Advertisement
Inflammation and insulin resistance
Steven E. Shoelson, Jongsoon Lee, and Allison B. Goldfine
Find articles by Shoelson, S. in: JCI | PubMed | Google Scholar
Find articles by Lee, J. in: JCI | PubMed | Google Scholar
Find articles by Goldfine, A. in: JCI | PubMed | Google Scholar
Published August 1, 2006 - More info
J Clin Invest. 2006;116(8):2308–2308. https://doi.org/10.1172/JCI29069C1.
© 2006 The American Society for Clinical Investigation
Related article:
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
Original citation: J. Clin. Invest.116:1793-1801 (2006). doi:10.1172/JCI29069
Citation for this corrigendum: J. Clin. Invest.116:2308 (2006). doi:10.1172/JCI29069C1
In the original article, reference 77 was cited incorrectly. The corrected reference appears below.
Cinti, S., et al. 2005. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J. Lipid Res.46:2347-2355.
The authors regret this error.
Copyright © 2024 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)