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Nutrient Requirements

Fractional Intestinal Absorption of Magnesium Is Directly Proportional to Dietary Magnesium Intake in Rats¹

Centre de Recherche en Nutrition Humaine d’Auvergne, Unité Maladies Métaboliques et Micro-nutriments, INRA, Theix, 63122 St Genès Champanelle, France

²To whom correspondence should be addressed. E-mail: coudray{at}clermont.inra.fr.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS Calculations RESULTS DISCUSSION LITERATURE CITED

 
The precise mechanisms of intestinal Mg absorption are still unclear and the possibility of an adaptative rise in the fraction of Mg absorbed as Mg intake is lowered is controversial. Mg deficiency has been studied extensively in rats where it is readily produced by dietary depletion. In this study, we investigated the effect of Mg intake on fractional absorption of Mg acutely and after adaptation to graded Mg intake in rats. For this purpose, male Wistar rats (n = 30) were fed a basal semipurified diet containing 600 mg Mg/kg (MgO) for 7 d. Three groups of 10 rats were then formed and fed the basal semipurified diet with 600, 300 or 150 mg Mg/kg, for 28 d. Apparent and true intestinal absorptions and fecal endogenous excretion of Mg were determined at the beginning and end of the experiment. As expected, plasma Mg levels were lower in the deficient groups than in the control by d 4 and differences were more marked at the end of the experiment. Erythrocyte Mg levels were significantly lower at the end of the experiment in the group fed the diet containing 150 mg Mg/kg. The amounts of Mg absorbed were directly proportional to the dietary Mg intakes in all three experimental groups at both testing periods. This indicated that the apparent and true intestinal absorption percentages of Mg were not different in rats fed the three different levels of dietary Mg. These results also show that fecal endogenous excretion of Mg was nearly directly proportional to the dietary Mg intakes. These results argue in favor of a passive diffusional process for intestinal Mg absorption.

KEY WORDS: • magnesium • intake • intestinal absorption • endogenous excretion • stable isotope • rats

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS Calculations RESULTS DISCUSSION LITERATURE CITED

 
Magnesium (Mg) is an essential mineral that plays a key role in many fundamental biological processes. Current research illustrates the importance of Mg in human health and diseases (1 ,2 ). A large number of people in industrialized countries consume less than the dietary intakes recommended internationally (3 ), and there is emerging evidence that habitually low intakes of Mg are associated with etiologic factors in various metabolic diseases (2 ,4 ). It has been reported that efficient mechanisms exist in both the gastrointestinal tract and the kidney that closely regulate Mg homeostasis (5 ). The kidney is the organ that most closely regulates Mg metabolism. There exists a threshold of filtered Mg in the kidney below which Mg is avidly conserved as well as one above which Mg is excreted completely (6 ). Mg is absorbed throughout the intestinal tract, although apparently most efficiently in the distal parts of the intestine (7 ,8 ). Mg is likely absorbed by active transport and passive diffusion across the intestinal mucosa. Early data suggest that the active transport system may account for greater fractional Mg absorption at low dietary intake (9 ,10 ). Mg absorption, however, continues at high dietary intakes, albeit at a lower fractional rate due to a passive absorption component (11 ). However, other data suggest that Mg absorption occurs primarily by passive diffusion and solvent drag mechanisms at usual Mg dietary intake (12 –14 ). There is still great uncertainty concerning the precise mechanisms of intestinal Mg absorption (15 ) and whether there is a compensatory adaptative rise in the fraction of Mg absorbed as Mg intake is lowered. Mg deficiency has been studied extensively in rats where it is readily produced by dietary depletion (16 ,17 ). The aim of the present study was to assess whether fractional intestinal Mg absorption varies inversely with dietary Mg intake and whether there is an increase in fractional intestinal Mg absorption when Mg intake is acutely lowered or after a period of adaptation.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS Calculations RESULTS DISCUSSION LITERATURE CITED

 
Reagents and equipment.

²⁵Mg (96.7%) enriched with 2.2% ²⁴Mg and 1.1% ²⁶Mg, (200 mg) in 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 made using an inductively coupled plasma mass spectrometry (ICP/MS) instrument (a Plasma quad-II system from Fisons Instruments, Manchester, UK), equipped with a Meinhard nebulizer. A Perkin Elmer 560 atomic absorption spectrometer (Perkin Elmer, St-Quentin-en-Yvelines, France) was used for total Mg measurements.

Animals and diets.

Male Wistar rats (n = 30; from the laboratory animal colony of the National Institute of Agronomic Research, Clermont-Ferrand-Theix, France) were fed a commercial pelleted diet (U.A.R, Villemoisson-sur-Orge, France) until body weights reached 230 g (8 wk). This diet contained (mg/kg): Ca, 8300; Mg, 2000; P, 5900; Zn, 85; iron, 240. All rats were then fed the basal semipurified diet, containing 600 mg Mg/kg for 7 d. We formulated a modified AIN-76 salt mix by omitting MgO. The composition of this diet is given in Table 1 . The chemical composition was (mg/kg): calcium, 5000; phosphorous, 5000; Mg, 50; zinc, 35; iron, 35 (18 ). Three groups of 10 rats each were then formed and fed the purified diets prepared by adding MgO to the Mg-deficient mixture to produce final Mg levels of 150, 300 or 600 mg Mg/kg (control). The rats were given fresh food and distilled water daily, which they consumed ad libitum. Food consumption and body weight were recorded weekly. During the experiment, the rats were housed two per cage (wire-bottomed to limit coprophagy) and maintained in a temperature-controlled room (22°C) with the dark period from 2000 h to 0800 h. Two intestinal Mg absorption tests were conducted using the ²⁵Mg stable isotope technique. The first test started on d 3 and lasted only 2 d to minimize the effect of Mg status change on Mg absorption. The second test started on d 24 and lasted 4 d. On the morning of each test, the rats were gavaged once with 1.5 mL of ²⁵Mg stable isotope solution and individually housed in metabolic cages fitted with urine/feces separators. In the first absorption test, the rats were fed 300, 600 or 1200 µg ²⁵Mg for the 150, 300 and 600 mg diet groups, respectively, and feces and urine were collected for two consecutive days. In the second absorption test, the rats were fed twice these doses; the feces and urine collection period was twice as long as that of the first test. Food intake was controlled daily by weighing the offered meal and the leftover food for each rat. Whole feces and urine for each rat were collected during these balance days to determine total and isotope Mg balances. All of the procedures complied with the Institute’s guide for the care and use of laboratory animals.

