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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 3

Potential mechanisms for adiposity-induced inflammation in the liver.

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Potential mechanisms for adiposity-induced inflammation in the liver.
He...
Healthy liver contains a broad repertoire of cells that participate in inflammatory and immune responses, including resident hepatic macrophages (Kupffer cells), B and T cells, NK and NKT cells, DCs, liver sinusoidal endothelial cells, hepatic stellate cells, and hepatocytes. Hepatic steatosis and obesity are accompanied by the activation of inflammatory signaling pathways in liver. Proinflammatory cytokines and FFAs, produced either by hepatocytes in response to steatosis or by abdominal fat tissue, may activate Kupffer cells. Numbers of regulatory NKT cells decrease in parallel with the Kupffer cell activation.

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