Roles of Long Non-Coding RNAs on Hepatic Insulin Resistance

Insulin resistance is the common pathophysiological mechanism of obesity and type 2 diabetes. The liver is an important target organ for insulin-mediated glucose uptake, metabolism and utilization, and an important site for insulin resistance. Studies have shown that liver gluconeogenesis signaling pathway, insulin signaling pathway, lipid production signaling pathway, autophagy and reactive oxygen species are closely related to liver insulin resistance. The liver can produce a variety of lncRNAs (long non-coding RNAs). When lncRNAs are up-regulated (eg. Blnc1, Risa, MALAT1, MEG3, SRA, Gm10768, H19 and Gomafu) or down-regulated (eg. lncSHGL), lncRNAs can orchestrate the liver gluconeogenesis signaling pathway, insulin signaling pathway, lipid signaling pathway, autophagy and reactive oxygen species, so as to participate in the occurrence and development of the hepatic insulin resistance. The elucidation of the relationship between lncRNAs and hepatic insulin resistance in this paper will deepen our understanding of the function of lncRNAs and the mechanism of hepatic insulin resistance, and provide a new direction for the prevention and treatment of diabetes. LncRNAs are expected to become a new target for the treatment of insulin resistance and diabetes.

CSTR: 32200.14.cjcb.2020.04.0018