Cited by 205Retinoids in leukemia and cellular processesLiver physiology and pathologyCholesterol and Lipid Metabolism

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Hepatic metabolism of retinoids and disease associations

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Shirakami, Yohei, Lee, Seung-Ah, Clugston, Robin D., Blaner, William S.·2012·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

DOI 10.1016/j.bbalip.2011.06.023PMC PMC3488285

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Abstract

The liver is the most important tissue site in the body for uptake of postprandial retinoid, as well as for retinoid storage. Within the liver, both hepatocytes and hepatic stellate cells (HSCs) are importantly involved in retinoid metabolism. Hepatocytes play an indispensable role in uptake and processing of dietary retinoid into the liver, and in synthesis and secretion of retinol-binding protein (RBP), which is required for mobilizing hepatic retinoid stores. HSCs are the central cellular site for retinoid storage in the healthy animal, accounting for as much as 50-60% of the total retinoid present in the entire body. The liver is also an important target organ for retinoid actions. Retinoic acid is synthesized in the liver and can interact with retinoid receptors which control expression of a large number of genes involved in hepatic processes. Altered retinoid metabolism and the accompanying dysregulation of retinoid signaling in the liver contribute to hepatic disease. This is related to HSCs, which contribute significantly to the development of hepatic disease when they undergo a process of cellular activation. HSC activation results in the loss of HSC retinoid stores and changes in extracellular matrix deposition leading to the onset of liver fibrosis. An association between hepatic disease progression and decreased hepatic retinoid storage has been demonstrated. In this review article, we summarize the essential role of the liver in retinoid metabolism and consider briefly associations between hepatic retinoid metabolism and disease. This article is part of a Special Issue entitled Retinoid and Lipid Metabolism.

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Authors: Shirakami, Y., Lee, S.-A., Clugston, R. D., & Blaner, W. S.
Affiliations: Columbia University (US)
Corresponding author: Blaner, William S.
ORCID: Shirakami, Yohei
Lee, Seung-Ah
Clugston, Robin D.
Blaner, William S.
Venue: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
Publisher: Elsevier BV
Published: 2012-01
Volume: 1821
Issue: 1
Pages: 124-136
ISSN: 1388-1981 (ISSN-L)
DOI: 10.1016/j.bbalip.2011.06.023
PMC: PMC3488285
OpenAlex: W2003289032
Cited by: 203
References: 177
Citations by year: 2026: 10 · 2025: 10 · 2024: 10 · 2023: 11 · 2022: 13 · 2021: 30 · 2020: 13 · 2019: 14 · 2018: 11 · 2017: 9 · 2016: 16 · 2015: 12 · 2014: 12 · 2013: 17 · 2012: 14
FWCI: 1.29
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (RC2 AA019413, R01 DK68437, R01 DK079221)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Keywords: vitamin A metabolism, liver, hepatocytes, hepatic stellate cells, retinol-binding protein, retinoic acid, retinoid receptors, retinoid signaling, liver fibrosis, hepatic stellate cell activation, extracellular matrix deposition, liver disease
MeSH terms: Animals, Biological Transport, Humans, Liver, Liver Diseases, Retinoids, Retinol-Binding Proteins, Signal Transduction, Lipid Metabolism, Mice, Rats, Hepatic Stellate Cells

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