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Treatment of insulin resistance with peroxisome proliferator–activated receptor γ agonists
Jerrold M. Olefsky
Jerrold M. Olefsky
Published August 15, 2000
Citation Information: J Clin Invest. 2000;106(4):467-472. https://doi.org/10.1172/JCI10843.
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Perspective

Treatment of insulin resistance with peroxisome proliferator–activated receptor γ agonists

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Abstract

Authors

Jerrold M. Olefsky

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Figure 1

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Schematic diagram of the mechanisms of PPARγ action. In the unliganded s...
Schematic diagram of the mechanisms of PPARγ action. In the unliganded state (top), the PPARγ receptor exists as a heterodimer with the RXR nuclear receptor and the heterodimer is located on a PPAR response element (PPRE) of a target gene. The unliganded receptor heterodimer complex is associated with a multicomponent corepressor complex, which physically interacts with the PPARγ receptor through SMRT. The corepressor complex contains histone deacetylase (HDAC) activity, and the deacetylated state of histone inhibits transcription. After PPARγ ligand binding, the corepressor complex is dismissed and a coactivator complex is recruited to the heterodimer PPARγ receptor (bottom). The coactivator complex contains histone acetylase activity, leading to chromatin remodeling, facilitating active transcription. Adapted from Glass and Rosenfeld (29).

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