延边地区朝鲜族胰岛素受体底物1基因Gly972Arg多态性与2型糖尿病的相关性

[目的]研究延边地区朝鲜族人群胰岛素受体底物l(IRS-1)基因Gly972Arg多态性与2型糖尿病的关系.[方法]应用聚合酶链反应-单链构象多态性分析延边地区298人的IRS-1基因Gly972Arg突变位点基因型,其中2型糖尿病组为89人(朝鲜族42人,汉族47人),正常对照组为209人(朝鲜族120人,汉族89人).[结果]正常对照组中汉族的IRS-1基因Gly972Arg多态性的突变率(即G/A基因型频率)高于朝鲜族(3.37%,2.50%),但差异无统计学意义(χ2=1.39,P=0.709);2型糖尿病组中朝鲜族的G/A基因型频率略高于汉族(4.76%,2.13%),但差异亦无统计学意义(χ2=1.107,P=0.744).[结论]IRS-1基因Gly972Arg多态性可能不是延边地区朝鲜族人群2型糖尿病的重要遗传因素.     

胰岛素受体底物1和2基因多态性与抗精神病药源性体重增加的关联分析

目的：探讨胰岛素受体底物1（IRS—1）和2（IRS-2）基因多态性与抗精神病药源性体重增加的关联性。方法：采用PCR—RFLP法检测抗精神病药源性体重增加精神分裂症患者（86例）和健康对照者（96名）的胰岛素受体底物1（Gly972Arg）和胰岛素受体底物2（Gly1057Asp）单核苷酸多态性。比较两组间基因型和等位基因的频率。结果：（1）IRS-1基因的Arg972／Arg972变异的4例仅发现于患者组,频率为4．60％。（2）对于IRS-2基因,Asp1057等位基因频率病例组显著高于对照组（Z=2．10,P〈0．05）,而Gly1057等位基因（Z=2．10,P〈0．05）和Gly1057／Gly1057基因型频率（Z=1．96,P〈0．05）是病例组显著低于对照组。结论：IRS基因多态性关联于抗精神病药源性体重增加,尤其是IRS-2基因。这可能与肥胖相关胰岛素代谢紊乱有关。     

中国汉族迟发型2型糖尿病与胰高血糖素受体基因Gly40Ser突变的关系

目的：探讨胰高血糖素受体（GCG－R）基因外显子2Gly40Ser突变是否与中国人迟发型非胰岛素依赖型糖尿病（non-insulin-dependent diabetes millitus,NIDDM)相关。方法：选择湖南地区汉族人NIDDM患者82例及正常对照136例,应用聚合酶链反应－限制性片段长度多态分析方法,检测Gly40Ser突变。结果：受检者均不存在Gly40Ser的错义突变。结论：该突变不是引起中国人NIDDM的重要遗传因素。文献报道白种人CGC－R基因Gly40Ser与NIDDM相关,本研究提示此种相关有种族差异性。     

中国汉族迟发型2型糖尿病与胰高血糖素受体基因Gly40Ser突变的关系

目的 :探讨胰高血糖素受体 (GCG R)基因外显子 2Gly40Ser突变是否与中国人迟发型非胰岛素依赖型糖尿病 (non -insulin -dependentdiabetesmillitus,NIDDM)相关。方法 :选择湖南地区汉族人NIDDM患者 82例及正常对照136例 ,应用聚合酶链反应———限制性片段长度多态分析方法 ,检测Gly40Ser突变。结果 :受检者均不存在Gly40Ser的错义突变。结论 :该突变不是引起中国人NIDDM的重要遗传因素。文献报道白种人GCG R基因Cly40Ser与NIDDM相关 ,本研究提示此种相关有种族差异性     

胰岛素受体底物-2基因多态性在多囊卵巢综合征中的初步研究

目的探讨多囊卵巢综合征(PCOS)患者与对照组胰岛素受体底物-2(IRS-2)基因密码子1057甘氨酸/天冬氨酸(1057Gly/Asp)多态性的不同.方法应用PCR酶切方法(PCR-RFLP)检测60例PCOS患者和30例对照的IRS-2基因密码子1057G/A的等位基因分布及基因频率.结果IRS-2基因型分布及基因频率在两组间差异有显著性,两组间空腹胰岛素、胰岛素抵抗指数(HOMA1-IR)、促黄体生成素/促卵泡刺激素(LH/FSH)、游离睾酮(T)的差异也有显著性.结论IRS-2基因1057G/A多态性在PCOS患者和对照组之间差异有显著性,可能是PCOS患者发生胰岛素抵抗(IR)的机制之一,也可能是PCOS的易感基因.     

