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*
Department of Nutritional Sciences, University of California, Berkeley, CA 94720;
Western Human Nutrition Research Center, University of California, Davis, CA 95616; and
**
Department of Radiology, University of California, San Francisco, CA 94143
3To whom correspondence should be addressed. E-mail: jking{at}whnrc.usda.gov
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • zinc • zinc depletion • tracer kinetics • exchangeable zinc pools • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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. Because whole-body zinc homeostasis is readily
maintained by adjustments in fractional zinc absorption and endogenous
intestinal excretion, zinc intakes that are substantially lower than
the RDA may be adequate to maintain body zinc content (2)
.
However, the relationship between low zinc intake and the incidence of
mild-to-moderate zinc deficiency is difficult to assess because
reliable indicators of zinc status have not been identified
(3)
.
The zinc that maintains zinc-dependent functions is believed to be
mobilized from small, rapidly exchanging zinc pools found primarily in
the plasma and liver (4
,5)
. Miller and coworkers
(4)
estimated exchangeable zinc pool
(EZP)4
mass by analyzing plasma
samples taken between d 3 and 9 after zinc isotope infusion. They used
a single exponential term to represent the decay curve for this period,
and the y-intercept to calculate EZP. Using this method,
they found that EZP mass was dependent on zinc intake in healthy adults
on self-selected diets, and in two adults who were severely
zinc-restricted for a 1-wk period. It has been suggested that a
decline in one or more of the EZP could be associated with a depletion
of the zinc required for zinc-dependent functions and could lead to
symptoms of zinc deficiency (6)
. Also, rapid plasma zinc
flux has been used as an indicator of poor zinc status, although normal
values have not been established (7)
.
An assessment of the masses and turnover rates of EZP is possible using
compartmental modeling techniques that use stable isotopic tracer
labeling and frequent sampling of the plasma compartment. Lowe and
coworkers (8)
studied zinc turnover in healthy adults over
a 120-min period using intravenously administered
70Zn and found that the plasma tracer
disappearance response could be explained by a two-compartment
model. The approximate masses of the two compartments, believed to be
located in the plasma and a portion of the liver, were 3.5 mg and 17.5
mg zinc, respectively, in these subjects (8)
. Using a more
comprehensive kinetic model with sampling for 6 d, King and
coworkers (9)
studied the effect of severe zinc depletion
on EZP mass in five men given a purified diet containing 0.23 mg
zinc/d. The total EZP mass fell significantly when the men were
zinc-depleted, dropping from 166 mg at baseline to 106 mg after 5
wk of zinc restriction. Plasma zinc flux dropped from 475 to 231 mg/d
during this period (9)
.
In the present study, we used a kinetic modeling approach to investigate whether a reduction in zinc intake to 4.6 mg/d would result in changes in the masses or turnover rates of one or more of the EZP in healthy adult men. If EZP masses responded to a change in zinc intake and are accompanied by alterations in zinc function, EZP mass could be used as a potential indicator of zinc status. In addition, our analysis of short-term zinc kinetics would further characterize the metabolic responses to a low zinc diet.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The study was approved by the University of California Committee for
Protection of Human Subjects, and informed consent was obtained from
all subjects. Seven healthy men completed the study. Their ages ranged
from 27 to 47 y; all of the men were white. Their body mass
indices averaged 23.8 ± 3.8 kg/m2. The subjects were
screened to ensure that their plasma zinc concentrations were normal
(
12 µmol/L), their iron status was adequate, they were nonsmokers
and they regularly consumed meat. None of the subjects had a history of
acute or chronic illness, gastrointestinal surgeries, alcohol or drug
abuse or mineral megadosing.
Experimental design.
