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Type 2 diabetes (T2D) is a complex, multifactorial disorder with an estimated heritability ranging between 40% and 70%. Genome-wide association studies (GWAS) have shown that common T2D is highly polygenic, with more than 100 loci contributing to T2D risk. Elucidating the function of T2D-associated single nucleotide polymorphisms (SNPs) and target genes and their involvement in T2D pathophysiology may have major translational implications for precision medicine and for the development of novel treatments. A significant part of the T2D-associated SNPs also modulates fasting plasma glucose levels and the homeostatic model assessment of beta-cell function in non-diabetic individuals, suggesting that their main diabetogenic impact is on insulin secretion and not on insulin resistance. Ndiaye, Ortalli, Canouil et al. performed a comprehensive expression study of candidate T2D susceptibility genes closest to all GWAS-identified T2D SNPs in a large panel of human organs, tissues, and cells, followed by the functional analysis of the knockdown of these genes in human pancreatic beta-cell lines. Using this strategy, they found that the expression of tested candidate T2D susceptibility genes was significantly and specifically enriched in pancreatic beta cells, and they report functional evidence for a role in insulin secretion of four T2D susceptibility genes (PRC1, SRR, ZFAND3, and ZFAND6) with previously unknown presence and function in pancreatic beta cells.

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The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.

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Brandon L Roberts, Baylin Bennett
Oregon National Primate Research Center, Beaverton, Oregon, USA
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