Inflammation and insulin resistance
Abstract
Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients. This should have been an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently. Together with the discovery of an important role for tissue macrophages, these new findings are helping to reshape thinking about how obesity increases the risk for developing T2D and the metabolic syndrome. The evolving concept of insulin resistance and T2D as having immunological components and an improving picture of how inflammation modulates metabolism provide new opportunities for using antiinflammatory strategies to correct the metabolic consequences of excess adiposity.
Footnotes
Nonstandard abbreviations used: AGE, advanced glycation end product; CRP, C-reactive protein; CVD, cardiovascular disease; IKKβ, IκB kinase-β; IRS-1, insulin receptor substrate-1; MCP-1, monocyte chemoattractant protein-1; MIP, macrophage inflammatory protein; PAI-1, plasminogen activator inhibitor-1; RAGE, receptor for advanced glycation end products; T2D, type 2 diabetes; TZD, thiazolidinedione.
Conflict of interest: The authors have declared that no conflict of interest exists.
Citation for this article:J. Clin. Invest.116:1793–1801 (2006). doi:10.1172/JCI29069.
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