The subjects were housed in a metabolic unit for all but the first 3 wk
of the 20-wk study. The subjects initially lived at home but were given
their meals at the research center so that the baseline period could be
extended while minimizing the length of confinement. A controlled, 3-d
rotating diet was provided throughout the study. Zinc intakes were
adjusted during the baseline and repletion periods by giving zinc
gluconate supplements, and placebos were given during the low zinc
period. During the 5-wk baseline and 5-wk repletion periods, the zinc
intakes of the subjects totaled 13.7 mg/d, an amount chosen because it
was close to the 1989 RDA for zinc of 15 mg (10)
. In the
low zinc phase of the study, the subjects consumed 4.6 mg of zinc for
10 wk. The phytate:zinc molar ratio of the diet was low, averaging
5.5:1 during the low zinc period. During the periods of zinc
supplementation, the phytate:zinc molar ratio averaged 1.8:1.
Study diet.
The study diet consisted of conventional foods. Table 1
lists the foods given on d 3 of the 3-d cycle menu, and Table 2
shows the calculated average nutrient composition for the 3-d menu. An
extra-energy formula made from oil, sugar and dextromaltose was
added to diets to meet individual energy needs. Energy intake was
adjusted to maintain body weights during the baseline period of the
study. Egg albumen powder was added to the diets to provide at least
0.8 g protein per kg body (protein RDA) for each subject. The diet
met or exceeded the RDA for all nutrients except magnesium and calcium;
supplements of 125 mg/d and 200 mg/d, respectively, were given to meet
the RDA for these minerals. Iron supplements (3 mg/d) were also
provided to compensate for losses of iron due to blood sampling.
Subjects consumed deionized water ad libitum, and the amounts consumed
were recorded daily.
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Body composition measurements, which included bone mineral content,
total body water and body density, were performed four times during the
study: at the end of baseline, 3 wk and 10 wk after the start of the
low zinc period, and at the end of the 5-wk repletion period. Bone
mineral content was measured with a Lunar dual-energy X-ray
absorptiometer (Lunar Corp., Madison, WI) using software, Version 3.6z.
Total body water was estimated using a multiple-frequency
bioelectrical impedance analyzer (Model 4000; Xitron Technologies, San
Diego, CA). Body density was determined from underwater weight
following the procedures of Akers and Buskirk (11)
, and
corrections were made for intestinal volume (estimated at 100 mL) and
residual lung volume, which was measured using an oxygen dilution
method described by Wilmore (12)
. Percent body fat was
calculated using the Selinger equation for a four-compartment
model: % body fat = (2.747/Db - 0.714W +
1.1298B - 2.037) x 100, where Db = body
density, W = % total body water and B = % bone mineral.
Isotopic tracer preparation and administration.
The masses and turnover rates of the EZP were estimated by analyses of the plasma tracer disappearance data after intravenous administration of a stable isotopic zinc tracer given four times during the study: at the end of the baseline period, 3 wk after the start of the low zinc period (when metabolic adjustments to the low zinc intake were thought to be completed), at the end of the 10-wk low zinc period and at the end of the 5-wk repletion period. The tracer, highly enriched in 70Zn (85.03% abundance) was purchased as zinc oxide (Oak Ridge National Laboratory, Oak Ridge, TN). It was dissolved in a minimal volume of concentrated ultrapure hydrochloric acid (Optima; Fisher Scientific, Pittsburgh, PA) and diluted to a zinc concentration of 0.592 g/L with triply deionized water. Sterilization and pyrogen testing was performed at a University of California, San Francisco pharmacy, where it was divided into aliquots in sealed, sterile vials for intravenous use.
On the morning of a tracer study day, an indwelling catheter was placed
into the antecubital vein and a 6-mL blood sample was collected from
fasting subjects. After breakfast was consumed, the isotopic zinc
tracer (
0.5 mg Zn) was injected intravenously into the opposite arm
of the subject. Blood samples (6 mL) were collected into zinc-free
polypropylene Monovette syringes with ammonium heparin-coated beads
(Sarstedt, Newton, NC) at 2, 5, 10, 20, 30, 45, 60 min; 2, 3, 6, 9,
12 h; and 1, 2, 4, 6 and 8 d after infusion. The samples were
immediately placed on ice and the plasma separated from RBC by
centrifugation at 230 x g for 10 min using a
refrigerated Sorvall RC-5C centrifuge (DuPont, Wilmington, DE), and the
plasma was frozen at -20°C for later analysis.
