Role of vitamin A in human metabolic processes

July 12, 2011

Role of vitamin A in human metabolic processes

Vitamin A (retinol) is an essential nutrient needed in small amounts by humans for the normal functioning of the visual system; growth and development; and maintenance of epithelial cellular integrity, immune function, and reproduction. These dietary needs for vitamin A are normally provided for as preformed retinol (mainly as retinyl ester) and provitamin A carotenoids.

Vitamin-A-Supplements

Overview of vitamin A metabolism

Preformed vitamin A in animal foods occurs as retinyl esters of fatty acids in association with membrane-bound cellular lipid and fat-containing storage cells. Provitamin A carotenoids in foods of vegetable origin are also associated with cellular lipids but are embedded in complex cellular structures such as the cellulose-containing matrix of chloroplasts or the pigment-containing portion of chromoplasts. Normal digestive processes free vitamin A and carotenoids from food matrices, which is a more ef?cient process from animal than from vegetable tissues. Retinyl esters are hydrolysed and the retinol and freed carotenoids are incorporated into lipid-containing, water-miscible micellar solutions. Products of fat digestion (e.g. fatty acids, monoglycerides, cholesterol, and phospholipids) and secretions in bile (e.g. bile salts and hydrolytic enzymes) are essential for the ef?cient solubilization of retinol and especially for solubilization of the very lipophilic carotenoids (e.g. a- and bcarotene, b-cryptoxanthin, and lycopene) in the aqueous intestinal milieu.
Micellar solubilization is a prerequisite to their ef?cient passage into the lipidrich membrane of intestinal mucosal cells (i.e. enterocytes) (1–3). Diets critically low in dietary fat (under about 5–10 g daily) (4) or disease conditions that interfere with normal digestion and absorption leading to steatorrhoea (e.g. pancreatic and liver diseases and frequent gastroenteritis) can therefore impede the ef?cient absorption of retinol and carotenoids. Retinol and some carotenoids enter the intestinal mucosal brush border by diffusion in accord with the concentration gradient between the micelle and plasma membrane of enterocytes. Some carotenoids pass into the enterocyte and are solubilized into chylomicrons without further change whereas some of the provitamin A carotenoids are converted to retinol by a cleavage enzyme in the brush border. Retinol is trapped intracellularly by re-esteri?cation or binding to speci?c intracellular binding proteins. Retinyl esters and unconverted carotenoids together with other lipids are incorporated into chylomicrons, excreted into intestinal lymphatic channels, and delivered to the blood through the thoracic duct.
Tissues extract most lipids and some carotenoids from circulating chylomicrons, but most retinyl esters are stripped from the chylomicron remnant, hydrolysed, and taken up primarily by parenchymal liver cells. If not immediately needed, retinol is re-esteri?ed and retained in the fat-storing cells of the liver (variously called adipocytes, stellate cells, or Ito cells). The liver parenchymal cells also take in substantial amounts of carotenoids. Whereas most of the body’s vitamin A reserve remains in the liver, carotenoids are also deposited elsewhere in fatty tissues throughout the body. Usually, turnover of carotenoids in tissues is relatively slow, but in times of low dietary carotenoid intake, stored carotenoids are mobilized. A recent study in one subject using stable isotopes suggests that retinol can be derived not only from conversion of dietary provitamin carotenoids in enterocytes—the major site of bioconversion—but also from hepatic conversion of circulating provitamin carotenoids. The quantitative contribution to vitamin A requirements of carotenoid converted to retinoids beyond the enterocyte is unknown.