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对氧磷酶1 L55M/Q192R基因多态性与糖尿病大血管病变及糖尿病微血管病变易感性的关联:一项Meta分析。

The Associations between Paraoxonase 1 L55M/Q192R Genetic Polymorphisms and the Susceptibilities of Diabetic Macroangiopathy and Diabetic Microangiopathy: A Meta-Analysis.

作者信息

Wu Chenfang, Wu Diling, Lin Minjie, Zhong Yanjun

机构信息

ICU Center, The Second Xiangya Hospital, Central South University, Furong, Changsha, China.

Clinical Skills Training Center, The Second Xiangya Hospital, Central South University, Furong, Changsha, China.

出版信息

Diabetes Ther. 2018 Aug;9(4):1669-1688. doi: 10.1007/s13300-018-0466-5. Epub 2018 Jul 9.

DOI:10.1007/s13300-018-0466-5
PMID:29987647
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6064588/
Abstract

INTRODUCTION

Plenty of studies have focused on the associations of paraoxonase 1 Q192R and L55M genetic polymorphisms with diabetic macroangiopathy and microangiopathy susceptibility, but these associations remain controversial. Therefore, this meta-analysis was conducted to demonstrate these relationships.

METHODS

Relevant studies published in English or Chinese were identified in PubMed, Embase, Wanfang Database, and CNKI by applying specific inclusion and exclusion criteria. Statistical analyses were performed using the STATA 12.0 statistical software.

RESULTS

25 Case-control studies were included in the meta-analyses: six on the association between paraoxonase 1 L55M genetic polymorphism and diabetic macroangiopathy risk, nine on the association between L55M and diabetic microangiopathy risk, 12 on the association between Q192R and diabetic macroangiopathy risk, and 12 on the association between Q192R and diabetic microangiopathy risk. Paraoxonase 1 L55M genetic polymorphism was significantly associated with diabetic microangiopathy susceptibility in the dominant model [odds ratio (OR) 0.53, 95% confidence interval (CI) 0.33-0.83, P = 0.006], the homozygous model (OR 0.37, 95% CI 0.16-0.86, P = 0.021), the allelic contrast model (OR 0.62, 95% CI 0.43-0.90, P = 0.011), the recessive model (OR 12.04, 95% CI 8.02-18.06, P = 0.000), and the heterozygous model (OR 0.57, 95% CI 0.38-0.85, P = 0.006), but L55M was not significantly associated with macroangiopathy susceptibility. Paraoxonase 1 Q192R genetic polymorphism was significantly associated with diabetic macroangiopathy susceptibility in the homozygous model (OR 1.88, 95% CI 1.06-3.32, P = 0.030), the allelic contrast model (OR 1.31, 95% CI 1.02-1.69, P = 0.038), and the recessive model (OR 1.55, 95% CI 1.11-2.16, P = 0.010), but not in the dominant and heterozygous models. Meanwhile, there was no significant association between paraoxonase 1 Q192R genetic polymorphism and diabetic microangiopathy susceptibility.

CONCLUSION

Paraoxonase 1 L55M and Q192R genetic polymorphisms play important roles in diabetic macroangiopathy and microangiopathy susceptibility. Further well-designed studies based on large samples are needed to confirm these results.

摘要

引言

大量研究聚焦于对氧磷酶1(PON1)Q192R和L55M基因多态性与糖尿病大血管病变及微血管病变易感性之间的关联,但这些关联仍存在争议。因此,开展了此项荟萃分析以阐明这些关系。

方法

通过应用特定的纳入和排除标准,在PubMed、Embase、万方数据库和中国知网中检索以英文或中文发表的相关研究。使用STATA 12.0统计软件进行统计分析。

结果

荟萃分析纳入了25项病例对照研究:6项关于PON1 L55M基因多态性与糖尿病大血管病变风险的关联,9项关于L55M与糖尿病微血管病变风险的关联,12项关于Q192R与糖尿病大血管病变风险的关联,以及12项关于Q192R与糖尿病微血管病变风险的关联。在显性模型中(优势比[OR] 0.53,95%置信区间[CI] 0.33 - 0.83,P = 0.006)、纯合子模型(OR 0.37,95% CI 0.16 - 0.86,P = 0.021)、等位基因对比模型(OR 0.62,95% CI 0.43 - 0.90,P = 0.011)、隐性模型(OR 12.04,95% CI 8.02 - 18.06,P = 0.000)和杂合子模型(OR 0.57,95% CI 0.38 - 0.85,P = 0.006)中,PON1 L55M基因多态性与糖尿病微血管病变易感性显著相关,但L55M与大血管病变易感性无显著关联。在纯合子模型中(OR 1.88,95% CI 1.06 - 3.32,P = 0.030)、等位基因对比模型(OR 1.31,95% CI 1.02 - 1.69,P = 0.038)和隐性模型中(OR 1.55,95% CI 1.11 - 2.16,P = 0.010),PON1 Q192R基因多态性与糖尿病大血管病变易感性显著相关,但在显性和杂合子模型中无此关联。同时,PON1 Q192R基因多态性与糖尿病微血管病变易感性之间无显著关联。

结论

PON1 L55M和Q192R基因多态性在糖尿病大血管病变和微血管病变易感性中起重要作用。需要进一步开展基于大样本的精心设计研究以证实这些结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/82e0db250910/13300_2018_466_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/c93a0eca5985/13300_2018_466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/935370eedcb4/13300_2018_466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/a9124ad954cb/13300_2018_466_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/82e0db250910/13300_2018_466_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/c93a0eca5985/13300_2018_466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/935370eedcb4/13300_2018_466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/a9124ad954cb/13300_2018_466_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9187/6064588/82e0db250910/13300_2018_466_Fig4_HTML.jpg

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