Preparation and analysis of plasma samples.
Blood samples were collected weekly from fasting subjects to monitor plasma zinc concentrations, which were analyzed using flame atomic absorption spectroscopy on a Smith-Hieftje 22 spectrometer (Thermo Jarrell Ash Corporation, Franklin, MA). The plasma samples were diluted eightfold in 0.125 mol/L nitric acid (Trace Metal Grade; Fisher Scientific), and a bovine liver standard (National Institute of Standards and Technology, Gaithersburg, MD) was analyzed with each run as an internal control.
Only ultrapure acids (Optima; Fisher Scientific) were used for zinc purification and analysis. Plasma samples (2 mL) were digested in 5 mL concentrated HNO3 using microwave digestion (MDS 2000; CEM Corporation,Matthews,NC), evaporated completely in Teflon beakers (Chemware; Norton Performance Plastics Corporation, Wayne, NJ) and resuspended in 10 mL of 2.5 mol/L HCl. Zinc was purified from samples by ion-exchange chromatography using an anion-exchange resin (AG1-X8 resin, 100–200 mesh, chloride form; Bio-Rad Laboratories, Hercules, CA) that was equilibrated in 0.005 mol/L HCl, packed into polypropylene chromatography columns and acidified using 10 mL sequential additions of 0.005 mol/L, 0.5 mol/L and 2.5 mol/L HCl. The digest (in 2.5 mol/L HCl) was added to columns, washed with 5 mL of 2.5 mol/L and 1 mL of 0.5 mol/L HCl and zinc was eluted from columns using 0.005 mol/L HCl. This fraction was evaporated to dryness in Teflon beakers and resuspended in 1% nitric acid to yield a concentration of 0.25 ppm (mg/L) zinc. Stable zinc isotopic ratios were analyzed using inductively coupled plasma mass spectrometry on a Sciex ELAN 6000 inductively coupled plasma mass spectrometry equipped with a Ryton crossflow nebulizer and AS-90 autosampler (Perkin-Elmer Sciex Instruments, Concord, Ontario, Canada). Zinc standards (0.25 ppm) were analyzed with each run to calibrate isotopic ratio values and to monitor drift.
Kinetic analysis of isotopic data.
The isotopic ratio data were converted to tracer-tracee ratios to
correct for zinc isotopic masses present in the tracer preparation and
plasma samples, as described previously (13)
. The
tracer-tracee ratio (m/M) is defined as the ratio between moles of
zinc in the tracer (m) and moles of naturally occurring zinc in the
sample (M). For 70Zn, the simplified equation for the
tracer:tracee ratio in a sample is:
 |
where m66, m67 and m70 are the moles of 66Zn, 67Zn and 70Zn in the tracer, respectively.
The masses and turnover of the EZP were estimated from the
tracer-tracee plasma disappearance data, using SAAM II kinetic
modeling software (SAAM Institute, Seattle, WA). The data obtained
within the first 3 h after tracer administration were analyzed by
two-compartment kinetics, as illustrated in Figure 1
A. Data collected during the full 190-h (8-d) protocol were
best fit by a three-compartment model, shown in Figure 1
B. The circles shown in the model represent kinetically
distinct zinc compartments, and the arrows, designated as
ki,j, indicate the rate constants of
zinc transfer from compartment j to compartment
i, per hour. The plasma mass, into which the isotopic tracer
was introduced, is represented by Qa, the rapidly
exchanging zinc compartments by Qb and
Qc, and the sum of the mass of the model’s
compartments represents the total EZP mass. Other parameters were
calculated as follows: fluxi,j =
ki,j x mass of compartment
j; plasma fractional turnover = sum of rate constants
exiting from Qa; plasma zinc flux = plasma
fractional turnover x Qa mass. The
uncertainty estimates of computed measures of the compartmental models
were determined from the covariance matrix at the least squares fit.
