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Centre de Recherche en Nutrition Humaine d’Auvergne, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 St Genès Champanelle, France and * U.S. Department of Agriculture/ARS Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030
1To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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170 g
were fed a control diet (500 mg Mg/kg), a marginally Mg-deficient
diet (200 mg/kg) or a severely Mg-deficient diet (60 mg Mg/kg) for
2 wk. Subsequently, rats were administered an intravenous injection of
25Mg, and the plasma 25Mg disappearance curve
was followed for the next 7 d. The following two methods were
employed to analyze the exchangeable pools of Mg: 1)
formal compartmental modeling and 2) a simplified
determination of the total mass of the rapidly exchangeable Mg pool
(EMgP). The mass of the three exchangeable pools (two extracellular
pools and one intracellular pool) determined by compartmental analysis
decreased in proportion to dietary Mg intake. EMgP, the combined pools
of Mg that exchange with the plasma Mg within 48 h, decreased
significantly as dietary Mg was lowered. It was positively correlated
with conventional markers of Mg status (total Mg in plasma, erythrocyte
and tibia Mg levels). Compartmental analysis assesses Mg exchangeable
pools more accurately, but determination of EMgP is simpler and faster.
Our findings demonstrate that the exchangeable pools of Mg constitute a
good marker of Mg status in rats.
KEY WORDS: • magnesium • exchangeable pool • status • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Mg deficiency leads to severe biochemical changes and
neuromuscular disorders, and increasing evidence suggests that Mg
deficiency as well as abnormalities in Mg metabolism may play an
important role in alcoholism, diabetes mellitus and cardiovascular
diseases (Durlach 1988
, Rude 1998
). In
developed countries, marginal Mg intake may increase the prevalence of
Mg deficiency (Galan et al. 1997
, Pennington and Schoen 1996
). Conventional Mg status markers represent only the
extracellular Mg level (plasma and urinary Mg). Only severe
deficiencies can be detected using these markers or erythrocyte Mg as a
marker of Mg status. The assessment of deep tissue Mg status is more
interesting. However, although Mg tissue measurements are available for
animal studies, the use of tissue markers is not practical in humans
(Rude 1998
, Shils 1994
).
The concept of the exchangeable pool, measured using either radioactive
or stable isotopes, has been developed to estimate mineral
bioavailability and status in humans, including growing children
(Abrams and Ellis 1998
). We showed recently, using
severely Mg-deficient rats, that exchangeable pool measurement of
Mg status can be performed in rats (Feillet-Coudray et al. 2000
). The purpose of this study was to explore the
exchangeable pools of Mg in rats of varied Mg status (control, marginal
and severe deficiency). The following two methods were employed to
analyze exchangeable pools of Mg: 1) compartmental analysis
with a model described by Avioli and Berman (1966)
and
2) determination of the total size of the rapidly
exchangeable Mg pool (EMgP), using the method of Miller et al. (1994)
.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Enriched Mg (200 mg; 96.7% 25Mg, 2.2% 24Mg and 1.1% 26Mg) in the oxide form, was obtained from Chemagas (Paris, France). Suprapure HNO3, suprapure H2O2, suprapure HCl, lanthanum oxide and standard solutions of Mg (1 g/L) were obtained from Merck (Darmstadt, Germany). All other chemicals were of the highest quality available, and demineralized water was used throughout. The Mg isotope-ratio measurements were performed using an inductively coupled plasma/mass spectrometry (ICP/MS) instrument (Plasma Quad-II System, Fisons Instruments, Manchester, UK), equipped with a Meinhard nebulizer. An atomic absorption spectrometer, Perkin Elmer 560 (Perkin Elmer, St-Quentin en Yvelines, France), was used for total Mg measurements.
Animals and diets.
Male Wistar rats (IFFA-CREDO, L’Arbresle, France) weighing 170 g
were used. They were housed under conditions of constant temperature
(20–22°C), humidity (45–50%) and a standard dark cycle (2000–0800
h). Our institutional guidelines for the care and use of laboratory
animals were observed.
