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妊娠期糖尿病与2型糖尿病之间的遗传关联

The genetic interface between gestational diabetes and type 2 diabetes.

作者信息

Konig Manige, Shuldiner Alan R

机构信息

Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

出版信息

J Matern Fetal Neonatal Med. 2012 Jan;25(1):36-40. doi: 10.3109/14767058.2012.626926. Epub 2011 Dec 7.

DOI:10.3109/14767058.2012.626926
PMID:22145702
Abstract

OBJECTIVE

Although the Western diet and lifestyle has contributed to an increase in the prevalence of gestational diabetes (GDM) worldwide, genetic predisposition also plays an important role. This article reviews the current state of knowledge regarding the genetic interface between type 2 diabetes (T2D) and GDM.

METHODS

Review of the current literature on genetics of T2D and GDM.

RESULTS

Maturity Onset Diabetes of the Young (MODY) due to glucokinase mutations may account for as much as 5% of GDM patients. Knowledge of both maternal and fetal genotypes may be useful for individualizing glycemic goals during pregnancy in families harboring these mutations. Of the 38 common T2D susceptibility variants identified to date, several are also associated with GDM. Presumably, these mutations increase GDM risk through decreased ability of β-cells to compensate for the insulin resistance associated with pregnancy. The effect of these alleles on risk for GDM is modest (odds ratios (odds ratio (OR)~1.1-1.6); thus, they individually are poorly predictive.

CONCLUSIONS

Future studies must concentrate on understanding the biological underpinnings of known T2D risk alleles and the discovery of new alleles for both GDM and T2D. These insights may lead to more effective strategies for preventing and treating GDM.

摘要

目的

尽管西方饮食和生活方式导致全球妊娠期糖尿病(GDM)患病率上升,但遗传易感性也起着重要作用。本文综述了关于2型糖尿病(T2D)与GDM之间遗传关联的当前知识状况。

方法

回顾当前关于T2D和GDM遗传学的文献。

结果

由葡萄糖激酶突变引起的青年发病型成年糖尿病(MODY)可能占GDM患者的5%。对于携带这些突变的家庭,了解母亲和胎儿的基因型可能有助于在孕期确定个体化的血糖目标。在迄今确定的38个常见T2D易感变异中,有几个也与GDM相关。据推测,这些突变通过降低β细胞补偿与妊娠相关的胰岛素抵抗的能力来增加GDM风险。这些等位基因对GDM风险的影响较小(比值比(OR)约为1.1 - 1.6);因此,它们单独的预测能力较差。(注:原文中“odds ratio (OR)~1.1-1.6”多了一个括号,翻译时保留了原文表述问题)

结论

未来的研究必须专注于理解已知T2D风险等位基因的生物学基础,以及发现GDM和T2D的新等位基因。这些见解可能会带来预防和治疗GDM的更有效策略。

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