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Because EZP have been studied using a variety of methods
(4
,14
,15)
and experimental results can be difficult to
compare, our results will be presented in terms of the time dimension
over which data were collected and analyzed, as proposed by
Fairweather-Tait et al. (15)
. Zinc pools analyzed from
data obtained within 3 h after tracer infusion will hereafter be
termed EZP(0–3 h), and pools calculated using data from the full 190-h
protocol will be designated EZP(0–190 h).
Zinc-enzyme activity and clinical laboratory values.
To help monitor zinc status, blood samples were collected from fasting subjects and serum prepared at each metabolic period for the analysis for zinc-enzyme activity. Serum 5'nucleotidase activity was analyzed using a coupled-enzyme analysis kit (265 A; Sigma, St. Louis, MO) and automated spectrophotometric analyzer (Cobas FARA II; Roche, Palo Alto, CA), according to the manufacturer’s directions. Alkaline phosphatase was measured as part of a sequential multiple analysis (SMAC-20) blood panel performed by a private clinical laboratory (Chemzyme Plus; SmithKline Beecham Clinical Laboratories, San Francisco, CA). Values for serum iron, glucose, cholesterol, creatinine and albumin also were obtained from the SMAC-20 analyses. Hemoglobin and hematocrit values were obtained from analysis of whole blood samples from fasting subjects using a System 9000 DIFF automated cell counter (Biochem Immunosystems, Allentown, PA).
Statistical analysis.
Data were analyzed by repeated-measures ANOVA, followed by Tukey’s studentized range test for pair-wise comparisons. Differences with P < 0.05 were considered significant. When data were unavailable, estimates whose addition minimized the error mean square were substituted for missing values, and the degrees of freedom adjusted accordingly when performing statistical tests. These estimates were required for the baseline data of two subjects and for the 10-wk zinc restriction data of one subject. Analyses were performed using the Statistical Package for Social Sciences software (SPSS, Chicago, IL) located on mainframe computers at the University of California at Berkeley.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The subjects’ general health was stable during the study and all
clinical values were within normal ranges (Table 3
). Serum iron concentrations were significantly lower by the end of the
zinc restriction and repletion periods compared with baseline values
(P < 0.05). Fasting glucose concentrations increased
during the study, and they were significantly greater (P
< 0.05) at the end of depletion than they were at the end of
baseline. Subjects gained an average of 2.1 kg between the baseline
period and the end of the study, which was primarily due to a 1.7 kg
increase in fat mass.
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There were no significant changes in plasma zinc concentrations of
fasting subjects (Table 3)
. The activities of the zinc enzymes alkaline
phosphatase and 5'nucleotidase remained stable throughout the study.
Preliminary analyses of urine and fecal samples indicate that zinc
balance was unaffected during the study (16)
; these
results will be presented in a separate publication.
Compartmental analysis.
Typical fits of the two- and three-compartment models to the plasma
tracer-tracee data are shown in Figure 2
. The 3-h data for all subjects were fitted adequately by the
two-compartment model shown in Figure 1
A, and the 190-h
data required the three-compartment model shown in Figure 1
B. None of the pool masses or kinetic parameters changed
significantly during the study (Table 4
). In addition, the plasma zinc mass (Qa) and
total EZP masses did not change when values were expressed per kilogram
of body or fat-free mass (data not shown); the average
Qa value was 0.056 mg/kg fat-free mass, and
values for EZP(0–3 h) and EZP(0–90 h) masses were 0.329 and 2.63
mg/kg fat-free mass, respectively. However, the subjects’
individual values for total EZP mass were found to correlate with their
fat-free masses (Fig. 3
; r = 0.89 and 0.91 for EZP(0–3 h) and EZP(0–90 h)
masses, respectively; P < 0.01).