Rats were assigned randomly to three groups of 20. For 2 wk, each was
fed a semipurified diet containing 500 mg Mg/kg (control group), 200 mg
Mg/kg (marginally Mg-deficient group) or 60 mg Mg/kg (Mg-deficient
group) (Rock et al. 1995
). All rats had free access to
distilled water and food. The semipurified diets contained the
following (g/kg): casein 200, starch 650, corn oil 50, alphacel
(cellulose) 50, DL-methionine 3, choline bitartrate 2,
modified AIN-76 mineral mix 35, AIN-76A vitamin mix 10 (ICN
Biomedicals, Orsay, France) (AIN 1977
). The Mg level in
the three experimental diets was checked by flame atomic absorption
spectrometric analysis (Perkin Elmer 560, St-Quentin en Yvelines,
France).
Preparation of stable isotope solution.
Enriched Mg (200 mg; or 328 mg of MgO) was moistened with 2 mL of demineralized water; 2 mL of 12 mol/L HCl (suprapure) was added to transform the oxide into the soluble chloride of Mg. The solution was then neutralized with 2 mL of NaOH (1 mol/L) and 25 mL of NaHCO3 (1.67 mol/L), and adjusted to 100 mL with physiologic solution (NaCl, 9 g/L). The pH and the osmolarity of the obtained solution were 7.0 and 320 mOs, respectively. The concentration of Mg in this solution was 2 g/L. This solution was then filtered (0.45 µm) and distributed into seven bottles of 14–15 mL each. Total Mg concentration and isotope ratio were checked before use.
Isotope injection and sampling.
After 2 wk of consuming the experimental diets, each rat was administered an intravenous injection of 1.37 mg 25Mg. Because the number of blood samples that can be obtained from each rat is limited, it was necessary to use 20 rats/group. Half of each group was sampled at the following times: 15, 30, 60, 90 min and 2, 3, 4, and 6 h after 25Mg injection (short-term kinetics). The other half of each group was sampled at 1, 2, 3, 4, 5, 7 d after 25Mg injection (long-term kinetics). Rats in both groups were anesthetized at each time point and blood (0.5 mL) was collected by a catheter in the left carotid for the short-term kinetic and from the retroorbital sinus for the long-term kinetic. Blood samples were centrifuged (2500 g x 15 min) and the plasma was separated. Erythrocytes were collected at 6 h and 7 d, twice washed with saline solution and hemolized. The anesthetized rats were then killed, and the tibiae were collected at the end of the long-term kinetics for total Mg determination.
Analysis.
The 25Mg concentration of plasma samples was determined by
ICP/MS (PlasmaQuad II systems) (Coudray et al. 1997
).
Before analysis, the plasma was diluted in 0.16 mol/L HNO3;
natural Mg and beryllium were used as external and internal standards,
respectively. Total Mg concentrations in the analyzed samples were
50 µg/L. Within- and between-run percentage
residual standard deviations were as follows: 0.45 and 0.71% for
25Mg/26Mg for Mg standard solution,
respectively, and 0.58 and 0.86%, respectively, for plasma dilution.
For total Mg determination, plasma and hemolized erythrocytes were simply diluted in 1 g/L lanthanum chloride. For tibia analysis, the bone was first dried, dry-ashed, dissolved with HNO3 and H2O2 and heated at 110°C, and then dried down. The dry residue was then taken up with concentrated HNO3 and adequately diluted in 1 g/L of lanthanum chloride. Mg concentration was determined by atomic absorption spectrophotometry (Perkin Elmer 560) at 285 nm. Within- and between-run percentage residual standard deviations were as follows: 2.5 and 3.71% for Mg standard solution, 3.2 and 5.1% for plasma Mg, 3.7 and 5.6% for erythrocyte hemolysate Mg and 3.5% and 4.9%, respectively, for bone Mg measurements.
Kinetic analysis.
