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Interaction between cytokines and inflammatory cells in islet dysfunction, insulin resistance, and vascular disease
Journal article   Open access

Interaction between cytokines and inflammatory cells in islet dysfunction, insulin resistance, and vascular disease

Y Imai, A. D Dobrian, J.R Weaver, M.J Butcher, B.K Cole, E.V Galkina, M.A Morris, D.A Taylor-Fishwick and J.L Nadler
Diabetes, obesity & metabolism, Vol.15(3), pp.117-129
09/2013
DOI: 10.1111/dom.12161
PMCID: PMC3777698
PMID: 24003928
url
https://doi.org/10.1111/dom.12161View
Published (Version of record) Open Access

Abstract

Inflammation is an established pathogenic player in insulin resistance, islet demise, and atherosclerosis. The complex interactions between cytokines, immune cells, and affected tissues result in sustained inflammation in diabetes and atherosclerosis. 12- and 15-lipoxygenase (LO), such as 12/15LO, produces a variety of metabolites through peroxidation of fatty acids and potentially contributes to the complex molecular crosstalk at the site of inflammation. 12- and 15-LO pathways are frequently activated in tissues affected by diabetes and atherosclerosis including adipose tissue, islets, and the vasculature. Moreover, mice with whole body and tissue-specific knockout of 12/15-LO are protected against insulin resistance, hyperglycemia, and atherosclerosis supporting functional contribution of 12- and 15-LO pathways in diabetes and atherosclerosis. Recently it has emerged that there is a temporal regulation of the particular isoforms of 12- and 15-LO in human adipose tissue and islets during the development of type 1 and type 2 diabetes and obesity. Analyses of tissues affected by diabetes and atherosclerosis also implied the roles of interleukin (IL)-12 and NADPH oxidase 1 (NOX1) in islets and IL-17A in atherosclerosis. Future studies should aim to test the efficacy of inhibitions of these mediators for treatment of diabetes and atherosclerosis.
interleukin-17A NADPH oxidase-1 15-lipoxygenase 12-lipoxygenase interleukin-12

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