Antidiabetic actions of a non-agonist PPARγ ligand blocking Cdk5-mediated phosphorylation

Jang Hyun Choi, Alexander S. Banks, Theodore M. Kamenecka, Scott A. Busby, Michael J. Chalmers, Naresh Kumar, Dana S. Kuruvilla, Youseung Shin, Yuanjun He, John B. Bruning, David P. Marciano, Michael D. Cameron, Dina Laznik, Michael J. Jurczak, Stephan C. Schürer, Dušica Vidović, Gerald I. Shulman, Bruce M. Spiegelman () and Patrick R. Griffin ()
Additional contact information
Jang Hyun Choi: Harvard Medical School
Alexander S. Banks: Harvard Medical School
Theodore M. Kamenecka: Translational Research Institute, The Scripps Research Institute, Scripps Florida
Scott A. Busby: The Scripps Research Institute, Scripps Florida
Michael J. Chalmers: The Scripps Research Institute, Scripps Florida
Naresh Kumar: The Scripps Research Institute, Scripps Florida
Dana S. Kuruvilla: The Scripps Research Institute, Scripps Florida
Youseung Shin: Translational Research Institute, The Scripps Research Institute, Scripps Florida
Yuanjun He: Translational Research Institute, The Scripps Research Institute, Scripps Florida
John B. Bruning: Texas A&M University
David P. Marciano: The Scripps Research Institute, Scripps Florida
Michael D. Cameron: Translational Research Institute, The Scripps Research Institute, Scripps Florida
Dina Laznik: Harvard Medical School
Michael J. Jurczak: Howard Hughes Medical Institute, Yale University School of Medicine
Stephan C. Schürer: Center for Computational Science, University of Miami
Dušica Vidović: Center for Computational Science, University of Miami
Gerald I. Shulman: Howard Hughes Medical Institute, Yale University School of Medicine
Bruce M. Spiegelman: Harvard Medical School
Patrick R. Griffin: Translational Research Institute, The Scripps Research Institute, Scripps Florida

Nature, 2011, vol. 477, issue 7365, 477-481

Abstract: Towards better antidiabetic drugs The nuclear receptor PPARγ is the target of thiazolidinedione antidiabetics including rosiglitazone and pioglitazone. These full PPARγ agonists are effective and well tolerated in most patients, but cause fluid retention and weight gain in a minority. In this proof-of-concept study, Choi et al. show the development of specific PPARγ ligands that retain antidiabetic activity through blockade of Cdk5-mediated PPARγ phosphorylation, but that are not full PPARγ agonists. In mouse models, these ligands do not cause the side effects sometimes associated with full PPARγ agonists.

Date: 2011
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DOI: 10.1038/nature10383

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