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miRNAs in the Beta Cell—Friends or Foes?

Type 2 diabetes (T2D) develops due to insulin resistance and an inability of the pancreatic β-cells to increase secretion of insulin and reduce elevated blood glucose levels. Diminished β-cell function and mass have been implicated in impaired β-cell secretory capacity and several microRNAs (miRNAs)...

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Autores principales: Karagiannopoulos, Alexandros, Cowan, Elaine, Eliasson, Lena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10214274/
https://www.ncbi.nlm.nih.gov/pubmed/36869830
http://dx.doi.org/10.1210/endocr/bqad040
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author Karagiannopoulos, Alexandros
Cowan, Elaine
Eliasson, Lena
author_facet Karagiannopoulos, Alexandros
Cowan, Elaine
Eliasson, Lena
author_sort Karagiannopoulos, Alexandros
collection PubMed
description Type 2 diabetes (T2D) develops due to insulin resistance and an inability of the pancreatic β-cells to increase secretion of insulin and reduce elevated blood glucose levels. Diminished β-cell function and mass have been implicated in impaired β-cell secretory capacity and several microRNAs (miRNAs) have been reported to be involved in regulating β-cell processes. We believe miRNAs are nodes in important miRNA-mRNA networks regulating β-cell function and that miRNAs therefore can be targets for the treatment of T2D. MicroRNAs are short (≈19-23 nucleotides [nt]) endogenous noncoding RNAs which regulate gene expression by directly binding to the mRNA of their target genes. Under normal circumstances, miRNAs act as rheostats to keep expression of their gene targets at optimal levels for different β-cell outputs. In T2D, levels of some miRNAs are altered as part of the compensatory mechanism to improve insulin secretion. Other miRNAs are differentially expressed as part of the process of T2D pathogenesis, which results in reduced insulin secretion and increased blood glucose. In this review, we present recent findings concerning miRNAs in islets and in insulin-secreting cells, and their differential expression in diabetes, with a specific focus on miRNAs involved in β-cell apoptosis/proliferation and glucose-stimulated insulin secretion. We present thoughts around miRNA-mRNA networks and miRNAs as both therapeutic targets to improve insulin secretion and as circulating biomarkers of diabetes. Overall, we hope to convince you that miRNAs in β-cells are essential for regulating β-cell function and can in the future be of clinical use in the treatment and/or prevention of diabetes.
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spelling pubmed-102142742023-05-27 miRNAs in the Beta Cell—Friends or Foes? Karagiannopoulos, Alexandros Cowan, Elaine Eliasson, Lena Endocrinology Mini-Review Type 2 diabetes (T2D) develops due to insulin resistance and an inability of the pancreatic β-cells to increase secretion of insulin and reduce elevated blood glucose levels. Diminished β-cell function and mass have been implicated in impaired β-cell secretory capacity and several microRNAs (miRNAs) have been reported to be involved in regulating β-cell processes. We believe miRNAs are nodes in important miRNA-mRNA networks regulating β-cell function and that miRNAs therefore can be targets for the treatment of T2D. MicroRNAs are short (≈19-23 nucleotides [nt]) endogenous noncoding RNAs which regulate gene expression by directly binding to the mRNA of their target genes. Under normal circumstances, miRNAs act as rheostats to keep expression of their gene targets at optimal levels for different β-cell outputs. In T2D, levels of some miRNAs are altered as part of the compensatory mechanism to improve insulin secretion. Other miRNAs are differentially expressed as part of the process of T2D pathogenesis, which results in reduced insulin secretion and increased blood glucose. In this review, we present recent findings concerning miRNAs in islets and in insulin-secreting cells, and their differential expression in diabetes, with a specific focus on miRNAs involved in β-cell apoptosis/proliferation and glucose-stimulated insulin secretion. We present thoughts around miRNA-mRNA networks and miRNAs as both therapeutic targets to improve insulin secretion and as circulating biomarkers of diabetes. Overall, we hope to convince you that miRNAs in β-cells are essential for regulating β-cell function and can in the future be of clinical use in the treatment and/or prevention of diabetes. Oxford University Press 2023-03-04 /pmc/articles/PMC10214274/ /pubmed/36869830 http://dx.doi.org/10.1210/endocr/bqad040 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Mini-Review
Karagiannopoulos, Alexandros
Cowan, Elaine
Eliasson, Lena
miRNAs in the Beta Cell—Friends or Foes?
title miRNAs in the Beta Cell—Friends or Foes?
title_full miRNAs in the Beta Cell—Friends or Foes?
title_fullStr miRNAs in the Beta Cell—Friends or Foes?
title_full_unstemmed miRNAs in the Beta Cell—Friends or Foes?
title_short miRNAs in the Beta Cell—Friends or Foes?
title_sort mirnas in the beta cell—friends or foes?
topic Mini-Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10214274/
https://www.ncbi.nlm.nih.gov/pubmed/36869830
http://dx.doi.org/10.1210/endocr/bqad040
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