Tuesday, July 3, 2007

Intestinal absorption of Vitamin C

General principles
Approximately 80–90% of the vitamin C content of
a given foodstuff exists in the reduced form, ascorbic
acid; the remainder is in the oxidized form, dehydroascorbic
acid. Ascorbic acid and dehydroascorbic
acid are absorbed by separate transport mechanisms
in animal species that depend upon dietary vitamin
C (Fig. 19.3). Inside the absorptive cell (enterocyte)
of the intestinal epithelium, dehydroascorbic acid is
enzymatically reduced and the accumulated ascorbic
acid is transported across the basolateral membrane
to the bloodstream. In addition to uptake at the
brush-border membrane, dehydroascorbic acid from
the bloodstream can be taken up at the basolateral
membrane, reduced within the cell, and returned to
the circulation in the form of the useful and non-toxic
ascorbic acid. The serosal uptake of dehydroascorbic
acid from the bloodstream and intracellular reduction
to ascorbic acid take place in animal species which do
not have a dietary vitamin C requirement as well as
those species that do. The ability of the enterocyte to
absorb dehydroascorbic acid effi ciently is important
because, apart from the indigenous dehydroascorbic
acid content of the diet, additional oxidation of
ascorbic acid occurs in the gastrointestinal tract as
the vitamin functions to maintain other nutrients
such as iron in the reduced state. The intestinal uptake
and reduction of dehydroascorbic acid explains
why this compound, orally administered, maintains
plasma concentrations of ascorbic acid and prevents
scurvy. The overall system of intestinal transport and
metabolism is designed to maximize the conservation
of vitamin C and also to maintain the vitamin in its
non-toxic reduced state, whether it is derived from the
diet .

Effi ciency of ascorbate absorption in humans
The usual dietary intake of vitamin C ranges from 30–
180 mg per day and over this range the effi ciency of
absorption is 70–90% (Institute of Medicine, 2000).
Brush-border uptake by the sodium-coupled, secondary
active transport mechanism reaches its maximum
rate at a relatively low luminal concentration. Beyond
physiological intakes, absorption becomes progressively
less effi cient, falling from 75% of a single 1-g
dose to 16% of a single 12-g dose (Table 19.2). This
fall-off in effi ciency occurs because absorption of
high luminal concentrations of vitamin C takes place
mainly by simple diffusion, and this passive movement
proceeds at a very low rate.
The ingestion of eight 0.125-g doses of ascorbate
spaced throughout the day produced a 72% increase
in absorption compared to a single 1-g dose (Yung et
al., 1981). The absorption effi ciency of a single dose
can be improved if the ascorbate is ingested in the
form of a sustained-release capsule (Sacharin et al.,
1976). The ingestion of 1 g of ascorbate immediately
after a fatty meal produced a 69% increase in absorption
compared to the same dose given on an empty
stomach (Yung et al., 1981). The divided dose effect
is consistent with a saturable absorption mechanism,
while the after-meal effect indicates a slowing of gastric
Adaptive regulation of ascorbate absorption in
guinea pigs
In the guinea pig, intestinal absorption of ascorbate
is adaptively regulated in a transient and reversible
manner by the level of dietary ascorbate (Karasov et
al., 1991). The mechanism of regulation is an increase
or decrease in the number of carriers at both brushborder
and basolateral membranes of enterocytes in
response to low or high concentrations of ascorbate
in the blood. The rationale for adaptive regulation
is that carriers are most needed at low dietary ascorbate
levels; at excessive levels the required amount of
ascorbate can be absorbed by fewer carriers, aided by
passive diffusion. As ascorbate does not provide metabolizable
energy, there is nothing to gain from the
cost of synthesizing and maintaining carriers when
the vitamin supply is in excess. The issue of adaptive
regulation has not been examined in humans.

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