Magnesium kinetics were determined using a multicompartmental model as
described by Avioli and Berman (1966)
and Sojka et al. (1997)
. A schematic of the model is shown in
Figure 1
. Compartmental modeling of the data was performed with the aid of the
SAAM II (Stimulation, Analysis, and Modeling) program (SAAM Institute,
Seattle, WA) (Barrett et al. 1998
). Plasma data were
expressed as tracer/tracee, with tracer = (25Mg from the injection) and tracee = (Mg
total - 25Mg from the injection). The mean
values (n = 8) at each sampling time were used in the
model development because of the use of different rats for the short
and long kinetic experiments. The mass of the different pools (M1, M2,
M3), the fractional transport rate [exchange constant between pools
(k1,2; k2,1; k1,3; k3,1)
and the irreversible loss of Mg from pool 3 (k 0,3)] were
determined from the model using the SAAM II program. Irreversible loss
from pool 1 (k 0,1) was approximated using the urinary
excretion values obtained from previous studies in rats subjected to
the same experimental conditions in our laboratory (data not shown).
Endogenous fecal losses were not taken into account in this
calculation.
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We evaluated EMgP size according to the method of Miller et al. (1994)
developed for zinc metabolism. EMgP is the system of
pools that exchange with the plasma at a rate fast enough to
essentially intermix completely within a 48-h period. EMgP size is
equivalent to the mass of isotope administered divided by the
tracer/tracee value at the y-intercept of the linear
regression of a semilog plot of the plasma tracer/tracee data between d
3 and 7 (Fig. 2
).
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Results were expressed as means ± SD. Statistical analyses were based on one-way ANOVA followed by a Tukey-Kramer multiple comparisons test and on Spearman’s correlation coefficients. The limit of statistical significance was set at P < 0.05. Statistical analyses were performed using the GraphPad program (V3.00, GraphPad Software, San Diego, CA).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The weight of rats fed the Mg-deficient diet was significantly less
than that of those fed the control diet (Table 1
). However, the weight of the marginally Mg-deficient group was not
significantly different from that of the other groups. Conventional Mg
markers (Mg concentration in plasma, erythrocytes and tibia) were
significantly lower in the Mg-deficient group compared with the
control group. In the marginally Mg-deficient rats, Mg
concentrations in plasma and in tibia were significantly lower than
those observed in the controls. However, the erythrocyte Mg
concentration did not differ between marginally Mg-deficient and
control rats.
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Semilogarithmic plots of the model fit to plasma data for control,
marginally Mg-deficient and Mg-deficient rats are shown in
Figure 3
. The pattern of the curve was similar in appearance for the three
experimental groups, showing a rapid disappearance of tracer during the
first 10 h, followed by a slow decline that extended through at
least 170 h. However, all tracer/tracee values were greater for
Mg-deficient rats compared with control rats and the marginally
Mg-deficient group. Tracer/tracee values were also higher for
marginally Mg-deficient rats compared with control rats.
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). Mg-deficient rats had smaller pool masses compared
with control rats, and marginally Mg-deficient rats had
intermediate masses (Table 2
). Pool 3 accounted for 89% of total exchangeable Mg in control rats,
for 91% in marginally Mg-deficient rats and for 88% in
Mg-deficient rats. In the Mg-deficient group, the masses of
pools 1, 2 and 3 were 40, 32 and 40% lower, respectively, than those
of control group, and in the marginally Mg-deficient group the
masses were 32, 29 and 16% lower, respectively. M3 was positively
correlated with plasma Mg (Table 3
). The correlation tended to be significant (P = 0.07)
between M3 and tibia Mg. No correlation was obtained for M1 and M2 with
plasma, erythrocytes or tibia Mg levels.
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. Moreover, irreversible
loss from pool 1 (calculated from a previous experiment, results not
published) was 89% lower in Mg-deficient rats and 50% lower in
the marginally Mg-deficient group than in control rats. A slight
decrease was observed for irreversible loss from pool 3 as the Mg level
in the diet decreased. EMgP and classical markers of Mg status.
EMgP was significantly different among the experimental groups (Table 2)
. It decreased with dietary Mg restriction. EMgP was positively
correlated with plasma Mg concentration, erythrocyte Mg concentration
and tibia Mg concentration on an individual animal basis (Table 3)
. It
was positively correlated with plasma Mg and tended to be correlated
with tibia Mg (P = 0.06) on a mean data basis.
Moreover, EMgP was positively correlated with M3 (r = 0.9998, P < 0.05).
Variations of conventional markers of Mg status and pool sizes with dietary Mg intake.