变性高效液相色谱检测IRS-2基因3′-非翻译区单核苷酸多态性

目的：探讨变性高效液相色谱(DHPLC)在胰岛素受体底物-2(IRS-2)基因3′-非翻译区单核苷酸多态性(SNP)检测中的应用。方法：采用聚合酶链式反应(PCR)，DHPLC，单链构象多态性(SSCP)和DNA序列分析对30例正常对照和30例2型糖尿病患者IRS-2基因3′-非翻译区进行SNP和突变检测。结果：PCR-DHPLC检测出4例PCR-SSCP分析未能发现的2型糖尿病患者IRS-2基因3′-非翻译区的SNP，并得到测序验证。结论：DHPLC是一种快速、自动化程度高、操作简单、检测片段长、准确率高的SNP检测技术。它为进一步研究IRS-2基因3′-非翻译区的变异与2型糖尿病的关系奠定了基础。     

胰岛素受体底物-2基因多态性在多囊卵巢综合征中的初步研究

目的：探讨多囊卵巢综合征（PCOS）患者与对照组胰岛素受体底物-2（IRS-2）基因密码子1057甘氨酸/天冬氨酸（1057Gly/Asp）多态性的不同。方法：应用PCR酶切方法（PCR-RFLP）检测60例PCOS患者和30例对照的IRS-2基因密码子1057G/A的等位基因分布及基因频率。结果：IRS-2基因型分布及基因频率在两组间差异有显著性,两组间空腹胰岛素、胰岛素抵抗指数（HOMA1-IR）、促黄体生成素/促卵泡刺激素（LH/FSH）、游离睾酮（T）的差异也有显著性。结论：IRS-2基因1057G/A多态性在PCOS患者和对照组之间差异有显著性,可能是PCOS患者发生胰岛素抵抗（IR）的机制之一,也可能是PCOS的易感基因。     

Toll样受体基因多态性与中国江苏地区汉族人群和白种人群炎症性肠病的相关性

目的 探讨Toll样受体基因多态性与中国人群和白种人群炎症性肠病(IBD)易感性的相关性.方法 采用聚合酶链反应.限制性片段长度多态性方法,检测113例江苏地区汉族IBD患者与120名正常对照者TLR2基因Arg677Trp、Arg753Glu,TLR4基因Asp299Gly、Thr399Ile及TLR9基因1237T/C基因型,分析这些Toll样受体基因位点的多态性与IBD发病的相关性;对白种人群中TLR4Asp299Gly、Thr399Ile两个单核苷酸多态性位点的多态性与IBD易感性及临床表型的关系进行荟萃分析.结果 在所检测的IBD患者和正常对照者中有2例溃疡性结肠炎(UC)患者、1例克罗恩病(CD)患者及1名正常对照者存在TLR91237T/C杂合突变(CD:P=0.361,UC:P=0.569),差异无统计学意义,在IBD患者及正常人群中均未发现TLR2基因Arg677Trp、Arg753Glu,TLR4基因Asp299Gly、Thr399Ile突变型;荟萃分析发现白种人CD和UC患者TLR4基因Asp299Gly(CD:OR=1.29,95%CI:1.08～1.54,P=0.004;UC:OR=1.28,95%CI:1.08～1.51,P:0.004)、Thr399Ile(CD:OR=1.37,95%CI:1.12～1.68,P=0.002;UC:OR=1.46,95%CI:1.13～1.88,P=0.003)突变发生率均明显高于正常对照者,Asp299Gly多态性与CD临床表型无明显相关性.结论 未发现TLR2基因Arg677Trp、Arg753Glu,TLR4基因Asp299Gly、Thr399Ile及TLR9基因1237T/C多态性与江苏地区汉族人群IBD的易感性相关;荟萃分析显示,TLR4基因Asp299Gly、Thr399Ile多态性与白种人CD和UC发病相关,IBD的遗传易感性具有种族差异性.     

