MiR-184 regulates insulin secretion through repression of Slc25a22
Author(s) -
Sumiyo Morita,
Takuro Horii,
Mika Kimura,
Izuho Hatada
Publication year - 2013
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.162
Subject(s) - secretion , insulin , glucose homeostasis , microrna , pancreatic islets , psychological repression , endocrinology , medicine , biology , type 2 diabetes , microbiology and biotechnology , homeostasis , diabetes mellitus , islet , insulin resistance , gene , gene expression , biochemistry
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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