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Submitted on April 3, 2007
Accepted on July 19, 2007
The National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, The Chinese Academy of Medical Sciences and Peking Union Medical College, Tsinghua University, Beijing-100005, China; Department of Molecular Parasitology, Humboldt University, Berlin 10115, Germany
* To whom correspondence should be addressed. E-mail: fangfd{at}vip.sina.com.
MicroRNAs (miRNAs) have been suggested to play pivotal roles in multifarious diseases associated with the post-transcriptional regulation of protein-coding genes. In this study, we aimed to investigate the function of miRNAs in type 2 diabetes mellitus (T2DM). The miRNAs expression profiles were examined by microRNA microarray analysis of skeletal muscles from healthy and Goto-Kakizaki rats. We identified 4 upregulated miRNAs, and 11 miRNAs that were down-regulated relative to normal individuals. Amongst induced miRNAs were three paralogs of miR-29, miR-29a, miR-29b and miR-29c. Northern blotting further confirmed their elevated expression in three important target tissues of insulin action: muscle, fat and liver of diabetic rats. Adenovirus-mediated over-expression of miR-29a/b/c in 3T3-L1 adipocytes could largely repress insulin-stimulated glucose uptake, presumably through inhibiting Akt activation. The increase in miR-29 level caused insulin resistance, similar to that of incubation with high glucose and insulin in combination, which in turn induced miR-29a and miR-29b expression. We demonstrate, Akt is not the direct target gene of miR-29 and the negative effects of miR-29 on insulin signaling might be mediated by other unknown intermediates. Taken together, these data reveal the crucial role of miR-29 in type 2 diabetes.
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