What Can Diabetes-Associated Genetic Variation in TCF7L2 Teach Us About the Pathogenesis of Type 2 Diabetes?

被引：9

作者：

Adams, J. D. ^{[1
]}

Vella, Adrian ^{[1
]}

机构：

[1] Mayo Clin, Coll Med, Endocrine Res Unit, Dept Endocrinol Diabet & Nutr, 200 First St SW,Rm 5-194 Joseph, Rochester, MN 55905 USA

来源：

METABOLIC SYNDROME AND RELATED DISORDERS | 2018年 / 16卷 / 08期

基金：

美国国家卫生研究院;

关键词：

common genetic variation; insulin secretion; insulin action; type; 2; diabetes; PATHWAY EFFECTOR TCF7L2; INSULIN-SECRETION; BETA-CATENIN; SUSCEPTIBILITY GENE; GLUCOSE-METABOLISM; PROGLUCAGON GENE; CELL FUNCTION; WNT; POLYMORPHISMS; EXPRESSION;

D O I：

10.1089/met.2018.0024

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Type 2 diabetes mellitus (T2DM) is a polygenic metabolic disorder characterized by hyperglycemia occurring as a result of impaired insulin secretion and/or insulin resistance. Among the various genetic factors associated with T2DM, a common genetic variant within the transcription factor 7-like 2 locus (TCF7L2) confers the greatest genetic risk for development of the disease. However, the mechanism(s) by which TCF7L2 predisposes to diabetes remain uncertain. Here we review the current literature pertaining to the potential mechanisms by which TCF7L2 confers risk of T2DM, using genetic variation as a probe to understand the pathogenesis of the disease.

引用

页码：383 / 389

页数：7

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