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

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

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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  1. [41]Green MH Green JB Hargrove JL Berdanier CD The application of model-based compartmental analysis to the study of the kinetic behavior of vitamin A in vitamin A-sufficient rats: Validation of a theoretical model Mathematical modeling in nutrition and toxicology Mathematical Biology Press Athens 2005 175 187

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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.
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)
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
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
  • Health Sciences › Medicine › Surgery › 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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