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      Genomics of Islet (Dys)function and Type 2 Diabetes

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          Abstract

          Pancreatic islet dysfunction and beta cell failure are hallmarks of type 2 diabetes (T2D) pathogenesis. In this review, we discuss how genome-wide association studies (GWASs) and recent developments in islet (epi)genome and transcriptome profiling (particularly single cell analyses) are providing novel insights into the genetic, environmental, and cellular contributions to islet (dys)function and T2D pathogenesis. Moving forward, study designs that interrogate and model genetic variation (e.g., allelic profiling and (epi)genome editing) will be critical to dissect the molecular genetics of T2D pathogenesis, to build next-generation cellular and animal models, and to develop precision medicine approaches to detect, treat, and prevent islet (dys)function and T2D.

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          Author and article information

          Journal
          8507085
          7839
          Trends Genet
          Trends Genet.
          Trends in genetics : TIG
          0168-9525
          17 March 2017
          27 February 2017
          April 2017
          01 April 2018
          : 33
          : 4
          : 244-255
          Affiliations
          [1 ]The Jackson Laboratory for Genomic Medicine, Farmington, CT, 06032, USA
          [2 ]Department of Genetics & Genome Sciences, University of Connecticut, Farmington, CT, 06032, USA
          [3 ]Institute for Systems Genomics, University of Connecticut, Farmington, CT, 06032, USA
          Author notes
          Article
          PMC5458785 PMC5458785 5458785 nihpa856282
          10.1016/j.tig.2017.01.010
          5458785
          28245910
          55f7032b-f18d-49f1-a182-c173063b7efb
          History
          Categories
          Article

          Type 2 diabetes (T2D),genomics,single cell,transcriptomics,epigenomics,pancreatic islets

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