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and increased to
near-baseline values by the end of the 10-wk restriction period.
Values obtained from three-compartment modeling showed that plasma
zinc flux dipped 10.7% after 3 wk of zinc restriction but was only
3.4% lower at the end of the 10-wk restriction period. |
DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Although the subjects’ dietary zinc intake was restricted to 4.6 mg of
highly available zinc (42% of the 2001 RDA), they remained in good
health throughout the study and showed no indication of zinc
deficiency. Plasma zinc concentrations and zinc-enzyme activities
of fasting subjects were maintained during the 10-wk zinc restriction
period (Table 3)
. The phytate:zinc ratio of the experimental diet used
in this study was lower than is customarily found in Western diets and
much lower than that of typical diets in developing countries, and,
therefore, a diet containing 4.6 mg of zinc might not be adequate when
zinc is less available.
The 28% drop in average serum iron concentrations (Table 3)
was
probably due to the high volume of blood taken for analyses, because
each subject donated 1000 mL of blood during the 20-wk study. This
suggests that the supplemental iron that was given was insufficient to
maintain iron stores. However, all of the subjects’ serum iron values
remained within normal ranges throughout the study.
It is not clear why fasting plasma glucose concentrations were
significantly higher at the end of the zinc restriction period compared
with baseline values (Table 3)
. It is possible that the increase was
related to some aspect of the study diet or protocol, because the
values remained elevated during repletion. Alternatively, the
subjects’ response could reflect changes in carbohydrate metabolism
that resulted from ingesting a low zinc diet. Solomon and King
(17)
reported that blood glucose concentrations of fasting
subjects increased significantly, from 5.09 ± 0.23 mmol/L to 5.61
± 0.26 mmol/L, when six healthy men consumed a diet containing
5.5 mg zinc/d for 54 d; there was no significant difference in
their responses to a standard glucose tolerance test, however. As in
the study of Solomon and King, all of our subjects’ fasting plasma
glucose values remained within normal ranges during the study.
Zinc pool mass.
Previous studies suggest that the total EZP mass in healthy individuals
(4)
and in populations (18)
may correlate
with zinc intakes. One of our primary objectives was to verify this
putative influence of zinc intake on EZP mass, and to determine whether
a decline in total EZP mass correlates with losses in
zinc-dependent functions, which would indicate that EZP mass is a
dependable indicator of zinc status. However, our two- and
three-compartment modeling results did not reveal any significant
changes in any of the zinc pool masses during the zinc restriction
period (Table 4)
. Thus, the 4.6 mg/d zinc intake either supplied
sufficient zinc to maintain the subjects’ zinc pools or the length of
the zinc restriction period was not long enough to elicit a decline.
Also, previous studies (4
,18)
reporting correlations
between EZP masses and zinc intakes used a single slope method to
approximate the isotopic plasma disappearance rather than a kinetic
model fitted to all the data, which included early as well as late
values. Possibly, the two approaches may represent different aspects of
zinc metabolism and are not comparable.
Our first kinetic measurement during the zinc restriction period was
done after subjects were zinc restricted for 3 wk. It is possible that
changes in the masses and rate constants of the EZP occurred when zinc
restriction was initiated and the kinetic values had returned toward
baseline before measurements were made after 3 wk. Our
three-compartment modeling results suggest that the half-lives
for compartments Qa, Qb and
Qc are 8 min, 85 min and 14 h,
respectively. Thus, zinc pool masses could return to a new steady state
within 1 wk and any earlier changes would be missed by 3 wk. For this
reason, total EZP mass may be a poor indicator of modest changes in
zinc status because of the apparently rapid rate at which a new steady
state is reestablished. Acute zinc depletion may have a more notable
effect. In our previous zinc depletion study in which five healthy men
consumed a formula diet containing 0.23 mg zinc/d for 5 wk
(9)
, there was a marked 65% drop in plasma zinc
concentrations and average total EZP mass (based on isotopic data
collected from 0 to 144 h) declined 36%. Possibly, EZP mass may
not change unless there is a critical loss of whole-body zinc.
