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Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility

Type 2 diabetes usually ensues from the inability of pancreatic beta cells to compensate for incipient insulin resistance. The loss of beta cell mass, function, and potentially beta cell identity contribute to this dysfunction to extents which are debated. In recent years, long non-coding RNAs (lncR...

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Detalles Bibliográficos
Autores principales: Pullen, Timothy J., Rutter, Guy A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076741/
https://www.ncbi.nlm.nih.gov/pubmed/25071823
http://dx.doi.org/10.3389/fgene.2014.00193
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author Pullen, Timothy J.
Rutter, Guy A.
author_facet Pullen, Timothy J.
Rutter, Guy A.
author_sort Pullen, Timothy J.
collection PubMed
description Type 2 diabetes usually ensues from the inability of pancreatic beta cells to compensate for incipient insulin resistance. The loss of beta cell mass, function, and potentially beta cell identity contribute to this dysfunction to extents which are debated. In recent years, long non-coding RNAs (lncRNAs) have emerged as potentially providing a novel level of gene regulation implicating critical cellular processes such as pluripotency and differentiation. With over 1000 lncRNAs now identified in beta cells, there is growing evidence for their involvement in the above processes in these cells. While functional evidence on individual islet lncRNAs is still scarce, we discuss how lncRNAs could contribute to type 2 diabetes susceptibility, particularly at loci identified through genome-wide association studies as affecting disease risk.
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spelling pubmed-40767412014-07-28 Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility Pullen, Timothy J. Rutter, Guy A. Front Genet Genetics Type 2 diabetes usually ensues from the inability of pancreatic beta cells to compensate for incipient insulin resistance. The loss of beta cell mass, function, and potentially beta cell identity contribute to this dysfunction to extents which are debated. In recent years, long non-coding RNAs (lncRNAs) have emerged as potentially providing a novel level of gene regulation implicating critical cellular processes such as pluripotency and differentiation. With over 1000 lncRNAs now identified in beta cells, there is growing evidence for their involvement in the above processes in these cells. While functional evidence on individual islet lncRNAs is still scarce, we discuss how lncRNAs could contribute to type 2 diabetes susceptibility, particularly at loci identified through genome-wide association studies as affecting disease risk. Frontiers Media S.A. 2014-07-01 /pmc/articles/PMC4076741/ /pubmed/25071823 http://dx.doi.org/10.3389/fgene.2014.00193 Text en Copyright © 2014 Pullen and Rutter. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Pullen, Timothy J.
Rutter, Guy A.
Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title_full Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title_fullStr Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title_full_unstemmed Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title_short Roles of lncRNAs in pancreatic beta cell identity and diabetes susceptibility
title_sort roles of lncrnas in pancreatic beta cell identity and diabetes susceptibility
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076741/
https://www.ncbi.nlm.nih.gov/pubmed/25071823
http://dx.doi.org/10.3389/fgene.2014.00193
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