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Retraction Open Access | 10.1172/JCI170315

CDK4 is an essential insulin effector in adipocytes

Sylviane Lagarrigue, Isabel C. Lopez-Mejia, Pierre-Damien Denechaud, Xavier Escoté, Judit Castillo-Armengol, Veronica Jimenez, Carine Chavey, Albert Giralt, Qiuwen Lai, Lianjun Zhang, Laia Martinez-Carreres, Brigitte Delacuisine, Jean-Sébastien Annicotte, Emilie Blanchet, Sébastien Huré, Anna Abella, Francisco J. Tinahones, Joan Vendrell, Pierre Dubus, Fatima Bosch, C. Ronald Kahn, and Lluis Fajas

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Published March 15, 2023 - More info

Published in Volume 133, Issue 6 on March 15, 2023
J Clin Invest. 2023;133(6):e170315. https://doi.org/10.1172/JCI170315.
© 2023 Lagarrigue et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published March 15, 2023 - Version history
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Related article:

CDK4 is an essential insulin effector in adipocytes
Sylviane Lagarrigue, … , C. Ronald Kahn, Lluis Fajas
Sylviane Lagarrigue, … , C. Ronald Kahn, Lluis Fajas
Research Article Endocrinology Metabolism

CDK4 is an essential insulin effector in adipocytes

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Abstract

Insulin resistance is a fundamental pathogenic factor that characterizes various metabolic disorders, including obesity and type 2 diabetes. Adipose tissue contributes to the development of obesity-related insulin resistance through increased release of fatty acids, altered adipokine secretion, and/or macrophage infiltration and cytokine release. Here, we aimed to analyze the participation of the cyclin-dependent kinase 4 (CDK4) in adipose tissue biology. We determined that white adipose tissue (WAT) from CDK4-deficient mice exhibits impaired lipogenesis and increased lipolysis. Conversely, lipolysis was decreased and lipogenesis was increased in mice expressing a mutant hyperactive form of CDK4 (CDK4R24C). We performed a global kinome analysis and found that mice lacking Cdk4 had impaired insulin signaling in the adipose tissue. Interestingly, our results demonstrated that insulin activates the cyclin D3-CDK4 complex, which, in turn, phosphorylates the insulin receptor substrate 2 (IRS2) at the Ser 388, likely creating a positive feedback loop to maintain adipocyte insulin signaling. Furthermore, we found that CCND3 expression and IRS2 serine 388 phosphorylation are increased in human obese subjects. Together, our results demonstrate that CDK4 is a major regulator of insulin signaling in WAT.

Authors

Sylviane Lagarrigue, Isabel C. Lopez-Mejia, Pierre-Damien Denechaud, Xavier Escoté, Judit Castillo-Armengol, Veronica Jimenez, Carine Chavey, Albert Giralt, Qiuwen Lai, Lianjun Zhang, Laia Martinez-Carreres, Brigitte Delacuisine, Jean-Sébastien Annicotte, Emilie Blanchet, Sébastien Huré, Anna Abella, Francisco J. Tinahones, Joan Vendrell, Pierre Dubus, Fatima Bosch, C. Ronald Kahn, Lluis Fajas

×

Original citation: J Clin Invest. 2016;126(1):335–348. https://doi.org/10.1172/JCI81480

Citation for this retraction: J Clin Invest. 2023;133(6):170315. https://doi.org/10.1172/JCI170315

At the request of the corresponding author, the JCI is retracting this article. The authors became aware that the genotype of the mice described as Cdk4neo/neo Rip-Cre was incorrect. The correct mouse genotype was Cdk4neo/neo Rip-Cdk4R24C. The model used transgenically expresses the Cdk4R24C allele under the control of the rat insulin promoter (Rip-Cdk4R24C) rather than expressing Cdk4R24C in the Cdk4 locus as described in the article. Due to this unintentional error, the corresponding author requested retraction.

Footnotes

See the related article at CDK4 is an essential insulin effector in adipocytes.

Version history
  • Version 1 (March 15, 2023): Electronic publication

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