Our data suggest that total EZP mass is related to body size in healthy
individuals, because the EZP masses correlated well with the
fat-free masses of the subjects (Fig. 3
; r = 0.89
and 0.91 for EZP(0–3 h) and EZP(0–90 h) masses, respectively;
P < 0.01). This is what might be expected because zinc
is an integral part of the protein mass in lean tissue. These results
suggest that EZP may be more meaningful if expressed in terms of
fat-free mass and that body size should be taken into account when
the EZP values of individuals are compared.
Plasma zinc flux.
Results of two- and three-compartment modeling showed that plasma
zinc flux tended to decline 10% after subjects were zinc restricted
for 3 wk (Table 4
; P = 0.11 and P = 0.06 for the two- and three-compartment models, respectively). This
suggests that there is a temporary reduction in the amount of zinc
available from the plasma compartment when an individual lowers the
amount of zinc in his diet. Plasma zinc flux declined markedly in our
earlier zinc depletion study in which five healthy men were given 0.23
mg zinc/d (9)
. Kinetic modeling data from that study
showed that plasma zinc flux at the end of the baseline period was 475
mg/d and fell to 231 mg/d after 5 wk of severe zinc restriction. The
decreased flux was explained by lower plasma zinc content rather than
by changes in plasma rate constants. Data from our
three-compartment model showed that plasma zinc mass decreased
slightly in five of the seven subjects, and the rate constant
k2,1 decreased in all subjects. The fall in both
the plasma mass and the rate constant contributed to the
near-significant decrease in plasma zinc flux. The
three-compartment modeling results also show an increase in
k1,2 values in six of the seven subjects between
wk 3 and 10 of zinc restriction; this accounts for the increase in the
plasma zinc flux back to baseline values. The shift in zinc flux
between the plasma compartment and compartment two, which is believed
to consist primarily of liver zinc (19)
, suggests that the
liver plays a role in maintaining plasma zinc content.
Plasma zinc flux has been used to evaluate zinc status in other
studies. Not all of these studies were in malnourished populations.
Yokoi et al. (7)
used the
67Zn-enrichment values of plasma samples
collected between 30 and 60 min after tracer infusion to calculate
67Zn disappearance constants and zinc turnover
rates. Faster zinc turnover was used to identify subjects believed to
be in poorer zinc status (on average, rates were 32% higher); however,
no other indicators of zinc nutriture were reported in that study.
Using a similar method, Prasad (20)
found that zinc
turnover rates in zinc-deficient Egyptian subjects were 50%
greater than those of normal controls. Jackson et al. (21)
compared plasma 67Zn turnover rates of poor,
lactating Amazonian women on consistently low dietary zinc intakes with
the much slower zinc turnover rate found in a single healthy British
man (14)
to help gauge the women’s zinc nutriture; his
estimates were derived from the slopes of semilogarithmically plotted
plasma responses. The use of single disappearance constants for
monitoring plasma zinc flux has not been validated using zinc
restriction studies, and the optimum protocol for calculating zinc flux
remains in question. Our results suggest that plasma zinc flux
initially decreases and then recovers when dietary zinc is restricted
in healthy adults.
In summary, seven men were able to maintain good health and showed no
signs of zinc deficiency when they consumed 4.6 mg of highly available
zinc/d over a 10-wk period. Other than a transient reduction in plasma
zinc flux during early restriction, measures of zinc kinetics, plasma
zinc and zinc-enzyme activity did not change, and they do not seem
to be useful indicators for identifying short-term marginal zinc
intakes. We were unable to confirm an association between total EZP
mass and zinc intakes, as reported previously (4
,18)
.
Instead, total EZP mass was maintained on short-term zinc intakes
of 4.6 mg/d.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Presented at Experimental Biology 1998, the annual meeting of the Federation of American Societies for Experimental Biology [Pinna, K., Woodhouse, L. R., Sutherland, B., Shames, D. M. & King, J. C. Effect of a low zinc diet on plasma zinc turnover and exchangeable zinc pools in healthy men. FASEB J. 13: A569 (abs. 448.6)].
