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USDA/ARS Western Human Nutrition Research Center, University of California, Davis, CA 95616
2To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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KEY WORDS: • zinc • zinc homeostasis • zinc absorption • zinc kinetics • zinc excretion
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). Changes in zinc absorption and excretion in the
gastrointestinal tract are the primary mechanisms for maintaining zinc
homeostasis. Adjustments in renal excretion also occur with extremely
low or high intakes of zinc. Tissue and cellular redistribution of zinc
may contribute further to the maintenance of zinc homeostasis. The
purpose of this report is to describe how these adjustments in zinc
homeostasis occur in animals and humans. |
Changes in zinc intake and whole body zinc content |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). When the zinc intakes of weanling experimental animals
ranged from 10 to 100 mg/kg, the content of the whole body zinc content
remained constant at ~30 mg/kg. Changes in the concentration of zinc
in the whole body changed only when very low (<10 mg/kg) or very high
(>100 mg/kg) intakes were consumed. The homeostatic mechanisms were
insufficient to maintain body zinc content with these extremes in
intake, and there was either a loss or an accumulation of zinc within
the body.
In humans, the effect of changes in dietary zinc on whole body zinc
content cannot be measured directly. Measurements of zinc balance,
however, provide a means for estimating changes in whole body zinc
content with changes in intake. Typically, human zinc intakes range
from 107 to 231 µmol/d; this is equivalent to ~14–30 mg/kg for
comparison with rat diets. These intakes support crude zinc balance
(i.e., replace fecal and urinary losses) in healthy adults, but balance
can be achieved when as little as 22 µmol/d (2.8 mg/kg) or as much as
306 µmol/d (40 mg/kg) is fed (Johnson et al. 1993
).
With these extreme reductions or increases in zinc intake, zinc losses
either fell or increased during the first 6–12 d after the dietary
change so that balance was achieved. Thus, humans appear to have the
capacity to regulate whole body zinc content over a 10-fold change in
intake, as has been observed in experimental animals.
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Intestinal regulation of zinc homeostasis |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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In detailed metabolic balance studies in rats (Weigand and Kirchgessner 1978
), the efficiency of zinc absorption decreased
from nearly 100% when a zinc-free diet was fed (group I) to
~55% when 7 µmol (0.5 mg) of zinc was fed daily (group IV)
(Fig. 1
). Endogenous fecal zinc (EFZ)3
excretion varied
30-fold, from 0.1 to 3.0 µmol/d, over the same range of intakes. In
groups I, II and III, endogenous zinc represented the major portion of
the total fecal zinc. From groups II to IV, each doubling of the
dietary zinc intake caused a fourfold increase in EFZ. The excretion of
endogenous zinc by the gastrointestinal tract is of major importance in
maintaining zinc balance just above and below optimal intakes. However,
it increases further with high intakes to fine tune the primary
adjustment in zinc absorption. Adjustments in urinary zinc excretion
were relatively minor in comparison with the gastrointestinal
adjustments.
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determined the changes in intestinal zinc absorption and
endogenous excretion in a man consuming 110, 230 or 473 µmol zinc/d
during three consecutive 8-d periods. With each increase in dietary
zinc, endogenous zinc excretion increased promptly (i.e., within the
first 4 d of each study period), going from 46 to 68 µmol/d from
period I to II and to 96 µmol/d in period III. Marked changes in zinc
absorption also occurred, but this did not occur until the last 4 d of each period (Fig. 2
). For example, during the first 4 d of period I, 58% of the zinc
intake was absorbed; during the second 4-d period, it dropped to 47%.
When zinc intake was doubled during the next 4 d in period II,
45% of the intake was absorbed during the first 4 d. This dropped
to 32% in the second 4-d period. Because the changes in endogenous
zinc excretion occurred promptly before the adjustment in zinc
absorption, it appears that the regulation of gastrointestinal zinc
endogenous excretion is independent of the regulation of absorption.
Urinary zinc excretion was essentially unchanged during the three
dietary treatments.
