Abstract

Carotenoids are currently under intense scrutiny regarding their potential to modulate chronic disease risk and prevent vitamin A deficiency, and renewed emphasis has been placed on achieving a better understanding of the metabolic fate of these compounds in humans. The development of new animal models, and use of human metabolic studies and stable tracer methods have greatly improved our knowledge of how carotenoids are absorbed, metabolized, and transported to tissues; however, many important issues remain unresolved. For example, intestinal uptake of carotenoids occurs by passive diffusion, but the lumenal or intracellular factors limiting this process are obscure. The intestinal mucosa plays a key role in the metabolism of provitamin A carotenoids such as beta-carotene, thus greatly influencing their bioavailability. Most recent evidence supports a central oxidation mechanism of cleavage of beta-carotene to retinal in the intestinal mucosa, but the extent and site(s) of postabsorptive metabolism in the human is unknown. While the human and other species clearly absorb non-provitamin A carotenoids, little is known of the extent and pathways of their metabolism and elimination. The metabolic fate of cis isomers of beta-carotene is a subject of recent interest, since 9-cis retinoic acid can apparently be formed from 9-cis beta-carotene in vitro and in vivo. Substantial cis-trans isomerization of at least small oral doses of 9-cis beta-carotene occurs in the human, although the site of isomerization is not yet known. Carotenoids are transported in plasma exclusively by lipoproteins, with the distribution among lipoprotein classes determined in large part by the physical properties of the carotenoid. The consequences of differential distribution in terms of tissue uptake and retention are not clear at present. Improved knowledge of the metabolic fate of carotenoids will assist in the development and testing of hypotheses regarding their potential to influence biological processes in the human.

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