MiR-184 regulates insulin secretion through repression of Slc25a22

Sumiyo Morita; Takuro Horii; Mika Kimura; Izuho Hatada

doi:10.7717/peerj.162

MiR-184 regulates insulin secretion through repression of Slc25a22

PeerJ. 2013 Sep 24:1:e162. doi: 10.7717/peerj.162. eCollection 2013.

Authors

Sumiyo Morita¹, Takuro Horii, Mika Kimura, Izuho Hatada

Affiliation

¹ Laboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University , Japan.

Abstract

Insulin secretion from pancreatic β-cells plays an essential role in blood glucose homeostasis and type 2 diabetes. Many genes are involved in the secretion of insulin and most of these genes can be targeted by microRNAs (miRNAs). However, the role of miRNAs in insulin secretion and type 2 diabetes has not been exhaustively studied. The expression miR-184, a miRNA enriched in pancreatic islets, negatively correlates with insulin secretion, suggesting that it is a good candidate for miRNA-mediated regulation of insulin secretion. Here we report that miR-184 inhibits insulin secretion in the MIN6 pancreatic β-cell line through the repression of its target Slc25a22, a mitochondrial glutamate carrier. Our study provides new insight into the regulation of insulin secretion by glutamate transport in mitochondria.

Keywords: Diabetes; Insulin; miRNA.

Grants and funding

This work was supported in part by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Ministry of Health, Labour and Welfare of Japan; the National Institute of Biomedical Innovation; and the Takeda Science Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.