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Adjustments in fractional zinc absorption |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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, Turnlund et al. 1982
, 1986
,
Wada et al. 1985
) (Table 1
). All of the studies were performed with healthy adults who consumed
diets with adequate amounts of zinc before implementation of the study
diet. Four studies compared the response to different levels of zinc
intake. When the zinc intake was reduced from 252 to 85 µmol/d in a
study of six men (Wada et al. 1985
), fractional zinc
absorption increased from 25 to 49%. In another study, when zinc
intake was reduced from 192 to 63 µmol/d, fractional absorption
increased from 44 to 63% (Lee et al. 1993
). A study of
a reduction to a very low intake (85–12 µmol/d) caused fractional
zinc absorption to increase to 93% (Taylor et al. 1991
). Doubling the zinc intake from 109 to 224 to 472 µmol/d
caused fractional absorption to decline from 47 to 32 to 21%; the
lower the intake of zinc, the higher the rate of fractional zinc
absorption. Because fractional zinc absorption responds so dramatically
to large changes in zinc intake, it is a gross indicator of the amount
of zinc consumed. However, the fractional absorption of zinc varies
sufficiently within a group of individuals fed the same amount of zinc
that it becomes impossible to predict zinc intakes from the efficiency
of absorption measured at a single time.
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), permitted 11 µmol of
zinc to be absorbed rather than only 4.5 µmol if the fractional
absorption had remained at 40%. This adjustment in the efficiency of
zinc absorption provided an additional 6.5 µmol of zinc to the
tissues.
When the zinc intake is very low, absorption occurs primarily by a
carrier-mediated process (Cousins 1996
). Kinetic
studies performed in rats show that the increased efficiency in
absorption that occurs with reductions in intake is due to an increase
in the rate of transfer of zinc on the carrier across the mucosal
membrane rather than a change in the affinity of the carrier for zinc.
It is not known how this increased transfer of zinc by the carrier
occurs. Several investigators have proposed that the exocrine pancreas
secretes a ligand that enhances jejunal zinc absorption. When the
ligand is unsaturated with zinc, it binds dietary zinc in the lumen of
the intestine and somehow facilitates its absorption (Van Wouwe and Uijlenbroek 1994
). It is thought that this ligand might be
metallothionein (De Lisle et al. 1996
, Finley et al. 1994
, McClain 1990
, Oberlas 1996
, Van Wouwe and Uijlenbroek 1994
).
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Adjustments in endogenous fecal zinc excretion |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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), EFZ
dropped by 16 µmol/d. The up-regulation of zinc absorption
conserved only 6.5 µmol/d. The larger decline in EFZ than that
conserved by absorptive changes shows that the change in EFZ is not due
to shifts in absorption alone.
EFZ excretion is made up of two components of zinc metabolism: the
inevitable metabolic, or obligatory, loss and the endogenous loss that
is in excess of the obligatory loss and contributes to homeostasis by
increasing or decreasing the retention of absorbed zinc (Weigand and Kirchgessner 1980
). The obligatory EFZ loss can be
estimated from the amount of zinc excreted in the stools when a
zinc-free diet is fed; this is ~6–8 µmol/d (Baer and King 1984
).
The net effect of the adjustments in gastrointestinal absorption and
endogenous excretion with changes in intake is an overall shift in the
physiological capacity to provide zinc to the tissues. As dietary zinc
declines, the efficiency in zinc utilization increases, allowing the
reduced intake of zinc to be absorbed with a higher efficiency. Also,
the lower total zinc absorption is associated with a lower endogenous
excretion. These two actions result in an overall increased metabolic
efficiency (Weigand and Kirchgessner 1980
).
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Gastrointestinal regulation of zinc homeostasis in individuals with chronically low zinc intakes |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). Fractional zinc absorption, on the other hand, is only
influenced by current zinc intake. This suggests that the adjustment to
a high zinc intake by a population in marginal zinc status due to a
typical diet that is low in zinc would alter EFZ losses differently
than if the high zinc diet were fed to a population in good zinc
status.
