Journal article
PPARγ: No SirT, No Service
Circulation research, Vol.112(3), pp.411-414
02/2013
DOI: 10.1161/CIRCRESAHA.113.300870
PMCID: PMC3580855
PMID: 23371897
Abstract
A novel mechanism has been defined for controlling PPARγn activity in response to thiazolidinedione ligands, in which deacetylation of PPARγ by SirT1 remodels the transcriptional complex. This change favors expression of genes associated with increased energy utilization and insulin sensitization in white adipose tissue, and is required for a portion of the beneficial effects of thiazolidinediones. More broadly, PPARγ acetylation and other recently identified regulatory modifications are clarifying the mechanisms by which thiazolidinediones exert their antidiabetic effects in fat cells and other tissues.
Details
- Title: Subtitle
- PPARγ: No SirT, No Service
- Creators
- Frederick W Quelle - From the Department of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IACurt D Sigmund - From the Department of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA
- Resource Type
- Journal article
- Publication Details
- Circulation research, Vol.112(3), pp.411-414
- DOI
- 10.1161/CIRCRESAHA.113.300870
- PMID
- 23371897
- PMCID
- PMC3580855
- ISSN
- 0009-7330
- eISSN
- 1524-4571
- Language
- English
- Date published
- 02/2013
- Academic Unit
- Molecular Physiology and Biophysics; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040494902771
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