Intestinal absorption

Ingested retinyl esters and provitamin A carotenoids
are liberated from their association with membranes
and lipoproteins by the action of pepsin in the stomach
and of proteolytic enzymes in the small intestine.
In the stomach the free carotenoids and retinyl esters
congregate in fatty globules, which then pass into the
duodenum. In the presence of bile salts, the globules
are broken up into smaller globules, which renders
them more easily digestible by a variety of pancreatic
lipases and results in the formation of mixed micelles.
Extensive hydrolysis of retinyl esters takes place within
the duodenum, catalysed mainly by a non-specifi c
pancreatic hydrolase that can act on a wide variety of
esters as substrates. Retinyl ester hydrolysis is completed
by brush-border hydrolases. With the exception
of esterifi ed xanthophylls, which are hydrolysed
by esterases, carotenoids are absorbed without prior
metabolic conversion.
The retinol and carotenoids contained within the
mixed micelles cross the unstirred layer of the intestinal
lumen and are released as a result of micelle
dissociation in the brush-border region. Physiological
concentrations of retinol derived from natural food
sources are absorbed by facilitated diffusion; at higher
concentrations a process of simple diffusion takes over.
The carrier-mediated absorption of retinol shows specifi
city toward all-trans retinol and 3-dehydroretinol;
uptake of 9-cis and 13-cis retinol and retinaldehyde
takes place by simple diffusion (Dew & Ong, 1994).
Carotenoid absorption is also by simple diffusion.
Preformed vitamin A and provitamin A carotenoids
(provitamins) of dietary origin differ in their effi ciency
of absorption. When foods containing normal physiological
amounts of these compounds are ingested,
retinol is absorbed with an effi ciency of 70–90%
compared with 20–50% for the provitamins. The
absorption effi ciency of retinol remains high as the
amount ingested increases beyond physiological levels,
whereas that of the provitamins falls markedly with
increased ingestion to less than 10%. Whereas crystalline
β-carotene in antioxidant-stabilized commercial
form is absorbed with an effi ciency of about 50%, the
absorption of carotenoids from raw carrot can be as
low as 1%. The cooking of vegetables increases absorption,
probably as a result of dissociation of carotenoids
from plant cell membranes and lipoproteins.
In a human study of β-carotene absorption, Blomstrand
& Werner (1967) fed single small doses of
radioactive β-carotene dissolved in vegetable oil to
hospitalized patients in whom cannulae had been
inserted into the thoracic duct. The percentages of
administered radioactivity recovered in the lymph of
three patients were 14.6, 8.7 and 16.8. In these patients
most of the radioactivity was found in the retinyl ester
fraction which contained 68 to 88% of the total radioactivity
in the lymph lipids. Smaller amounts of
radioactivity (1.7, 11.3 and 27.9%) were recovered in
the β-carotene fractions. These results demonstrate
that only a part of β-carotene consumed is absorbed
in the intestine. Most of that absorbed is converted in
the enterocytes to retinaldehyde and further to retinol
and retinyl esters; some remains as intact β-carotene.
There is a large variability, three- to four-fold
among healthy male humans, in effi ciency of carotenoid
absorption (Brown et al., 1989). In some people
there is no plasma response to a single oral dose of
β-carotene. Johnson & Russell (1992) measured β-
carotene concentrations in plasma and various lipoproteins
in healthy males for 10 days after a single oral
dose (120 mg) of β-carotene in capsule form. Seven of
the eleven subjects were nonresponders, showing little
or no increase in plasma β-carotene and only a small
response in chylomicrons. This lack of response may
be caused by ineffi cient uptake of luminal β-carotene
by enterocytes, ineffi cient incorporation of β-carotene
into chylomicrons, or extensive conversion of
β-carotene to retinyl esters. Of interest with the four
responders was that surges of chylomicron β-carotene
occurred every few days following the single dose,
suggesting delayed release of β-carotene from enterocytes.
It is possible that these surges were the result
of re-uptake of β-carotene from the intestinal lumen
following sloughing off of the epithelial cells.