4 Abbreviations used: EZP, exchangeable zinc pool; EZP(0–3 h), exchangeable zinc pools, based on data collected from 0 to 3 hours after tracer infusion and analyzed by two-compartment modeling; EZP(0–190 h), exchangeable zinc pools, based on data collected from 0 to 190 hours after tracer infusion and analyzed by three-compartment modeling.
Manuscript received January 8, 2001. Initial review completed February 5, 2001. Revision accepted June 12, 2001.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Food and Nutrition Board, Institute of Medicine (2001) Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2001 National Academy Press Washington, DC. .
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King J. C., Shames D. M. & Woodhouse L. R. (2000) Zinc homeostasis in humans. J. Nutr. 130:1360S-1366S.
3. King J. C. (1990) Assessment of zinc status. J. Nutr. 120:1474-1479.
4. Miller L. V., Hambidge K. M., Naake V. L., Hong Z., Westcott J. L. & Fennessey P. V. (1994) Size of the zinc pools that exchange rapidly with plasma zinc in humans: alternative techniques for measuring and relation to dietary zinc intake. J. Nutr. 124:268-276.
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6. Golden M.H.N. (1989) The diagnosis of zinc deficiency. Mills C. F. eds. Zinc in Human Biology 1989:323-333 Springer-Verlag London, England. .
7. Yokoi K., Alcock N. W. & Sandstead H. H. (1994) Iron and zinc nutriture of premenopausal women: associations of diet with serum ferritin and plasma zinc disappearance and of serum ferritin with plasma zinc and plasma zinc disappearance. J. Lab. Clin. Med. 124:852-861.[Medline]
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King J. C., Shames D. M., Lowe N. M., Woodhouse L. R., Sutherland B., Abrams S. A., Turnlund J. R. & Jackson M. J. (2001) Effect of acute zinc depletion in men on zinc homeostasis and plasma zinc kinetics. Am. J. Clin. Nutr. 74:116-124.
10. Food and Nutrition Board, National Research Council (1989) Recommended Dietary Allowances 1989 National Academy Press Washington, DC. .
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Akers R. & Buskirk E. R. (1969) An underwater weighing system utilizing "force cube" transducers. J. Appl. Physiol. 26:649-652.
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Lowe N. M., Shames D. M., Woodhouse L. R., Matel J. S., Roehl R., Saccomani M. P., Toffolo G., Cobelli C. & King J. C. (1997) A compartmental model of zinc metabolism in healthy women using oral and intravenous stable isotope tracers. Am. J. Clin. Nutr. 65:1810-1819.
14. Jackson M. J., Jones D. A. & Edwards R.H.T. (1984) Zinc homeostasis in man: studies using a new stable isotope-dilution technique. Br. J. Nutr. 51:199-208.[Medline]
15. Fairweather-Tait S. J., Jackson M. J., Fox T. E., Wharf S. G., Eagles J. & Croghan P. C. (1993) The measurement of exchangeable pools of zinc using the stable isotope 70Zn. Br. J. Nutr. 70:221-234.[Medline]
16. Mertz S. D., Woodhouse L. R., Pinna K., Sutherland B. & King J. C. (2000) Adjustments in fractional and total zinc absorption in men fed low zinc diets. FASEB J 14:A226 (abs. 164.2).
17. Solomon S. J. & King J. C. (1983) Effect of low zinc intake on carbohydrate and fat metabolism in men. Fed. Proc 42:391A (abs. 574).
18.
Sian L., Mingyan X., Miller L. V., Tong L., Krebs N. F. & Hambidge K. M. (1996) Zinc absorption and intestinal losses of endogenous zinc in young Chinese women with marginal zinc intakes. Am. J. Clin. Nutr. 63:348-353.
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