The relationships between conventional markers of Mg status and pool
sizes with dietary Mg intake relative values (the value 1 was given to
the control group) were calculated for each variable. As expected,
plasma Mg decreased the most as dietary Mg decreased (Fig. 4
). EMgP and M3 decreased similarly to tibia Mg. The variation of
erythrocyte Mg with dietary Mg was of lower magnitude and was less
sensitive.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Various biochemical markers of Mg status are available. However, they
have some important limitations. Serum Mg represents <1% of total
body Mg; thus, the serum Mg concentration may not reflect intracellular
magnesium status. Because ionized Mg is physiologically active, the
measurement of ionized Mg would be useful. Recently, Mg
ion-selective electrodes have become available. However, it has
been demonstrated that ionized Mg concentration measured in serum
depends on the analyzer used (Huijgen et al. 1999
).
Therefore, improvements are still necessary. Routine determinations of
the Mg in the blood constituents (erythrocytes and peripheral
lymphocytes) (Mazur et al. 1997
) are inconsistently
correlated with each other, and may vary in different physiologic and
pathologic conditions (Elin 1991
). The parenteral Mg
load test has been suggested as a diagnostic test for Mg status. This
test is based on the fact that the normal kidney regulates the body
stores of Mg, excreting an excess in normal subjects and retaining the
mineral in deficient subjects. However, applied tests vary among
laboratories and a standardized procedure is not available
(Mazur et al. 1997
). Skeletal muscle and bone biopsies
are invasive markers, they are time consuming, and there is a poor
correlation between these two methods (Alfrey and Miller 1973
). Thus, there is a pressing need to develop additional and
potentially more suitable methods for assessment of Mg tissue status.
The concept of the exchangeable pool of a given element has been
developed to estimate trace element status and has been validated for
selenium (Janghorbani 1990
) and zinc
(Fairweather-Tait et al. 1993
, Lowe et al. 1991
). In our initial studies in rats, we evaluated the
exchangeable pool in severely Mg-deficient rats
(Feillet-Coudray et al. 2000
). We observed alterations
in both pool masses and turnover rates with Mg deficiency.
In this study, we found that plasma, erythrocyte and tibia Mg
concentrations were considerably lower in Mg-deficient rats
compared with control rats. These conventional markers of Mg status
confirmed a severe Mg deficiency in the Mg-deficient rats. In
marginally Mg-deficient rats, plasma and tibia Mg concentrations
were also significantly decreased, whereas erythrocyte Mg
concentrations were not different from control levels. Thus,
erythrocyte Mg was not sensitive enough to detect a marginal Mg
deficiency. Moreover, most studies have shown no correlation between
erythrocyte Mg concentration and other tissue pools of Mg (Elin 1989
); an apparent genetic regulation of erythrocyte Mg may be
a factor in this lack of correlation (Henrotte 1982
).
The exchangeable pools of Mg can be measured according to the model of
Avioli and Berman (1966)
. Using
28Mg as a tracer, these authors first proposed a
multicompartmental model of exchangeable magnesium. However, the short
half-life of 28Mg (21.3 h) did not allow the
determination of turnover rates of Mg in the slowly exchangeable pool.
Moreover, 28Mg tracer studies had been limited as
a result of their apparent inability to identify Mg-deficient
conditions clinically (Wallach 1987
). Recently, with
improvements in analytical techniques, the use of the Mg stable
isotopes, 25Mg and 26Mg,
has been developed. The multicompartmental model described by
Avioli and Berman (1966)
was validated by Sojka et al. (1997)
and Abrams and Ellis (1998)
using
stable isotopes of Mg in children and adolescents. This technique has
the disadvantage of requiring a large number of blood samples but
allows accurate characterization of exchangeable pools and turnover
rates. In this model, there are three exchangeable Mg pools with varied
rates of turnover. In fact, the plasma concentration of
25Mg fit a sum of three exponentials
(Avioli and Berman 1966
). Pools 1 and 2 represent pools
with a relatively fast turnover. Together, these pools approximate
extracellular fluid distribution. Avioli and Berman (1966)
demonstrated in several individual studies that plasma
28Mg consisted of at least two compartments
because the integral of the plasma curve was not proportional to the
cumulative urine curve. Pool 3 is an intracellular pool containing
>70% of the exchanging Mg, with a turnover one half that of the most
rapid pool. There is also a pool 5, which is a loss pathway
representing deposition into tissues (Sojka et al. 1997
).
