Peroxisome Proliferator-activated Receptor γ Stimulation of Adipocyte ApoE Gene Transcription Mediated by the Liver Receptor X Pathway
Open accessAbstract
Peroxisome proliferator-activated receptor (PPARgamma) agonists increase insulin sensitivity in humans and are useful for treating human diabetes. Treatment with these agonists leads to increased apoE expression and triglyceride accumulation in adipocytes. The importance of apoE for adipocyte triglyceride accumulation is demonstrated by observations that triglyceride accumulation is impaired in apoE knockout adipocytes treated with PPARgamma agonists. The current studies investigate the molecular mechanism for PPARgamma stimulation of the adipocyte apoE gene and demonstrate that the liver receptor X (LXR) response element within an apoE gene downstream enhancer is required for the apoE response to PPARgamma agonists. The response of the apoE gene to treatment with PPARgamma agonists was delayed beyond 12 h suggesting the involvement of an intermediary pathway. The combined addition of PPARgamma and LXR agonists did not increase apoE response beyond that observed with addition of either alone. Deletion or mutation of the LXR response element completely eliminated the adipocyte apoE gene response to a PPARgamma agonist. Chromatin immunoprecipitation analyses performed using isolated adipocytes, or adipose tissue from mice treated with PPARgamma agonists, showed increased LXR binding to the apoE gene after PPARgamma agonist treatment. Knockdown of LXR expression completely eliminated the increase in apoE message, protein, and triglyceride in response to PPARgamma stimulation. Th…
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Peripherally, LXRs and PPARγ participate in a coupled metabolic pathway in which activation of PPARγ induces expression of LXRα and its target genes abca1 and apoE.
“Peripherally, LXRs and PPARγ participate in a coupled metabolic pathway, whereby activation of PPARγ induces expression of LXRα and its target genes abca1 and apoE (Chawla et al., 2001; Seo et al., 2004; Yue and Mazzone, 2009).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Yue and Mazzone, 2009
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- Authors
- Yue, L., & Mazzone, T.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Mazzone, Theodore
- ORCID
- Yue, Lili
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 284
- Issue
- 16
- Pages
- 10453-10461
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2667732
- OpenAlex
- W2152032545
- Cited by
- 49
- References
- 30
- Citations by year
- 2026: 5 · 2025: 1 · 2023: 2 · 2021: 3 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 3 · 2013: 5 · 2012: 9
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK71711)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- PPARγ, liver X receptor, adipocytes, triglyceride accumulation, enhancers, PPARγ agonists, cholesterol homeostasis, triglyceride homeostasis, transcriptional regulation
- MeSH terms
- Liver X Receptors, Animals, Apolipoproteins E, DNA-Binding Proteins, Humans, Hypoglycemic Agents, Ligands, Mice, Inbred C57BL, Triglycerides, Signal Transduction, Transcriptional Activation, Mutagenesis, Site-Directed, Adipocytes, Genes, Reporter, Receptors, Cytoplasmic and Nuclear, 3T3-L1 Cells, Thiazolidinediones, PPAR gamma, Mice, Gene Knockdown Techniques, Orphan Nuclear Receptors
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