Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

IL-4/STAT6 immune axis regulates peripheral nutrient metabolism and insulin sensitivity

Roberto R. Ricardo-Gonzalez, Alex Red Eagle, Justin I. Odegaard, Hani Jouihan, Christine R. Morel, Jose E. Heredia, Lata Mukundan, Davina Wu, Richard M. Locksley, Ajay Chawla and Ronald M. Evans
Proceedings of the National Academy of Sciences of the United States of America
Vol. 107, No. 52 (December 28, 2010), pp. 22617-22622
Stable URL: http://www.jstor.org/stable/25770688
Page Count: 6
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
IL-4/STAT6 immune axis regulates peripheral nutrient metabolism and insulin sensitivity
Preview not available

Abstract

Immune cells take residence in metabolic tissues, providing a framework for direct regulation of nutrient metabolism. Despite conservation of this anatomic relationship through evolution, the signals and mechanisms by which the immune system regulates nutrient homeostasis and insulin action remain poorly understood. Here, we demonstrate that the IL-4/STAT6 immune axis, a key pathway in helminth immunity and allergies, controls peripheral nutrient metabolism and insulin sensitivity. Disruption of signal transducer and activator of transcription 6 (STAT6) decreases insulin action and enhances a peroxisome proliferator-activated receptor α (PPARα) driven program of oxidative metabolism. Conversely, activation of STAT6 by IL-4 improves insulin action by inhibiting the PPARα-regulated program of nutrient catabolism and attenuating adipose tissue inflammation. These findings have thus identified an unexpected molecular link between the immune system and macronutrient metabolism, suggesting perhaps the coevolution of these pathways occurred to ensure access to glucose during times of helminth infection.

Page Thumbnails

  • Thumbnail: Page 
[22617]
    [22617]
  • Thumbnail: Page 
22618
    22618
  • Thumbnail: Page 
22619
    22619
  • Thumbnail: Page 
22620
    22620
  • Thumbnail: Page 
22621
    22621
  • Thumbnail: Page 
22622
    22622