Rehman Kanwal, Akash Muhammad Sajid Hamid, Liaqat Aamira, Kamal Shagufta, Qadir Muhammad Imran, Rasul Akhtar
Institute of Pharmacy, Physiology and Pharmacology, University of Agriculture, Faisalabad, Pakistan.
Department of Pharmaceutical Chemistry, Government College University Faisalabad, Pakistan.
Crit Rev Eukaryot Gene Expr. 2017;27(3):229-236. doi: 10.1615/CritRevEukaryotGeneExpr.2017019712.
Interleukin-6 (IL-6) is a proinflammatory cytokine that decisively induces the development of insulin resistance and pathogenesis of type 2 diabetes mellitus (T2DM) through the generation of inflammation by controlling differentiation, migration, proliferation, and cell apoptosis. The presence of IL-6 in tissues is a normal consequence, but its irregular production and long-term exposure leads to the development of inflammation, which induces insulin resistance and overt T2DM. There is a mechanistic relationship between the stimulation of IL-6 and insulin resistance. IL-6 causes insulin resistance by impairing the phosphorylation of insulin receptor and insulin receptor substrate-1 by inducing the expression of SOCS-3, a potential inhibitor of insulin signaling. In this article, we have briefly described how IL-6 induces the insulin resistance and pathogenesis of T2DM. The prevention of inflammatory disorders by blocking IL-6 and IL-6 signaling may be an effective strategy for the treatment of insulin resistance and T2DM.
白细胞介素-6(IL-6)是一种促炎细胞因子,它通过控制细胞分化、迁移、增殖和凋亡来引发炎症,从而决定性地诱导胰岛素抵抗的发展和2型糖尿病(T2DM)的发病机制。组织中IL-6的存在是正常现象,但其产生不规则且长期暴露会导致炎症的发展,进而诱发胰岛素抵抗和显性T2DM。IL-6的刺激与胰岛素抵抗之间存在机制上的联系。IL-6通过诱导胰岛素信号潜在抑制剂SOCS-3的表达,损害胰岛素受体和胰岛素受体底物-1的磷酸化,从而导致胰岛素抵抗。在本文中,我们简要描述了IL-6如何诱导胰岛素抵抗和T2DM的发病机制。通过阻断IL-6和IL-6信号传导来预防炎症性疾病可能是治疗胰岛素抵抗和T2DM的有效策略。