J. Lipid Res.
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A more recent version of this article appeared on January 1, 2005

Papers In Press, published online ahead of print November 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400341-JLR200
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Submitted on September 9, 2004
Revised on October 21, 2004
Accepted on October 26, 2004

Thioredoxin interacting protein (Txnip) deficiency disrupts the fasting-feeding metabolic transition

Sonal S. Sheth, Lawrence W. Castellani, Soumya Chari, Cory Wagg, Christopher K. Thipphavong, Jackie S. Bodnar, Peter Tontonoz, Alan D. Attie, Gary D. Lopaschuk, and Aldons J. Lusis

Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095-1679

Corresponding Author: jlusis{at}mednet.ucla.edu

Through a positional cloning approach, the thioredoxin interacting protein gene (Txnip) was recently identified as causal for a form of combined hyperlipidemia in mice(1). We now show that Txnip deficient mice in the fed state exhibit an altered response to nutrition, including elevated levels of plasma ketone bodies and free fatty acids, decreased glucose, and increased hepatic expression of PPAR-gamma Coactivator-1alpha (PGC-1alpha ), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase (G6Pase), and acyl CoA oxidase (AOX). Dramatic differences in the expression of key metabolic enzymes were also observed in other tissues, and the fat to muscle ratio of Txnip deficient mice was increased by about 40%. We demonstrate an effect of Txnip on the redox status, as the Txnip deficient mice in the fed state had a significant increase in the ratio of NADH:NAD+. Surprisingly, we observed that Txnip deficient mice and wild-type mice had similar levels of thioredoxin activity, suggesting that the effects of Txnip deficiency may be mediated in part by other interactions. These results indicate a role for Txnip in the metabolic response to feeding and the maintenance of the redox status.


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