变性高效液相色谱检测IRS-2基因3''''-非翻译区单核苷酸多态性

目的探讨变性高效液相色谱(DHPLC)在胰岛素受体底物-2(IRS-2)基因3′-非翻译区单核苷酸多态性(SNP)检测中的应用.方法采用聚合酶链式反应(PCR),DHPLC,单链构象多态性(SSCP)和DNA序列分析对30例正常对照和30例2型糖尿病患者IRS-2基因3′-非翻译区进行SNP和突变检测.结果PCR - DHPLC检测出4例PCR-SSCP分析未能发现的2型糖尿病患者IRS-2基因3′-非翻译区的SNP,并得到测序验证.结论DHPLC是一种快速、自动化程度高、操作简单、检测片段长、准确率高的SNP检测技术.它为进一步研究IRS-2基因3′-非翻译区的变异与2型糖尿病的关系奠定了基础.     

β1肾上腺素受体Arg389Gly基因多态性与静息心率的关系研究

目的探讨β1肾上腺素受体(β1-AR)Arg389Gly基因多态性与静息心率的关系。方法选取2002年1月—2003年1月就诊于我院心内科门诊的高血压患者171例和血压正常者124例,采用听诊法检测受试者坐位静息心率,采用聚合酶链反应-限制酶片段长度多态性(PCR-RFLP)技术分析高血压受试者和血压正常受试者β1-ARArg389Gly基因多态性。结果高血压受试者Arg/Arg、Arg/Gly、Gly/Gly基因型频率分别为59.06%(101/171)、35.09%(60/171)、5.85%(10/171),血压正常受试者分别为43.55%(54/124)、45.97%(57/124)、10.48%(13/124)。高血压受试者与血压正常受试者3种基因型频率分布差异有统计学意义(χ2=7.420,P<0.05)。高血压患受试者Arg/Arg基因型静息心率最高(78±7)次/min,Gly/Gly基因型静息心率最低(72±8)次/min;Arg/Gly基因型静息心率居中(76±6)次/min,差异有统计学意义(F=5.599,P=0.004)。3种不同基因型男性和女性高血压受试者平均静息心率比较,差异均有统计学意义(F=6.600、5.010,P=0.002、0.009);3种不同基因型正常血压受试者无平均静息心率比较,差异无统计学意义(F=1.424,P=0.260)。结论静息心率与基因型有关,高血压受试者的β1-AR Arg389Gly基因多态性与静息心率相关;健康受试者β1-AR Arg389Gly基因多态性与静息心率无关。     

Lack of association between the insulin receptor substrates-1 Gly972Arg polymorphism and type-2 diabetes mellitus among Saudis from Eastern Saudi Arabia

Objectives:

To investigate the association between the insulin receptor substrate-1 (IRS1) Gly972Arg polymorphism and type-2 diabetes mellitus (T2DM) among Saudis from Eastern Saudi Arabia.

Methods:

This study was conducted between May and December 2014 at King Fahad Hospital of the University, Al-Khobar, Kingdom of Saudi Arabia. In a case-control study design, a total of 143 subjects (age range: 35-73 years) comprising 74 healthy controls and 69 patients with T2DM were examined. Blood samples were collected from subjects and subjected to genomic DNA extraction and chemical analysis. The IRS1 Gly972Arg polymorphism was then genotyped using the standard polymerase chain reaction-restriction fragment length polymorphism technique.

Results:

Eight out of 74 (10.8%) of the control group carried at least one copy of the mutated allele. The frequency (8.7%) of the IRS1 variant was also found in the diabetic group. Logistic regression analysis showed an adjusted odds ratio of 1.04, 95% confidence interval 0.28 - 3.95, and a p-value of 0.94.

Conclusion:

