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Critical Reviews™ in Eukaryotic Gene Expression

年間 6 号発行

ISSN 印刷: 1045-4403

ISSN オンライン: 2162-6502

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.6 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.2 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.3 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00058 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.33 SJR: 0.345 SNIP: 0.46 CiteScore™:: 2.5 H-Index: 67

Indexed in

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

巻 27, 発行 3, 2017, pp. 229-236
DOI: 10.1615/CritRevEukaryotGeneExpr.2017019712
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要約

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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