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真核基因表达评论综述™
影响因子: 1.734 5年影响因子: 1.848 SJR: 0.627 SNIP: 0.516 CiteScore™: 1.96

ISSN 打印: 1045-4403
ISSN 在线: 2162-6502

真核基因表达评论综述™

DOI: 10.1615/CritRevEukaryotGeneExpr.2017019712
pages 229-236

Role of Interleukin-6 in Development of Insulin Resistance and Type 2 Diabetes Mellitus

Kanwal Rehman
Institute of Pharmacy, Physiology and Pharmacology, University of Agriculture, Faisalabad, Pakistan
Muhammad Sajid Hamid Akash
Department of Pharmaceutical Chemistry, Government College University Faisalabad, Pakistan
Aamira Liaqat
Department of Pharmaceutical Chemistry, Government College University Faisalabad, Pakistan; Department of Biochemistry, Government College University Faisalabad, Pakistan
Shagufta Kamal
Department of Biochemistry, Government College University Faisalabad, Pakistan
Muhammad Imran Qadir
Institute of Molecular Biology and Biotechnology, Bahauddin Zakariya University, Bosan Road, Multan, Pakistan
Akhtar Rasul
Department of Pharmaceutics, Government College, University Faisalabad, Pakistan

ABSTRACT

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.


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