A 6-mo study of low zinc intakes (63 µmol/d) in men confirmed the
findings in rats, i.e., that EFZ losses are affected more by
long-term poor zinc intakes than is fractional zinc absorption
(Lee et al. 1993
) (Fig. 3
). After the men had been on the low zinc diet for 2 mo, fractional zinc
absorption increased 48%, from 44 to 65%. Although fractional
absorption increased, the total absorbed zinc declined from 85 to 41
µmol/d and endogenous fecal losses fell by 27%, from 65 to 48
µmol/d. During the 6 mo the men were on the low zinc diet, fractional
and total zinc absorptions remained relatively constant, but the
endogenous zinc losses continued to decline from 65 µmol/d during
baseline to 48, 40 and 27 µmol/d at 2, 4 and 6 mo, respectively.
After 6 mo, this reduction in EFZ losses allowed the men to achieve a
positive crude zinc balance on this very low zinc diet. Net crude
balance was 4.7 µmol/d at 6 mo. It is unlikely, however, that this
was sufficient to replace zinc losses in the integument and semen. Data
from this study suggest that adjustments in zinc homeostasis with very
low intakes do not occur rapidly; however, changes continue to occur
for months, possibly until equilibrium is eventually established.
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).
Another study of the homeostatic response to a chronic intake of diets
low in zinc was performed in two groups of Chinese women: a group of
rural women habitually consuming 5.2 mg zinc/d (80 µmol/d) and an
urban group consuming 8.1 mg/d (125 µmol/d) (Sian et al. 1996
). Although the urban women consumed ~35% more dietary
zinc than the rural women, fractional zinc absorption did not differ
between the two groups; the urban and rural women absorbed 34 and 31%
of their intakes, respectively. Thus, the absolute amount of zinc
absorbed by the urban women was higher than that of the rural women
because they consumed more zinc: 42 versus 25 µmol/d. This increased
amount of zinc absorbed by the urban women (17 µmol/d) was nearly
balanced by the increased amount of endogenous zinc excreted in the
feces: 15 µmol/d (i.e., 35 versus 20 µmol/d). Thus, the rural
women, who were consuming only 80 µmol zinc/d, achieved homeostasis
and zinc balance by reducing EFZ losses rather than changing the
fractional rates of zinc absorption.
These two studies of low zinc intakes (Lee et al. 1993
,
Sian et al. 1996
), as well as other studies performed in
healthy, young infants (Krebs et al. 1993
), show that
the EFZ excretion is directly related to the total amount of zinc
absorbed after individuals have established a state of equilibrium on
the level of intake. If total zinc absorption is low, EFZ losses are
also reduced. The quantity of zinc that is absorbed undoubtedly
influences the amount of zinc in endogenous tissue pools, which in turn
may be associated with the amount of endogenous zinc excreted in the
feces.
In situations in which the tissue demand for zinc is high, as occurs
during lactation, this relationship between true zinc absorption and
EFZ losses is likely to change. Fractional zinc absorption increases
during lactation (Fung et al. 1997
) to provide
additional zinc for milk synthesis. Endogenous fecal losses may be
unchanged. Data from a study of fractional zinc absorption in a group
of Amazonian women consuming low zinc diets support this hypothesis
(Jackson et al. 1988
). The women consumed only 129
µmol zinc/d before and during full lactation; fractional zinc
absorption increased from 59 to 84%. The amount of zinc absorbed
increased by 30 µmol/d, but the EFZ losses remained low to provide
additional zinc for milk synthesis.
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Renal adjustments with changes in dietary zinc |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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); urinary losses range from 8 to 11
µmol/d. When zinc intake is very low, i.e., <~50 µmol/d, urinary
losses decline. Johnson et al. (1993)
measured the
changes in urinary zinc excretion when diets providing 21.9, 37.5, 51.6
and 67.8 µmol/d were fed. They found that urinary zinc excretion did
not decline until zinc intake was reduced to <51.6 µmol/d.
The decline in urinary zinc occurs very rapidly, in 2–3 d, after the
initiation of a very low zinc intake (unpublished data). The urinary
excretion data from a young man fed a diet providing only 4.5 µmol/d
is shown in Figure 4
. This decline in urinary zinc occurs before there are any changes in
plasma zinc concentration or in fractional zinc absorption. The
regulation of urinary zinc losses is not well understood. Studies in
dogs showed that glucagon infusions increased urinary zinc without
changing plasma zinc concentrations (Victery et al. 1981
); this increase is inhibited by an infusion of insulin
(Vander et al. 1983
). These hormonal changes in urinary
zinc excretion occurred without altering glomerular filtration rates.
