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High-Throughput Approaches onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes

Laboratory of Cell Signaling and Metabolic Disorders, Nencki Institute of Experimental Biology of Polish Academy of Sciences, 02-093 Warsaw, Poland
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Genes 2018, 9(8), 374;
Received: 27 May 2018 / Revised: 20 July 2018 / Accepted: 23 July 2018 / Published: 26 July 2018
(This article belongs to the Special Issue Emerging Applications for Next Generation Sequencing)
Type 2 diabetes (T2D) is a complex disorder that is caused by a combination of genetic, epigenetic, and environmental factors. High-throughput approaches have opened a new avenue toward a better understanding of the molecular bases of T2D. A genome-wide association studies (GWASs) identified a group of the most common susceptibility genes for T2D (i.e., TCF7L2, PPARG, KCNJ1, HNF1A, PTPN1, and CDKAL1) and illuminated novel disease-causing pathways. Next-generation sequencing (NGS)-based techniques have shed light on rare-coding genetic variants that account for an appreciable fraction of T2D heritability (KCNQ1 and ADRA2A) and population risk of T2D (SLC16A11, TPCN2, PAM, and CCND2). Moreover, single-cell sequencing of human pancreatic islets identified gene signatures that are exclusive to α-cells (GCG, IRX2, and IGFBP2) and β-cells (INS, ADCYAP1, INS-IGF2, and MAFA). Ongoing epigenome-wide association studies (EWASs) have progressively defined links between epigenetic markers and the transcriptional activity of T2D target genes. Differentially methylated regions were found in TCF7L2, THADA, KCNQ1, TXNIP, SOCS3, SREBF1, and KLF14 loci that are related to T2D. Additionally, chromatin state maps in pancreatic islets were provided and several non-coding RNAs (ncRNA) that are key to T2D pathogenesis were identified (i.e., miR-375). The present review summarizes major progress that has been made in mapping the (epi)genomic landscape of T2D within the last few years. View Full-Text
Keywords: type 2 diabetes; NGS; epigenetics; GWAS; beta-cell failure; insulin resistance type 2 diabetes; NGS; epigenetics; GWAS; beta-cell failure; insulin resistance
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MDPI and ACS Style

Dziewulska, A.; Dobosz, A.M.; Dobrzyn, A. High-Throughput Approaches onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes. Genes 2018, 9, 374.

AMA Style

Dziewulska A, Dobosz AM, Dobrzyn A. High-Throughput Approaches onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes. Genes. 2018; 9(8):374.

Chicago/Turabian Style

Dziewulska, Anna, Aneta M. Dobosz, and Agnieszka Dobrzyn. 2018. "High-Throughput Approaches onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes" Genes 9, no. 8: 374.

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