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MiR-184 regulates insulin secretion through repression of Slc25a22.

Authors
  • Morita, Sumiyo1
  • Horii, Takuro
  • Kimura, Mika
  • Hatada, Izuho
  • 1 Laboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University , Japan. , (Japan)
Type
Published Article
Journal
PeerJ
Publisher
PeerJ
Publication Date
Jan 01, 2013
Volume
1
Identifiers
DOI: 10.7717/peerj.162
PMID: 24109547
Source
Medline
Keywords
License
Unknown

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.

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