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Review
. 2011 Jan;3(1):63-103.
doi: 10.3390/nu3010063.

Vitamin A metabolism: an update

Diana N D'Ambrosio  1 , Robin D Clugston, William S Blaner
Affiliations
Review

Vitamin A metabolism: an update

Diana N D'Ambrosio et al. Nutrients. 2011 Jan.

Abstract

Retinoids are required for maintaining many essential physiological processes in the body, including normal growth and development, normal vision, a healthy immune system, normal reproduction, and healthy skin and barrier functions. In excess of 500 genes are thought to be regulated by retinoic acid. 11-cis-retinal serves as the visual chromophore in vision. The body must acquire retinoid from the diet in order to maintain these essential physiological processes. Retinoid metabolism is complex and involves many different retinoid forms, including retinyl esters, retinol, retinal, retinoic acid and oxidized and conjugated metabolites of both retinol and retinoic acid. In addition, retinoid metabolism involves many carrier proteins and enzymes that are specific to retinoid metabolism, as well as other proteins which may be involved in mediating also triglyceride and/or cholesterol metabolism. This review will focus on recent advances for understanding retinoid metabolism that have taken place in the last ten to fifteen years.

Keywords: adipocyte; carotenoid; chylomicron; hepatic stellate cell; hepatocyte; lecithin:retinol acyltransferase (LRAT); retinol-binding protein (RBP).

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Figures

Figure 1
Figure 1
General scheme for the uptake and metabolism of dietary retinoids and proretinoid carotenoids within the intestine. Dietary proretinoid carotenoids, like β-carotene, are taken up into the enterocyte through a process that involves SR-B1. Once inside the enterocyte, β-carotene can be acted upon by BCMO1 and either converted to retinal, which binds CRBPII, or can be incorporated intact and unmodified along with dietary fat and cholesterol into nascent chylomicrons. The retinal produced from β-carotene cleavage must undergo reduction to retinol. This is catalyzed by one or more not well-characterized retinal reductases. Upon conversion to retinol, the retinol formed from dietary proretinoid carotenoids is metabolically indistinguishable from retinoid arriving in the diet as preformed retinoid. Dietary retinyl ester is either hydrolyzed in the lumen of the intestine by PTL or PLRP2 or undergoes hydrolysis at the intestinal brush border catalyzed by a brush border REH. Retinol taken into the enterocyte binds to CRBPII and is esterified to retinyl ester. In response to a physiological challenge of retinol, LRAT will catalyze approximately 90% of retinyl ester formation, while the intestinal acyl‑CoA:retinol acyltransferase, DGAT1, catalyzes the remainder of retinyl ester formation. The resulting retinyl ester is then packed along with dietary fat and cholesterol into nascent chylomicrons, which are secreted into the lymphatic system.
Figure 2
Figure 2
Carotenoids can undergo cleavage either symmetrically by BCMO1 or asymmetrically by BCMO2.
Figure 3
Figure 3
Uptake of retinoids into extrahepatic tissues. Retinoids in the circulation are present in several forms, including retinol bound to RBP (holo-RBP), retinyl esters in lipoproteins (primarily chylomicrons, but also VLDL, LDL, and HDL), and retinoic acid bound to albumin. The mechanisms that mediate cellular uptake of retinyl ester and retinoic acid are not fully understood. However, it has been established for certain tissues that LpL can hydrolyse retinyl ester to retinol, which can then be taken up by tissues and cells. The transmembrane protein STRA6 is able to bind holo-RBP and facilitate its uptake into cells.
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References

    1. To be consistent with our experiences in using and understanding modern nomenclature usage, we will use the term retinoid in place of vitamin A throughout this review. The word retinoid is a generic term that includes both naturally occurring compounds with vitamin A activity and synthetic analogs of retinol, with or without the biological activity (Goodman, D.S. Vitamin A Metabolism. Federation Proc. 1980, 39, 2716–2722; and Goodman, D.S. Vitamin A and Retinoids in Health and Disease. N. Engl. J. Med. 1984, 310, 1023–1031). The focus of this review will be solely on the uptake, storage and metabolism of natural retinoids or their precursor proretinoid carotenoids. Consequently, for the purposes of understanding this review, the terms retinoid and vitamin A should be considered to be synonymous.

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