Administration of the potent PPARα agonist, Wy-14,643, reverses nutritional fibrosis and steatohepatitis in mice
Open accessAbstract
Administration of a methionine and choline deficient (MCD) diet to rodents causes progressive fibrosing steatohepatitis pathologically similar to human metabolic steatohepatitis. We have previously shown that the peroxisome proliferator-activated receptor-α (PPARα) agonist, Wy-14,643, prevented the development of MCD diet-induced steatohepatitis. We have now tested whether Wy-14,643 ameliorates established steatohepatitis and fibrosis. Male C57BL6 mice were fed the MCD diet for 51 days to induce severe steatohepatitis. They were then treated with Wy-14,643 together with the MCD diet for 5 or 12 days; positive controls continued on the MCD diet for 5 or 12 days. After 5 days of Wy-14,643 treatment, alanine aminotransferase (ALT) levels were significantly decreased, steatohepatitis less severe, and hepatic lipoperoxides significantly reduced. After 12 days, hepatic triglycerides were normalized and there was near resolution of histological changes. MCD dietary feeding was associated with increased expression of vascular cell adhesion molecule (VCAM)-1, and increased numbers of activated macrophages in the liver. Treatment with Wy-14,643 reduced VCAM-1 expression and macrophage numbers. MCD diet-fed mice developed hepatic fibrosis with increased hepatic collagen α1(I), tissue inhibitor of metalloproteinases (TIMP)-1, TIMP-2, and matrix metalloproteinase (MMP)-13 mRNA levels. After treatment with Wy-14,643, expression of these genes was reduced in a manner that paralleled the reduction in activated hepatic stellate cells and near resolution of liver fibrosis. In conclusion, the present study shows that MCD diet-induced fibrosing steatohepatitis can be reversed by treatment with Wy-14,643. It is likely that activation of PPARα reverses fibrosis indirectly by reducing stimuli, such as lipid peroxides, and activation of cells responsible for promoting hepatic fibrosis. (Hepatology 2004;39:1286-1296.)
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Although fibrates are effective for improvement of NAFLD in animals, their efficacy in clinical settings is not established.
“Although fibrates were effective for improvement of NAFLD in animals [103–105], their efficacy in clinical settings is not established.”
From Pemafibrate, a new selective PPARα modulator: drug concept and its clinical applications for dyslipidemia and metabolic diseases (2020) · cites this paper as [103]
In rodent carbon tetrachloride or thioacetamide models, the PPAR-α ligand Wy14643 decreased liver fibrosis and hepatic stellate cell activation, reduced liver steatosis and even reversed histological liver fibrosis.
“Briefly, in rodent CCl 4 or thioacetamide models, the PPAR-α ligand Wy14643 has been shown to decrease liver fibrosis and HSC activation, reduce liver steatosis and even reverse histological liver fibrosis.[112,114]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [112]
In hepatic stellate cells, the role of PPAR-α is still poorly characterized, even though antifibrotic effects of the PPAR-α agonist Wy14643 have previously been demonstrated in murine models of liver fibrosis.
“In HSCs, however, the role of PPAR-α is still poorly characterized, even though antifibrotic effects of the PPAR-α agonist Wy14643 have previously been demonstrated in murine models of liver fibrosis.[112,113]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [112]
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- Authors
- Ip, E., Farrell, G., Hall, P., Robertson, G., & Leclercq, I.
- Affiliations
- The University of Sydney (AU)
- University of Cape Town (ZA)
- Corresponding author
- Farrell, Geoff
- Venue
- Hepatology
- Published
- 2004-05
- Volume
- 39
- Issue
- 5
- Pages
- 1286-1296
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2080361134
- Cited by
- 383
- References
- 51
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 22 · 2023: 17 · 2022: 12 · 2021: 25 · 2020: 18 · 2019: 13 · 2018: 19 · 2017: 23 · 2016: 19 · 2015: 21 · 2014: 18 · 2013: 21 · 2012: 16
- FWCI
- 14.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion)
- Funders
- Université Catholique de Louvain
- Medical Research Council
- National Health and Medical Research Council (153899)
- National Cancer Institute
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- Wy-14,643, PPARα agonist, steatohepatitis, liver fibrosis, methionine-choline-deficient diet, metabolic steatohepatitis, hepatic stellate cells, macrophages, VCAM-1, lipid peroxidation, hepatic collagen, matrix metalloproteinase-13, tissue inhibitors of metalloproteinases, hepatic triglycerides, fibrosis reversal
- MeSH terms
- Animals, Dietary Fats, Fatty Liver, Lipid Peroxides, Liver Cirrhosis, Male, Mice, Inbred C57BL, Pyrimidines, Transcription Factors, Triglycerides, Cell Adhesion Molecules, Gene Expression, Transforming Growth Factor beta, Immediate-Early Proteins, Receptors, Cytoplasmic and Nuclear, Peroxisome Proliferators, Hepatocytes, Intercellular Signaling Peptides and Proteins, Mice, Transforming Growth Factor beta1, Connective Tissue Growth Factor
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