We failed to find any association between the IRS1 Gly972Arg polymorphism and T2DM.Diabetes mellitus (DM) is a major medical and public health concern worldwide. In 2014, it has been estimated that there were 382 million sufferers of diabetes worldwide.1 The prevalence of diabetes in Saudi Arabia is 23.9%, which is among the highest in the gulf area and the world.1,2 Type-2 diabetes mellitus (T2DM) represents approximately 90-95% of all diabetes cases.3 Type-2 diabetes mellitus is characterized by high blood glucose due to the inability of body cells to respond to insulin, a phenomenon known as insulin resistance.4 The genetic factors behind the insulin resistance are not well-understood and are under intensive research. Insulin is a metabolically important peptide hormone secreted from ß-cells of the pancreas in response to high blood glucose. Insulin signaling starts with binding of the insulin molecule to its cognate membrane insulin receptor (IR). This binding triggers conformational changes in the juxtamembrane intracellular region of the receptor causing autophosphorylation of certain tyrosine residues. The activated receptor then phosphorylates and activates a family of intracellular effector proteins known as insulin receptor substrates 1 to 4 (IRS-1 to 4).5 These activated proteins then interact with the regulatory subunit (p85) of the enzyme phosphatidylinositol (PI) 3-kinase causing glucose transporter-4 (Glut-4) translocation to the cell membrane to increase glucose uptake.6 In this signaling pathway, IRS1 seems to play a major role as suggested by IRS1 knockout mice studies.7 Additionally, several polymorphisms in the IRS1 gene were associated with insulin resistance, obesity, and T2DM.8,9 The single nucleotide polymorphism (SNP) (rs1801278) in the IRS1 gene causing an amino acid substitution where glycine (GGG) is replaced by arginine (AGG) at codon 972 was first described by Almind et al.10 It is the most widely studied candidate of the IRS1 gene variants by testing its association with insulin resistance and T2DM.11 However, the association of this polymorphism with the development of T2DM has not been consistent around the world. In a study focusing on Mexican participants, Burguete-Garcia et al8 found that the IRS1 Gly972Arg variant was significantly associated with T2DM. Another study that also focused on Mexican population similarly found a significant association between Gly972Arg variant and genetic susceptibility to T2DM.12 A study on Indian population from Hyderabad also reported significant association with T2DM.13 A meta-analysis study conducted in 2009 of 30 studies had shown that there was no significant association between the IRS1 Gly972Arg variant and T2DM.11 In addition, previous studies also reported no association between the IRS1 Gly972Arg polymorphism and T2DM.14-18 There is no report on the frequency of this polymorphism and its association with T2DM in the Eastern Province of Saudi Arabia. Thus, the aim of the current work is to examine the association between the IRS1 Gly972Arg polymorphism with T2DM among Saudis.     

Association between peroxisome proliferator-activated receptor-γ coactivator-1α gene polymorphisms and type 2 diabetes in southern Chinese population: role of altered interaction with myocyte enhancer factor 2C

Background Some single nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α gene have been reported to be associated with type 2 diabetes in different populations, and studies on Chinese patients yielded controversial results. The objective of this case-control study was to explore the relationship between SNPs of PGC-1α and type 2 diabetes in the southern Chinese population and to determine whether the common variants: Gly482Ser and Thr394Thr, in the PGC-1α gene have any impacts on interaction with myocyte enhancer factor (MEF) 2C.Methods The SNPs in all exons of the PGC-1α gene was investigated in 50 type 2 diabetic patients using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and direct sequencing. Thereafter, 263 type 2 diabetic patients and 282 healthy controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). A bacterial two-hybrid system and site-directed mutagenesis were used to investigate whether Gly482Ser and Thr394Thr variants in the PGC-1α gene alter the interaction with MEF2C.Results Three frequent SNPs (Thr394Thr, Gly482Ser and Thr528Thr) were found in exons of the PGC-1α gene. Only the Gly482Ser variant had a different distribution between diabetic patients and healthy subjects, with the 482Ser allele more frequent in patients than in controls (40.1% vs 29.3%, P&lt;0.01). Even in controls, the 482Ser(A) carriers were more likely to have higher levels of total cholesterol and low-density lipoprotein cholesterol than the 482Gly(G) carriers. The 394A-482G-528A haplotype was associated with protection from diabetes, while the 394A-482A-528A was associated with the susceptibility to diabetes. The bacterial two-hybrid system and site-directed mutagenesis revealed that the 482Ser variant was less efficient than the 482Gly variant to interact with MEF2C, whereas the 394Thr (A) had a synergic effect on the interaction between 482Ser variant and MEF2C.Conclusions The results suggested that the 482Ser variant of PGC-1α conferred the susceptibility to type 2 diabetes in the southern Chinese population. The underlying mechanism may be attributable, at least in part, to the altered interaction between the different variants (Gly482Ser, Thr394Thr) in the PGC-1α gene and MEF2C.     

