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CorrigendumMetabolism Free access | 10.1172/JCI21480C1

c-Cbl-deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action

Juan C. Molero, Thomas E. Jensen, Phil C. Withers, Michelle Couzens, Herbert Herzog, Christine B.F. Thien, Wallace Y. Langdon, Ken Walder, Maria A. Murphy, David D.L. Bowtell, Edna Hardeman, Majid Ghoddusi, David E. James, and Gregory J. Cooney

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Published February 1, 2005 - More info

Published in Volume 115, Issue 2 on February 1, 2005
J Clin Invest. 2005;115(2):476–476. https://doi.org/10.1172/JCI21480C1.
© 2005 The American Society for Clinical Investigation
Published February 1, 2005 - Version history
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c-Cbl–deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action
Juan C. Molero, … , David E. James, Gregory J. Cooney
Juan C. Molero, … , David E. James, Gregory J. Cooney
Article Metabolism

c-Cbl–deficient mice have reduced adiposity, higher energy expenditure, and improved peripheral insulin action

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Abstract

Casitas b-lineage lymphoma (c-Cbl) is an E3 ubiquitin ligase that has an important role in regulating the degradation of cell surface receptors. In the present study we have examined the role of c-Cbl in whole-body energy homeostasis. c-Cbl–/– mice exhibited a profound increase in whole-body energy expenditure as determined by increased core temperature and whole-body oxygen consumption. As a consequence, these mice displayed a decrease in adiposity, primarily due to a reduction in cell size despite an increase in food intake. These changes were accompanied by a significant increase in activity (2- to 3-fold). In addition, c-Cbl–/– mice displayed a marked improvement in whole-body insulin action, primarily due to changes in muscle metabolism. We observed increased protein levels of the insulin receptor (4-fold) and uncoupling protein-3 (2-fold) in skeletal muscle and a significant increase in the phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase. These findings suggest that c-Cbl plays an integral role in whole-body fuel homeostasis by regulating whole-body energy expenditure and insulin action.

Authors

Juan C. Molero, Thomas E. Jensen, Phil C. Withers, Michelle Couzens, Herbert Herzog, Christine B.F. Thien, Wallace Y. Langdon, Ken Walder, Maria A. Murphy, David D.L. Bowtell, David E. James, Gregory J. Cooney

×

Original citation: J. Clin. Invest.114:1326–1333(2004). doi:10.1172/JCI21480

Citation for this erratum: J. Clin. Invest.115:476 (2005). doi:10.1172/JCI21480C1

Edna Hardeman and Majid Ghoddusi were omitted from the original author list. The corrected list, with affiliations, is as follows:

Juan C. Molero,1 Thomas E. Jensen,1 Phil C. Withers,2 Michelle Couzens,3 Herbert Herzog,3 Christine B.F. Thien,4 Wallace Y. Langdon,4 Ken Walder,5 Maria A. Murphy,6 David D.L. Bowtell,6 Edna Hardeman,7 Majid Ghoddusi,7 David E. James,1 and Gregory J. Cooney1

1Diabetes and Obesity Program, The Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. 2Zoology Department, University of Western Australia, Perth, Western Australia, Australia. 3Neurobiology Program, The Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. 4Pathology Department, University of Western Australia, Perth, Western Australia, Australia. 5Metabolic Research Unit, Deakin University, Geelong, Victoria, Australia. 6Peter MacCallum Institute, Melbourne, Victoria, Australia. 7Children's Medical Research Institute, Westmead, New South Wales, Australia.

The authors regret the error.

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