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The Genetic and Epigenetic Basis of Type 2 Diabetes and Obesity
Author(s) -
Drong A W,
Lindgren C M,
McCarthy M I
Publication year - 2012
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.2012.149
Subject(s) - epigenetics , obesity , type 2 diabetes , genetics , body mass index , biology , trait , disease , genetic association , bioinformatics , family aggregation , genetic variation , quantitative trait locus , medicine , diabetes mellitus , genotype , single nucleotide polymorphism , gene , endocrinology , computer science , programming language
Type 2 diabetes (T2D) and obesity are complex disorders that constitute major public health problems. The evidence for familial aggregation of both T2D and obesity is substantial. To date, more than 150 genetic loci are associated with the development of monogenic, syndromic, or multifactorial forms of T2D or obesity. However, the proportion of overall trait variance explained by these associated loci is modest (~5–10% for T2D, ~2% for body mass index (BMI)). Some of the familial aggregation not attributable to known genetic variation, as well as many of the effects of environmental exposures, may reflect epigenetic processes. In this review, we discuss the evidence concerning the genetic contribution to individual risk of T2D and obesity, and explore the potential role of epigenetic mechanisms. We also explain how genetics, epigenetics, and environment are likely to interact to define the individual risk of disease. Clinical Pharmacology & Therapeutics (2012); 92 6, 707–715. doi: 10.1038/clpt.2012.149