Vldl

LDL-tcrtz

Lipids crt

Retinal

Tissues

Figure 3 Factors affecting digestion, absorption, metabolism, and transport of carotenoids. crt, carotenoids; CEH, carboxylic ester hydrolase, secreted by the pancreas; LPL, lipoprotein lipase; VLDL, very low-density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

levels in plasma after ingestion by 20-120%. The extent of this inhibition depends upon the amount of nonabsorbable compound ingested, as well as the particular carotenoid under consideration. The mechanism for this inhibition is apparently similar to the action of fiber, i.e., sequestration. The type of fat that is ingested along with carotenoids will also affect carotenoid absorption. As macerated food passes into the intestinal lumen, carotenoids freed from the food matrix then become incorporated into micelles, consisting of free fatty acids, monoglycer-ides, phospholipids, and bile acids. Many other factors can affect intestinal absorption such as micelle size, phospholipid composition, solubilization of car-otenoids into mixed micelles, and concentration of available bile salts, among others.

The presence of other carotenoids can affect the absorption of carotenoids into intestinal mucosal cells, since carotenoids can compete for absorption or facilitate the absorption of another. Data on carotenoid interactions are not clear. Human studies show that ^-carotene decreases lutein absorption, while lutein has either no effect or a lowering effect on ^-carotene absorption. Although not confirmed in humans, the inhibitory effect of lutein on ^-carotene absorption might be partly attributed to the inhibition of the ^-carotene cleavage enzyme by lutein shown in rats. Beta-carotene also seemed to lower absorption of canthaxanthin, whereas canthaxanthin did not inhibit ^-carotene absorption. Studies showed that ^-carotene increased lycopene absorption, although lycopene had no effect on ^-carotene. Alpha-carotene and cryptoxanthin show high serum responses to dietary intake compared to lutein. In addition, cis isomers of lyco-pene seem to be more bioavailable than the all-trans, and selective intestinal absorption of all-trans ^-carotene occurs, as well as conversion of the 9-cis isomer to all-trans ^-carotene. It is clear, then, that selective absorption of carotenoids takes place into the intestinal mucosal cell.

Another complicating factor in the intestinal muco-sal cell is the partial conversion of provitamin A car-otenoids (/3- and a-carotenes and cryptoxanthin) to vitamin A (primarily to retinyl esters). Therefore, in absorption studies these metabolic reactions must be accounted for in measuring intestinal transport. Non-provitamin A carotenoids such as lycopene, lutein, and zeaxanthin are incorporated intact, although some cleavage can occur. Earlier studies on rats indicated that lycopene and ^-carotene are absorbed by passive diffusion. However, recent evidence from the kinetics of ^-carotene transport through Caco-2 cell mono-layers indicates the involvement of a specific epithelial transporter that facilitates absorption.

In the intestinal mucosa, both carotenoids and retinyl esters are incorporated into chylomicrons and secreted into the lymph for transport to blood. In blood, lipoprotein lipase rapidly degrades the chylomicrons, and the liver sequesters the resulting carotenoid-containing fragments. The liver then secretes carotenoids back into the bloodstream in association with hepatic very low-density lipopro-teins (VLDL). Most carotenoids in fasting plasma are carried by low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Seventy-five per cent of the hydrocarbon carotenoids, e.g., lycopene and ^-carotene, are associated with LDL, the rest is associated with HDL and, in smaller amounts, with VLDL. More polar carotenoids such as lutein and zeaxanthin are found equally distributed between HDL and LDL. After ingestion, carotenoids first appear in the bloodstream in chylomicrons, resulting from excretion from intestinal mucosal cells (4-8 h). HDL carotenoid levels peak in the circulation between 16 and 28 h; LDL carotenoid levels peak between 24 and 48 h. The bloodstream then transports carotenoids to different tissues (e.g., liver, prostate gland, fat, ocular macula) where they are sequestered by various mechanisms.

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