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- Sean R. Pyper
- Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
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- Navin Viswakarma
- Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
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- Songtao Yu
- Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
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- Janardan K. Reddy
- Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
書誌事項
- 公開日
- 2010-01
- 権利情報
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- https://journals.sagepub.com/page/policies/text-and-data-mining-license
- DOI
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- 10.1621/nrs.08002
- 公開者
- SAGE Publications
この論文をさがす
説明
<jats:p> The peroxisome proliferator-activated receptor α (PPARα, or NR1C1) is a nuclear hormone receptor activated by a structurally diverse array of synthetic chemicals known as peroxisome proliferators. Endogenous activation of PPARα in liver has also been observed in certain gene knockout mouse models of lipid metabolism, implying the existence of enzymes that either generate (synthesize) or degrade endogenous PPARα agonists. For example, substrates involved in fatty acid oxidation can function as PPARα ligands. PPARα serves as a xenobiotic and lipid sensor to regulate energy combustion, hepatic steatosis, lipoprotein synthesis, inflammation and liver cancer. Mainly, PPARα modulates the activities of all three fatty acid oxidation systems, namely mitochondrial and peroxisomal β-oxidation and microsomal co-oxidation, and thus plays a key role in energy expenditure. Sustained activation of PPARα by either exogenous or endogenous agonists leads to the development of hepatocellular carcinoma resulting from sustained oxidative and possibly endoplasmic reticulum stress and liver cell proliferation. PPARα requires transcription coactivator PPAR-binding protein (PBP)/mediator subunit 1(MED1) for its transcriptional activity. </jats:p>
収録刊行物
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- Nuclear Receptor Signaling
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Nuclear Receptor Signaling 8 (1), e002-, 2010-01
SAGE Publications