Association of GYS1 and β3-AR gene with postprandial hyperglycemia and ser um uric acid in type 2 diabetes mellitus

Objective To determine the relationships of Met416Val and XbaI polymorphism of muscle glycogen synthase (GYS1) gene and Trg64Arg variant of the β3-adrenergic-receptor (β3-AR) gene with type 2 diabetes mellitus (DM) and its intermediate phenotypes in the Chinese population. Methods Polymerase chain reaction-oligonucleotide ligation assay and restriction fragment length polymorphism assay were used to evaluate the GYS1 and β3-AR gene polymorphisms in 102 pairs of case-control Chinese spouses.Results Subjects with Met416Val variant had a significantly higher 2-hour post-glucose level than subjects without this variant had in diabetic group (P=0.032).The Met416Val polymorphism of GYS1 gene was not significantly associated with the risk of type 2 DM (adjusted OR=1.67; 95% CI: 0.73-3.81, P=0.223). Subjects with Trp64Arg variant had a significantly higher serum uric acid level than subjects without this variant had in diabetic group (P=0.034). The combination of BMI and Arg64 allele carrier of the β3-AR gene increased the diabetic risk over four-fold (adjusted OR=4.00; 95%CI: 1.53-10.45, P=0.005).Conclusions In the Chinese population, Met416Val polymorphism is identified in a subgroup of diabetic subjects with high 2-hour post-glucose.It will explain why some diabetic patients appear to be genetically predisposed to developing high postpradial glucose level.The presence of the Arg64 allele in the β3-AR gene may predispose patients to higher serum uric acid level.     

MODY6基因在家族性2型糖尿病发病中的作用

目的探讨NeumD1／BETA2基因在中国北方地区家族性2型糖尿病发病中的作用。方法用PCR和单链构像多态性技术（PCR—SSCP）对188名2型糖尿病家系的先证者NeuroD1／BETA2基因的编码区序列进行突变筛查,对发现的变异进行DNA序列分析证实,并对130名正常人进行基因分型,比较两组的等位基因、基因型频率和临床表型的差别。结果在NeuroD1／BETA2基因的筛查中发现多态性A45T和突变Gly12Arg,其中A45T在病人和正常人中的频率分别是19．7％和10％,差异有统计学意义（P〈0．05）,在正常对照组发现携带A45T的个体比A45A个体有较低的B细胞功能。仅在一个家系中发现Gly12Arg突变,且与糖尿病共分离。在正常人未筛查到此突变。结论NeumD1／BETA2基因的多态性A45T在中国人群的家族性2型糖尿病相关,NeuroD1／BETA2基因或附近的基因与中国人群家族性2型糖尿病的发病中起一定的作用,而Gly12Arg可能是导致糖尿病的突变。     

Ghrelin基因Arg51Gln、Leu72Met多态性与甘肃回族2型糖尿病及血脂的关系

目的 探讨Ghrelin基因Arg51Gl(G-A)和Leu72Met(C-A)多态性与甘肃回族2型糖尿病及血脂的关系.方法 采用聚合酶链反应-限制性片段长度多态性方法检测甘肃回族人251例(2型糖尿病138例,对照组113例),Ghrelin基因Arg51Gln和Leu72Met各基因型,并测定其相关临床、生化指标....     

武汉地区汉人2型糖尿病合并肥胖及非肥胖患者Lepr基因变异的对比性分析

目的研究瘦素受体基因GIN223Arg与2型糖尿病合并肥胖的关系。方法运用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法测定无亲缘关系且具有完整资料的武汉地区汉人351例(其中2型糖尿病合并肥胖组131例、2型糖尿病非肥胖组148例、正常对照组72例)。结果①2型糖尿病合并肥胖组基因型AA、AG、GG(分别为0.398、0.480和0.122)与2型糖尿病非肥胖组的(0.196、0.223和0.581)和正常对照组分别为(0.208、0.264和0.528)比较有显著性差异(P<0.01)。②2型糖尿病合并肥胖组等位基因分布频率A、G分别为0.642及0.358,与非肥胖组及正常对照组比较有统计学意义(P<0.01)。③应用多重回归分析(NominalRegression)2型糖尿病与临床各变量的关系发现,2型糖尿病GIN223Arg变异(由A突变G)与BMI、收缩压、舒张压(分别为P=0.001,P=0.032,P=0.037)相关。结论瘦素受体基因GIN223Arg变异可能与2型糖尿病合并肥胖和高血压相关。     