We demonstrated that the sizes of pools 1, 2 and 3 decreased in proportion to Mg deficiency. Unfortunately, statistical analysis was not performed because two groups of rats were used (short kinetic and long kinetic) as a result of limitations on venesection. Determination of exchangeable pool sizes of Mg does appear sufficiently sensitive to assess Mg status in either marginal or severe Mg deficiency. The size of the exchangeable pools better reflects the state of Mg storage in the body than do plasma, erythrocyte and tibia levels of Mg. Indeed, the third exchangeable pool of Mg represents the Mg level in deep tissue, which the conventional markers of Mg cannot measure. The assessment of this deep body Mg is important to gain a better understanding of Mg metabolism and to link to it the effect of Mg intake and status. The fractional transport rate of Mg from pool 1 to pool 3 increased with marginal and severe Mg deficiency, suggesting a higher avidity of compartment 3 for Mg, which may prevent excessive depletion of intracellular Mg. On the other hand, the fractional transport rate from pool 3 to pool 1 was not modified by Mg deficiency. Moreover, the irreversible loss from pool 1 decreased with marginal and severe Mg deficiency. This irreversible loss accounts in large part for fecal and urinary excretions of Mg. This is in agreement with the compensatory mechanism occurring in the kidney, in the case of Mg deficiency, in which Mg is conserved when Mg status is low, resulting in a low urinary excretion of Mg.
EMgP decreased significantly as Mg was lowered in the diet. EMgP is
defined as the combined pools of Mg that exchange with the plasma Mg
within 48 h. This method requires determination of the coefficient
of the simple exponential decay function fitting plasma enrichment data
between 3 and 7 d after administration of the Mg stable isotope
tracer (Miller et al. 1994
). Collection of plasma
samples starting at day 3 is more feasible than the rapid early
sampling required for compartmental analysis, and analysis of the data
is easier and faster. However, this method of determining the size of
EMgP is accurate only to the extent that the following two conditions
are met: 1) the loss of tracer from EMgP occurs at a
monoexponential rate from the moment of tracer administration to the
end of the measurement period; and 2) the tracer is
homogeneously mixed throughout the EMgP during the measurement period
(Miller et al. 1994
). Because the initial rapid loss of
tracer from plasma is not accounted for by extrapolation of the
monoexponential loss rate during the measurement period, and because it
is extremely unlikely that the tracer exists at equal concentrations in
all compartments of the EMgP at any time, there are two potential
sources of error inherent in this method (Miller et al. 1994
), which result in an overestimation of EMgP size. In fact,
the Mg exchangeable pool size is overestimated with the method of
Miller by 25% for control and marginally deficient rats.
Nevertheless the overestimation is only 5% for Mg-deficient rats.
We also showed that EMgP is positively correlated with conventional markers of Mg status on an individual animal basis. The higher correlation was obtained with the tibia Mg concentration. Moreover, sensitivity to dietary Mg variation was the same for EMgP and tibia Mg concentration. This is an important result, because tibia Mg concentration is an excellent tissue marker that is not accessible in humans. Moreover, EMgP is at least as sensitive as M3 to dietary Mg variation.
In conclusion, this study demonstrates that the exchangeable pools of Mg represent a good marker of Mg status in rats. In fact, Mg exchangeable pool sizes vary with dietary Mg intake and are reduced by restriction of dietary Mg. M3 is adequate to reveal differences that depend on Mg status and represents the deep tissue Mg level, which conventional markers of Mg cannot measure. Compartmental modeling of Mg metabolism allows accurate characterization of exchangeable pools and turnover rates; however, its determination necessitates numerous blood samples. EMgP determination is a simple and alternative method and permits rapid determination of Mg status. Studies are now warranted to validate the utilization of the Mg exchangeable pool concept as a Mg status biomarker in humans.
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ACKNOWLEDGMENTS |
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Manuscript received March 8, 2000. Initial review completed March 24, 2000. Revision accepted April 25, 2000.
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