Also, there was no evidence that other cations were affected by
glucagon or insulin infusions. Possibly, the shifts in urinary zinc
excretion are mediated by adjustments in renal tubular zinc transport.
Cysteine infusion has been shown to increase urinary zinc excretion
dramatically by causing a rise in net tubular secretion
(Abu-Hamdan et al. 1981
).
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), but only 2–6 µmol zinc/d
was conserved by adjustments in renal excretion. Although the changes
in urinary zinc occur quickly and may be as much as 100-fold, the
amount of zinc excreted in the urine is much less than that excreted in
the feces, so less is conserved. Because renal adjustments have a
relatively small impact on zinc conservation, it seems logical that
adjustments in renal conservation are not induced unless the intakes
are extremely low.
The rapid changes in endogenous fecal and urinary zinc losses with low
zinc diets limit the drop in plasma zinc concentrations (unpublished
data) (Fig. 5
). When dietary zinc was reduced from 241 to 4 µmol/d, fecal and
urinary zinc losses dropped ~75% by the end of the second week,
whereas the plasma zinc concentrations were unchanged. When dietary
zinc intake was reduced from 252 to 85 µmol/d (Wada et al. 1985
), fecal zinc losses declined markedly; there were no
changes in plasma zinc concentrations. Plasma zinc concentrations
change very slowly, if at all, with changes in zinc intake reducing the
value of this measurement for assessing zinc status. Because the plasma
must provide zinc to all of the tissues, maintaining relatively
constant plasma zinc concentrations is essential to sustaining normal
function and health.
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Other sources of zinc loss |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). When zinc intakes were reduced to 55 µmol/d, surface
losses declined by ~50%. Surface losses also tended to rise with
high zinc intakes (518 µmol/d). These adjustments in surface losses
occurred even though plasma zinc remained within the normal range. It
is not known how this adjustment in integumental zinc losses is made
with changes in intake.
Semen is rich in zinc and can represent a significant source of zinc
loss with frequent ejaculations. One ejaculation contains ~ 9
µmol zinc. Semen zinc losses decline with zinc depletion; severe zinc
depletion caused a 50% decrease in the amount of zinc per ejaculum
(Baer and King 1984
). This reduction in semen zinc seems
to be due to a decrease in semen volume rather than a change in the
concentration of zinc in the semen (Hunt and Johnson 1990
).
Typical hair and nail growth account for only 0.5 µmol zinc loss/d
(Baer and King 1984
).
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Shifts in tissue zinc concentrations to conserve whole body zinc |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). Another 11% is found in the skin and liver. The remaining 2–3% of
the whole body zinc is in all of the other tissues (Jackson 1989
).
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), but zinc loss was
not uniform across all tissues. Hair, skin, heart and skeletal muscle
zinc concentrations remained constant, whereas plasma, liver, bone and
testes zinc concentrations dropped significantly. After the low zinc
diet was fed for 80 d, plasma zinc was 45% lower than that of
controls, testes zinc was 53% lower, bone zinc was 64% lower and
liver zinc was 19% lower. It is interesting that hair zinc
concentrations did not change in this study of experimental animals.
Hair zinc has been used as a measure of zinc status in humans
(Hambidge 1982
). Possibly, hair zinc concentrations
change with long-term, marginal intakes but not with severe
depletion as was studied in these experimental animals.
A set of tissue zinc measurements from three patients in whom zinc
metabolism was abnormal provides unique information about the effect of
zinc depletion on tissue zinc concentrations in humans (Jackson et al. 1982
). In one patient, hair and skeletal muscle samples
were collected; in a second patient, skin and plasma samples were
collected before death and tissue samples were removed postmortem. In
the third patient, an 11-y-old boy with thalassemia treated with a
zinc-chelating agent, liver, bone, testes, hair, heart and
quadriceps muscle were removed postmortem and analyzed for zinc. As was
observed in experimental rats, hair, skin, skeletal muscle and heart
zinc concentrations were unchanged in these patients, but bone, liver,
testes and plasma zinc levels were significantly below normal values.
