After you eat, your liver switches from producing glucose to storing it. At the same time, a cellular signaling pathway known as the unfolded protein response (UPR) is transiently activated, but it is not clear how this pathway contributes to the liver's metabolic switch. In this issue of the Journal of Clinical Investigation, researchers led by Phillip Scherer at the University of Texas Southwestern Medical Center report that activation of the UPR triggers the expression of Xbp1s, a protein that regulates genes needed for the metabolic switch. Scherer and colleagues found that they could induce changes in liver metabolism just by increasing expression of Xbps1. These results suggest that Xbps1 could play a role in metabolic disease.
The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism
Philipp E. Scherer
The University of Texas Southwestern Medical Center, Dallas, TX, USA
Phone: (214) 648-8715; Fax: (214) 648-8720; E-mail: email@example.com
View this article at: http://www.jci.org/articles/view/62819?key=17adb760d62c3d29b6fb
|Contact: Jillian Hurst|
Journal of Clinical Investigation