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The role of long non-coding RNAs in the regulation of pancreatic beta cell identity

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
Pages (from-to)2153-2161
Number of pages9
JournalBiochemical Society Transactions
Issue number5
Published1 Nov 2021

Bibliographical note

Funding Information: This work was supported by the joint King’s College London and Technische Universität Dresden IRTG programme and by Diabetes UK (grant number 19/0006062). Publisher Copyright: © 2021 Portland Press Ltd. All rights reserved.

King's Authors


Type 2 diabetes (T2D) is a widespread disease affecting millions in every continental population. Pancreatic β-cells are central to the regulation of circulating glucose, but failure in the maintenance of their mass and/or functional identity leads to T2D. Long non-coding RNAs (lncRNAs) represent a relatively understudied class of transcripts which growing evidence implicates in diabetes pathogenesis. T2D-associated single nucleotide polymorphisms (SNPs) have been identified in lncRNA loci, although these appear to function primarily through regulating β-cell proliferation. In the last decade, over 1100 lncRNAs have been catalogued in islets and the roles of a few have been further investigated, definitively linking them to β-cell function. These studies show that lncRNAs can be developmentally regulated and show highly tissue-specific expression. lncRNAs regulate neighbouring β-cell-specific transcription factor expression, with knockdown or overexpression of lncRNAs impacting a network of other key genes and pathways. Finally, gene expression analysis in studies of diabetic models have uncovered a number of lncRNAs with roles in β-cell function. A deeper understanding of these lncRNA roles in maintaining β-cell identity, and its deterioration, is required to fully appreciate the β-cell molecular network and to advance novel diabetes treatments.

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