Bone zinc was 1.68 µmol/g dry weight (normal range, 2.30–3.80
µmol/g dry weight). Liver zinc was 1.01 µmol/g dry weight (normal
range, 1.24–3.34 µmol/g dry weight). Testes zinc was 0.49 µmol/g
dry weight (normal range, 0.78–1.91 µmol/g dry weight), and plasma
zinc ranged from 4.5 to 11.7 µmol/L (normal range, 11.4–17.8
µmol/L).
These data from both experimental animals and humans show that even though the changes in whole body zinc are small with severe depletion, some tissues lose significant amounts of zinc. It is unclear why the bone, liver, testes and plasma give up zinc during deficiencies, whereas the concentration in muscle and skin are maintained. Possibly, the drop in plasma zinc after the initiation of a severely low zinc diet signals certain tissues to increase the release of zinc and other tissues to retain zinc.
The bone contains about one third of the whole body zinc. Studies in
experimental animals and humans suggest that it is a significant source
of endogenous zinc when the dietary supply is low (Jackson et al. 1982
). Bone is not a conventional zinc store, however,
because there is no way to enhance the release of bone zinc during a
deficiency. The decline in bone zinc with depletion may reflect a
reduction in bone zinc uptake in response to the decrease in plasma
zinc rather than an increased release. Recent research by Zhou et al. (1993)
shows that the zinc released from bone comes
primarily from a rapidly turning over pool that composes 10–20% of
the total bone zinc. The second major pool turns over more slowly and
does not release zinc as readily for use elsewhere in the body in times
of zinc need.
The bone can apparently accumulate zinc in times of excess. In studies
of chicks, the administration of a high zinc diet before zinc depletion
allowed the bone to accumulate zinc that was released later during zinc
depletion. Chicks fed a high zinc diet before depletion survived for
longer periods of time without developing any symptoms of zinc
deficiency than did chicks fed typical zinc intakes before depletion
(Emmert and Baker 1995
).
Bone seems to function, therefore, as a passive reserve of zinc that is released, but not replaced, when the dietary supply is very low. No specific mechanisms for increasing the rate of bone zinc release have been identified. The rate of loss seems to be governed by normal rates of bone turnover. This is in stark contrast to the situation in the muscle in which zinc deposition is maintained at a rate that maintains a normal concentration.
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Zinc depletion and plasma kinetics |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). Plasma zinc concentrations also fall in humans in
experimental zinc depletion studies (Baer and King 1984
,
Johnson et al. 1993
, Taylor et al. 1991
).
Physiological signs of zinc depletion and changes in tissue zinc
concentrations are not evident until a drop in plasma zinc
concentration occurs. One can argue, therefore, that the fall in plasma
zinc concentration may be part of a homeostatic mechanism to maintain
critical levels of zinc in those tissues most susceptible to zinc
depletion. This second line of defense may only come into play when
there is a large drop in dietary zinc, when chronically low zinc
intakes have been consumed for a long time or when zinc intakes are
marginal in times of increased need, i.e., growth or lactation. Plasma zinc represents <0.1% of whole body zinc. In an adult, the plasma contains ~3.5 mg of zinc. Because all of the absorbed zinc passes through the plasma, i.e., ~50–75 µmol/d, the flux of zinc out of the plasma must be rapid to maintain a constant concentration. Using an intravenous stable isotopic tracer of zinc, 70Zn, we measured indices of zinc kinetics in five men before and after 5–6 wk of severe zinc depletion (<5 µmol/d; unpublished data). At baseline, plasma zinc turned over ~150 times/d, and ~7400 µmol of zinc was moved into and out of the tissues daily. This is roughly equivalent to one third of the whole body zinc. However, at the end of depletion when plasma zinc concentrations had declined by two thirds, from 12 to 4 µmol/L, the fractional turnover rate increased about one third from ~150 to 200 times/d. Plasma zinc mass fell more than the turnover rate increased, however, and the total amount of zinc moved into the tissues declined from 7400 to 4150 µmol/d. This reduction in the amount of zinc available to the tissues was associated with the onset of the clinical symptoms of zinc depletion.
