Affiliation:
1. Islet Cell Exocytosis, Lund University Diabetes Centre; Department of Clinical Sciences Malmö, Lund University; and Clinical Research Centre, Skåne University Hospital, Malmö, Sweden
Abstract
Impaired insulin secretion from the pancreatic β-cells is central in the pathogenesis of type 2 diabetes (T2D), and microRNAs (miRNAs) are fundamental regulatory factors in this process. Differential expression of miRNAs contributes to β-cell adaptation to compensate for increased insulin resistance, but deregulation of miRNA expression can also directly cause β-cell impairment during the development of T2D. miRNAs are small noncoding RNAs that posttranscriptionally reduce gene expression through translational inhibition or mRNA destabilization. The nature of miRNA targeting implies the presence of complex and large miRNA–mRNA regulatory networks in every cell, including the insulin-secreting β-cell. Here we exemplify one such network using our own data on differential miRNA expression in the islets of T2D Goto-Kakizaki rat model. Several biological processes are influenced by multiple miRNAs in the β-cell, but so far most studies have focused on dissecting the mechanism of action of individual miRNAs. In this Perspective we present key islet miRNA families involved in T2D pathogenesis including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152. Finally, we highlight four challenges and opportunities within islet miRNA research, ending with a discussion on how miRNAs can be utilized as therapeutic targets contributing to personalized T2D treatment strategies.
Funder
Swedish Foundation for Strategic Research
Swedish Research Council
Region Skåne-ALF
Swedish Diabetes Foundation
Diabetes Wellness Network Sweden
Albert Påhlsson Foundation
Crafoord Foundation
Byggmästare Olle Engqvist Foundation
Syskonen Svenssons Fond
European Union’s Horizon 2020 Research and Innovation Programme
Publisher
American Diabetes Association
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Cited by
45 articles.
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