Abstract
Over the last 2 decades, mi(cro)RNAs have emerged as one of the key regulators of metabolic homeostasis. Most of the studies have highlighted that, in the cytoplasm, miRNAs directly bind to the 3'-UTR (untranslated region) of a mRNA. Conventional RNA-induced silencing complex (RISC) formation results in the post-transcriptional inhibition. This process is known to contribute to the development of metabolic diseases, including diabetes mellitus. Recent advancements with small RNA detection technologies have enabled us to identify miRNAs in the mitochondrial compartment of the cells. We have termed these miRNAs, which translocate into the mitochondria as mitochondrial miRNA, MitomiR. It has been demonstrated that MitomiRs can regulate gene expression, with some evidence even suggesting that, after translocation, MitomiRs can bind to the 3'-end of a mitochondrial gene, altering its regulation. Our main focus in this review is to highlight the potential role of MitomiR in the pathogenesis of metabolic disorders such as diabetes mellitus.