Parker R S
Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853-6301, USA.
FASEB J. 1996 Apr;10(5):542-51.
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.
目前,类胡萝卜素因其调节慢性病风险和预防维生素A缺乏的潜力而受到密切关注,人们重新强调要更好地了解这些化合物在人体内的代谢归宿。新动物模型的开发以及人体代谢研究和稳定示踪方法的应用,极大地增进了我们对类胡萝卜素如何被吸收、代谢并转运至组织的了解;然而,许多重要问题仍未得到解决。例如,类胡萝卜素通过被动扩散被肠道吸收,但限制这一过程的肠腔或细胞内因素尚不清楚。肠黏膜在β-胡萝卜素等维生素A原类胡萝卜素的代谢中起关键作用,从而极大地影响其生物利用度。最新证据支持在肠黏膜中β-胡萝卜素裂解为视黄醛的核心氧化机制,但人体吸收后代谢的程度和部位尚不清楚。虽然人类和其他物种显然能吸收非维生素A类胡萝卜素,但对其代谢和消除的程度及途径知之甚少。β-胡萝卜素顺式异构体的代谢归宿是近期研究的一个课题,因为9-顺式视黄酸显然可在体外和体内由9-顺式β-胡萝卜素形成。尽管异构化部位尚不清楚,但至少小剂量口服9-顺式β-胡萝卜素在人体内会发生大量顺反异构化。类胡萝卜素在血浆中仅通过脂蛋白运输,其在脂蛋白类别中的分布在很大程度上由类胡萝卜素的物理性质决定。目前,不同分布对组织摄取和保留的影响尚不清楚。更好地了解类胡萝卜素的代谢归宿将有助于开发和检验关于其影响人体生物学过程潜力的假说。