均无显著意义；ＮＩＤＤＭ合并肾病者（ＤＮ）的基因型与未合并肾病者无显著性差异，但等位基因则有显著性差异（Ｄ、Ｉ等位基因为０４５和０５５对０３０和０７０）（Ｐ＜００２）；ＮＩＤＤＭ病程≤１年即伴有肾病者与病程≥５年仍无肾病者比较，ＤＤ型及Ｄ等位基因均显著高于无肾病组（Ｐ均＜００５），后者以Ｉ型及Ｉ等位基因占绝对优势。结论ＡＣＥ基因多态性与ＮＩＤＤＭ发病无关，而与其肾脏合并症则明显相关，ＤＤ型是ＤＮ的易感基因，而Ｉ型则为其保护基因。
Objective To investigate the relationship between angiotensin converting enzyme (ACE) gene insertion / deletion (I / D) polymorphism and type 2 diabetes mellitus (NIDDM) and its incidence of renal complications. Methods ACE gene I / D polymorphism was detected by polymerase chain reaction (PCR) amplification in 109 patients with NIDDM and 155 healthy controls. Results The I / D polymorphism at the 16th intron of ACE gene was amplified by PCR and divided into three genotypes: homozygous deletion (DD), homozygous insertion (I) and heterozygous insertion / deletion Type (ID). There was no significant difference in genotype and allele frequencies between 109 cases of NIDDM and 155 cases of normal controls. There was no significant difference in genotype between NIDDM with nephropathy (DN) and no nephropathy, but allele There was a significant difference (D, I alleles 0 45 and 0 55 pairs 0 30 and 0 70) (P <0 02); NIDDM duration ≤ 1 year with renal disease and duration ≥ 5 Compared with those without nephropathy, the DD and D alleles were significantly higher than those without nephropathy (all P <005), while those with type I and I alleles had the absolute advantage. Conclusion ACE gene polymorphism has nothing to do with the incidence of NIDDM, but with renal complications, DD is the susceptibility gene of DN, and I is its protective gene.