Vitamin A status regulates hepatic lecithin: retinol acyltransferase activity in rats.
Open accessAbstract
The activity of lecithin:retinol acyltransferase (LRAT) was determined in microsomes from the liver and small intestine of rats with differing vitamin A status. In animals depleted of retinol, as judged by undetectable liver vitamin A stores and low plasma retinol concentrations, hepatic LRAT activity was almost undetectable, whether assayed with retinol bound to cellular retinol-binding protein or solvent-dispersed retinol. In contrast, neither the activity of intestinal LRAT nor that of acyl-CoA:retinol acyltransferase in either liver or intestine differed from that of vitamin A-adequate rats. During the course of vitamin A depletion, liver LRAT activity fell progressively, nearly in parallel to the decrease in plasma retinol concentration. Oral repletion of vitamin A-depleted rats with 0.8 mg of retinol resulted in a very rapid restoration of plasma retinol concentration and full recovery of hepatic LRAT activity within 24 h, together with deposition of retinyl ester in the liver. These data strongly implicate LRAT activity in liver as responsible for the storage of hepatic retinyl esters. Retention of the intestine's capacity to esterify retinol during vitamin A deficiency provides a mechanism for capture of dietary vitamin A, while reduced hepatic LRAT activity may function to redirect retinol in liver from storage to other metabolic pathways.
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LRAT activity was much lower in the liver of vitamin A deficient rats compared to control animals.
“The initial studies by Dr. Ross and colleagues indicated that LRAT activity was much lower in the liver of vitamin A deficient rats as compared to the control animals.”
From Molecular Basis for Vitamin A Uptake and Storage in Vertebrates (2016) · cites this paper as [117]
LRAT activity could be induced by retinoic acid or supplemental vitamin A.
“Interestingly, LRAT activity could be induced by retinoic acid or supplemental vitamin A [117,118].”
From Molecular Basis for Vitamin A Uptake and Storage in Vertebrates (2016) · cites this paper as [117]
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- Authors
- Randolph, R. K., & Ross, A. C.
- ORCID
- Ross, A.C.
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- Journal of Biological Chemistry
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- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hd016484-09)
- National Heart, Lung, and Blood Institute (P01-HL22633, P01HL022633)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK-41479)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R-01 HD-16484)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- LRAT, vitamin A status, vitamin A deficiency, retinol esterification, retinol-binding protein, plasma retinol, liver microsomes, small intestine
- MeSH terms
- Acyltransferases, Animals, Intestines, Kinetics, Liver, Male, Microsomes, Liver, Organ Specificity, Rats, Inbred F344, Vitamin A, Retinol O-Fatty-Acyltransferase, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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