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Use of tissue zinc as a reserve in severe zinc depletion |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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). When weanling rats were force fed a zinc-deficient
diet so that they were prevented from reducing their growth rates, the
rats rapidly became ill and died. In contrast, rats fed similar diets
ad libitum survive for several weeks longer, albeit with signs of zinc
deficiency. They survived, however, at the expense of the use of their
own tissue zinc. Typically, weanling animals fed zinc-deficient
diets develop a cyclic pattern of food intake that is 3–4 d in length
(O’Dell and Reeves 1989
). This cyclic pattern in food
intake causes the catabolism of tissues containing zinc, such as
muscle, and the release of that endogenous zinc for critical metabolic
functions. The prevention of tissue catabolism by force feeding the
animals seems to prevent a homeostatic response to an extremely low
zinc diet, and survival is impaired.
Zinc released from tissues during the catabolic phase is taken up and
retained very efficiently by other tissues. This was demonstrated by
Giugliano and Millward (1984)
. They measured the changes
in weight and zinc concentrations in various organs after weanling rats
had consumed a severely deficient diet for 24 d. During this
period, the net gain in total muscle zinc was ~25 µmol. This was
only ~5 µmol more than the amount of zinc lost from bone during the
same period. Apparently, muscle tissue gained weight and maintained its
zinc concentration by efficiently incorporating any zinc released by
the bone and small amounts obtained from the diet. This avid retention
of zinc in selected tissues during severe zinc deficiency contributes
to the marked drop in endogenous zinc losses and the overall efficient
use of dietary zinc.
Adjustments in gastrointestinal zinc absorption and intestinal endogenous zinc excretion are the primary means by which the body maintains constant tissue levels of zinc with varying intakes. With extremely low intakes or with prolonged marginal intakes, secondary homeostatic measures become operative. These secondary measures include a reduction in urinary zinc excretion, an increase in plasma fractional turnover rates and avid retention of zinc released from selected tissues, such as bone, in other tissues to maintain their zinc status.
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FOOTNOTES |
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3 Abbbreviation used: EFZ, endogenous fecal zinc.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONChanges in zinc intake...Intestinal regulation of zinc...Adjustments in fractional zinc...Adjustments in endogenous fecal...Gastrointestinal regulation of...Renal adjustments with changes...Other sources of zinc...Shifts in tissue zinc...Zinc depletion and plasma...Use of tissue zinc...REFERENCES |
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2.
Baer M. T., King J. C. Tissue zinc levels and zinc excretion during experimental zinc depletion in young men. Am. J. Clin. Nutr. 1984;39:556-570
3. Cousins R. J. Zinc. Ziegler E. E. Filer L. J., Jr eds. Present Knowledge in Nutrition 1996:293-306 ILSI Press Washington, DC.
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De Lisle R. C., Sarras M. P., Jr, Hidalgo J., Andrews G. K. Metallothionein is a component of exocrine pancreas secretion: implications for zinc homeostasis. Am. J. Physiol. 1996;271:C1103-C1110
5. Emmert J. L., Baker D. H. Zinc stores in chickens delay the onset of zinc deficiency symptoms. Poultry Sci 1995;74:1011-1021[Medline]
6. Finley J. W., Johnson P. E., Reeves P. G., Vanderpool R. A., Briske-Anderson M. Effect of bile/pancreatic secretions on absorption of radioactive or stable zinc: in vivo and in vitro studies. Biol. Trace Elem. Res. 1994;42:81-96[Medline]
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Fung E. B., Ritchie L. D., Woodhouse L. R., Roehl R., King J. C. Zinc absorption in women during pregnancy and lactation: a longitudinal study. Am. J. Clin. Nutr. 1997;66:80-88
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9.
Hambidge K. M. Hair analyses: worthless for vitamin, limited for minerals. Am. J. Clin. Nutr. 1982;36:943-949
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11. Jackson M. J. Physiology of zinc: general aspects. Mills C. F. eds. Zinc in Human Biology 1989:1-14 Springer-Verlag London.
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