Journal
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
Volume 11, Issue 4, Pages 371-377Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e32830349a1
Keywords
beta-cell dysfunction; genome-wide association; insulin secretion; obesity genetics; type-2 diabetes genetics
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Purpose of review Over the past 18 months, the number of gene loci robustly associated with type 2 diabetes has risen from three to 18. In this study, we focus on explaining the genome-wide approach that has led to most of these discoveries and discuss some of the early insights the new gene loci have provided into the aetiology of type 2 diabetes. Recent findings Recent genome-wide association studies have provided an important resource for furthering our understanding of type 2 diabetes disease mechanisms. Genes previously unsuspected of playing a role in diabetes are now implicated in the disease process. These include genes in cell cycling control (CDKN2A/2B, CDKAL1), transcription factors (TCF7L2, HHEX), and ion channels (SLC30A8). These variants are all associated with insulin-secretory defects in the general population and show little if any relationship to insulin resistance. Two common variants (near or in FTO and MC4R) alter diabetes risk through a primary effect on obesity. Summary Recent genome-wide association studies show that there are now 18 gene loci associated with the risk of type 2 diabetes. Most of these T2D gene loci affect insulin secretion.
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