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Inflammation and insulin resistance
Steven E. Shoelson, … , Jongsoon Lee, Allison B. Goldfine
Steven E. Shoelson, … , Jongsoon Lee, Allison B. Goldfine
Published July 3, 2006
Citation Information: J Clin Invest. 2006;116(7):1793-1801. https://doi.org/10.1172/JCI29069.
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Inflammation and insulin resistance

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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.

Authors

Steven E. Shoelson, Jongsoon Lee, Allison B. Goldfine

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Figure 4

Local, portal, and systemic effects of inflammation in insulin resistance and atherogenesis.

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Local, portal, and systemic effects of inflammation in insulin resistanc...
Increasing adiposity activates inflammatory responses in fat and liver, with associated increases in the production of cytokines and chemokines. Immune cells including monocytes and macrophages are recruited and/or activated, and together these cause local insulin resistance. Portal delivery of abdominal fat–derived cytokines and lipids contributes to hepatic inflammation and insulin resistance. Proinflammatory and proatherogenic mediators are produced in the adipose tissue and liver and associated immune cells. This creates a systemic inflammatory diathesis that promotes insulin resistance in skeletal muscle and other tissues and atherogenesis in the vasculature.

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