Role of peroxisome proliferator-activated receptor-α in fasting-mediated oxidative stress
Open accessAbstract
The peroxisome proliferator-activated receptor-alpha (PPARalpha) regulates lipid homeostasis, particularly in the liver. This study was aimed at elucidating the relationship between hepatosteatosis and oxidative stress during fasting. Fasted Ppara-null mice exhibited marked hepatosteatosis, which was associated with elevated levels of lipid peroxidation, nitric oxide synthase activity, and hydrogen peroxide accumulation. Total glutathione (GSH), mitochondrial GSH, and the activities of major antioxidant enzymes were also lower in the fasted Ppara-null mice. Consequently, the number and extent of nitrated proteins were markedly increased in the fasted Ppara-null mice, although high levels of protein nitration were still detected in the fed Ppara-null mice while many oxidatively modified proteins were only found in the fasted Ppara-null mice. However, the role of inflammation in increased oxidative stress in the fasted Ppara-null mice was minimal based on the similar levels of tumor necrosis factor-alpha change in all groups. These results with increased oxidative stress observed in the fasted Ppara-null mice compared with other groups demonstrate a role for PPAR alpha in fasting-mediated oxidative stress and that inhibition of PPAR alpha functions may increase the susceptibility to oxidative damage in the presence of another toxic agent.
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Chronic and excessive alcohol intake is known to cause liver injury from mild steatosis (AFLD) to more advanced liver disease such as ASH, fibrosis/cirrhosis, hepatic cancer, liver failure, and death.
“Chronic and excessive alcohol intake is known to cause liver injury from mild steatosis (simple fat accumulation in so-called alcoholic fatty liver disease, AFLD) to more advanced liver disease such as inflammation (alcoholic steatohepatitis, ASH), fibrosis/cirrhosis, hepatic cancer, liver failure, and death203–213.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [205]
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- Authors
- Abdelmegeed, M. A., Moon, K.-H., Hardwick, J. P., Gonzalez, F. J., & Song, B.-J.
- Affiliations
- National Institute on Alcohol Abuse and Alcoholism (US)
- Northeast Ohio Medical University (US)
- National Institutes of Health (US)
- Corresponding author
- Song, Byoung-Joon
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 47
- Issue
- 6
- Pages
- 767-778
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC2759705
- OpenAlex
- W2083870067
- Cited by
- 74
- References
- 68
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 8 · 2014: 3 · 2013: 12 · 2012: 4
- FWCI
- 2.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99‐AA999999)
- National Institute on Alcohol Abuse and Alcoholism (Z01AA000036)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- PPARα, fasting, oxidative stress, hepatic steatosis, lipid peroxidation, protein nitration, glutathione, antioxidant enzymes, mitochondrial glutathione, nitric oxide synthase, hydrogen peroxide, PPARalpha-null mice, TNF-α, inflammation, lipid homeostasis
- MeSH terms
- Animals, Fasting, Fatty Liver, Glutathione, Hydrogen Peroxide, Liver, Mitochondria, Liver, Nitro Compounds, Tumor Necrosis Factor-alpha, Lipid Peroxidation, Mice, Knockout, Oxidative Stress, Nitric Oxide Synthase, PPAR alpha, Mice
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