Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 381, Issue 1-2, Pages 230-240Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.08.004
Keywords
C2C12 myotubes; Insulin resistance; MicroRNA-106b; Mitofusin-2; Mitochondrial function; Peroxisome proliferator-activated receptor gamma coactivator-1 alpha
Categories
Funding
- National Natural Science Foundation of China [81100592, 81270800]
Ask authors/readers for more resources
MicroRNA-106b (miR-106b) is reported to correlate closely with skeletal muscle insulin resistance and type 2 diabetes. The aim of this study was to identify an mRNA targeted by miR-106b which regulates skeletal muscle insulin sensitivity. MiR-106b was found to target the 3' untranslated region (3' UTR) of mitofusin-2 (Mfn2) through miR-106b binding sites and to downregulate Mfn2 protein abundance at the post-transcriptional level by luciferase activity assay combined with mutational analysis and immunoblotting. Overexpression of miR-106b resulted in mitochondrial dysfunction and insulin resistance in C2C12 myotubes. MiR-106b was increased in insulin-resistant cultured C2C12 myotubes induced by TNF-alpha, and accompanied by increasing Mfn2 level, miR-106b loss of function improved mitochondrial function and insulin sensitivity impaired by TNF-alpha in C2C12 myotubes. In addition, both overexpression and downregulation of miR-106b upregulated peroxisome proliferator-activated receptor gamma coactivator (PGC)-l alpha and estrogen-related receptor (ERR)-alpha expression. MiR-106b targeted Mfn2 and regulated skeletal muscle mitochondrial function and insulin sensitivity. Therefor, Inhibition of miR-106b may be a potential new strategy for treating insulin resistance and type 2 diabetes. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available