PIK3R2基因错义变异所致MPPH综合征I型患儿遗传学分析

目的：总结1例罕见的巨脑畸形-多小脑回-多指（趾）畸形-脑积水（MPPH）综合征Ⅰ型患儿的临床特点及基因检测结果。方法：回顾性总结2021 年1月在温州医科大学附属第一医院新生儿科确诊的1例MPPH I型患儿的临床表现、影像学检查和基因检测结果等病例资料。并通过文献复习,分析和总结国内外已报道的MPPH I型综合征病例的临床特征及遗传学特点。同时对患儿进行全外显子组检测,对候选变异用Sanger测序进行家系验证。结果：先证者携带PIK3R2 基因c.1117（p.Gly373Arg）杂合错义变异,国内既往未见报道,其父母未携带相同变异。相关文献报道的16例MPPH I型患儿主要表现为不同程度的脑积水、巨脑畸形、癫痫发作、多指（趾）畸形、发育迟缓及智力发育障碍。共报道了3个基因突变位点,其中p.Gly373Arg杂合变异最多（14例）,罕见变异包括p.Leu401Pro变异1例和p.Asp557His变异1例。结论：PIK3R2 基因c.1117G＞A（p.Gly373Arg）杂合错义变异可能是该患儿发生MPPH I的原因,脑积水考虑与该综合征相关,其母亲再次怀孕时需接受产前诊断。     

2型糖尿病患者胰高糖素受体基因Gly40Ser突变的检测

为探讨中国人２型糖尿病与胰高糖素受体（ＧＣＧ－Ｒ）基因４０号密码子的错义突变（Ｇｌｙ４０Ｓｅｒ）是否存在关联,运用聚合酶链反应－限制性片段长度多态性（ＰＣＲ－ＲＦＬ－Ｐ）分析方法在１６０例无亲缘关系之中国云南昆明地区汉族人（２型糖尿病患者１００例,健康对照者６０例）中对ＧＣＧ－Ｒ基因Ｇｌｙ４０Ｓｅｒ突变进行了检测。结果显示：所有研究对象中无论是２型糖尿病患者还是健康对照者均无一例存在ＧＣＧ－Ｒ基因     

PON 1 192 Gln/Arg基因多态性与2型糖尿病并发冠心病风险的Meta分析

目的 采用Meta分析法综合评价对氧磷脂酶1 192Gln/Arg （PON1 Q192R）基因多态性与2型糖尿病并发冠心病的相关性。方法 截至2017年3月,在Pubmed、Embase、Web of Science、中国知网、万方等数据库可检索到的已发表论文,由两位评价者根据纳入排除标准独立筛选和评价文献质量。采用RevMan5.3和Stata12.0软件进行Meta分析,计算合并比值比（odds ratio,OR）及其95%可信区间（confidence intervals,CI）,并进行敏感度分析和发表偏倚评估。结果 9个病例-对照研究纳入本研究,包括1353例病例组（2型糖尿病并发冠心病组）和1360例对照组（单纯2型糖尿病组）。Meta分析结果显示,与单纯糖尿病组比较,5种基因模型均提示PON1Gln/Arg基因多态性和2型糖尿病并发冠心病显著相关[等位基因模型：R vs Q,OR=1.50,95% CI （1.23~1.83）;纯合子基因模型：RR vs QQ,OR=2.28,95% CI （1.52~3.42）;杂合子基因模型：QR vs QQ,OR=1.42,95% CI （1.18~1.71）;显性基因模型：RR+RQ vs QQ,OR=1.59,95% CI （1.33~1.89）;隐性基因模型：RR vs RQ+QQ,OR=1.74,95% CI （1.24~2.45）]。人口学的亚组分析提示,对氧磷脂酶1 192Gln/Arg基因多态性与2型糖尿病并发冠心病的相关性在亚洲和高加索人群中比较,差异无统计学意义。敏感度结果显示,合并的结果是稳定可靠的,漏斗图检测未发现发表偏倚。结论 PON1 192Gln/Arg基因多态性与2型糖尿病并发冠心病风险呈显著相关性,携带R等位基因的2型糖尿病人群相对于携带Q等位基因者,可能更易并发冠心病。