Long noncoding RNAs, including MEG3, H19, MALAT1, GAS5, and lncSHGL, play important roles in the pathogenesis of insulin resistance by regulating insulin signaling and metabolism.
Insulin resistance (IR), designated as the blunted response of insulin target tissues to physiological level of insulin, plays crucial roles in the development and progression of diabetes, nonalcoholic fatty liver disease (NAFLD) and other diseases. So far, the distinct mechanism(s) of IR still needs further exploration. Long non-coding RNA (lncRNA) is a class of non-protein coding RNA molecules with a length greater than 200 nucleotides. LncRNAs are widely involved in many biological processes including cell differentiation, proliferation, apoptosis and metabolism. More recently, there has been increasing evidence that lncRNAs participated in the pathogenesis of IR, and the dysregulated lncRNA profile played important roles in the pathogenesis of metabolic diseases including obesity, diabetes and NAFLD. For example, the lncRNAs MEG3, H19, MALAT1, GAS5, lncSHGL and several other lncRNAs have been shown to regulate insulin signaling and glucose/lipid metabolism in various tissues. In this review, we briefly introduced the general features of lncRNA and the methods for lncRNA research, and then summarized and discussed the recent advances on the roles and mechanisms of lncRNAs in IR, particularly focused on liver, skeletal muscle and adipose tissues.
Yang et al. (Fri,) conducted a review in Insulin resistance. Long noncoding RNAs (lncRNAs) was evaluated. Long noncoding RNAs, including MEG3, H19, MALAT1, GAS5, and lncSHGL, play important roles in the pathogenesis of insulin resistance by regulating insulin signaling and metabolism.