Blood was sampled on d 4 from the orbital vein under mild anesthesia to measure Mg plasma levels at this period. At the end of the experiment, the rats were anesthetized (40 mg/kg of sodium pentobarbital) and killed just after the dark period (between 0800 and 1000 h). Blood was sampled via the abdominal aorta. The blood was placed in microfuge tubes containing heparin and centrifuged at 5000 x g for 10 min. Plasma and RBC samples were stored at -20°C until Mg analysis. After blood sampling, the tibia was also removed for body Mg assay.

The urine was collected for two or four successive days. Individual urine from each rat was weighed and a subsample was acidified with 14 mol/L HNO₃ (acid final concentration, 0.14 mol/L) and kept at -20°C until Mg analysis. The whole feces of each rat were weighed, freeze-dried and reweighed. To obtain homogenous fecal samples, the dried feces were powdered for 60 s in an electronic spex industry grinder equipped with tubs and balls made of stainless steel. The powdered feces were then kept at room temperature until Mg analysis.

Mg determination by atomic absorption spectrometry.

Mg levels were determined in the plasma, RBC and urine after simple appropriate dilution in 1 g/L lanthanum. For solid samples, subsamples of diet, feces (0.25 g) or one tibia were first dried and then mineralized for 10 h at 500°C. The residue was then taken up in nitric acid (14 mol/L) and hydrogen peroxide (30%) on a heating plate until complete discoloration occurred. The products of mineralization were finally appropriately diluted in 1 g/L lanthanum. Mg concentration was measured using a flame atomic absorption spectrophotometer at 285 nm. Proper quality control and external calibration were ensured for each series of measurements. Within- and between-run percentage residual SD for total Mg measurement were as follows: on standard solutions of Mg, 1.21 and 1.86; on plasma samples, 2.76 and 4.67; on RBC samples, 3.11 and 4.78; on urine samples, 3.22 and 5.55; on fecal mineral solutions, 2.38 and 4.16.

Mg stable isotope determination.

Subsamples of feces (0.25 g) were dry-ashed at 500°C for 10 h. The ash was dissolved in 0.2 mL of concentrated HNO₃ and 9.8 mL of distilled water. In each case, an appropriate dilution with 1% HNO₃ was then performed before the ICP/MS analysis to ensure a total Mg concentration of 50 µg/L. Stable isotope solutions were also appropriately diluted with 1% HNO₃ and verified by ICP/MS. Mg stable isotope concentrations were determined by ICP/MS under the following conditions. The mass spectrometer settings and plasma conditions were optimized with a solution of 10 µg/L of indium and the instrument operating conditions were as follows: radio frequency generator, 27.12 MHz; forward RF power, 1350 W; reflected RF power, < 3W; outer argon flow rate, 14 L/min; intermediate argon flow rate, 0.7 L/min; nebulizer argon flow rate, 0.76 L/min; mass resolution, 0.9 amu at 10% of peak height. Data collection parameters were as follows: total replicates per integration, 5; signal integration time per replicate, 40 s; dwell time per sweep, 20.4 ms; scanning mode, peak hopping, five points per peak; sample uptake rate, 0.6 mL/min. The within- and between-run percentage residual SD for ²⁵Mg/²⁶Mg ratio were: on standard solutions of Mg, 0.31 and 0.65; on fecal mineral solutions, 0.43 and 0.67.

	Calculations

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS Calculations RESULTS DISCUSSION LITERATURE CITED

 
Apparent intestinal absorption of Mg.

Fractional apparent absorption (%) was determined as 100 x [(Mg intake - fecal Mg)/(Mg intake)], and absolute apparent absorption (mg/d) as (Mg intake - fecal Mg).

True intestinal absorption of Mg.

Fractional "true" intestinal absorption of Mg was calculated as 100 x [(administered ²⁵Mg - nonabsorbed ²⁵Mg excreted in the feces)/(administered ²⁵Mg)], whereas absolute true absorption (mg/d), based on fecal isotopic monitoring, was calculated as (Mg intake x fractional "true" intestinal absorption).

The nonabsorbed ²⁵Mg isotope present in the fecal sample was [total fecal Mg x (IR ²⁵Mg/²⁴Mg sample - IR ²⁵Mg/²⁴Mg baseline)]/[1.267 + (IR ²⁵Mg/²⁴Mg sample – R ²⁵Mg/²⁴Mg baseline)], where total fecal Mg (mg) was determined by atomic absorption spectrometry, IR is the isotopic ratio, and 1.267 is 1/0.789, to convert ²⁴Mg fecal quantity to total fecal Mg (19 ).

Fecal endogenous excretion of Mg.

Endogenous excretion of Mg in the feces (mg/d) was calculated as daily Mg intake (mg/d) x (fractional true absorption - fractional apparent absorption). The fractional endogenous excretion of Mg (%) was calculated as 100 x [endogenous excretion of Mg in the feces (mg/d)/Mg intake (mg/d)].

Mg balance.

Mg balance (mg/d) was calculated as follows : Mg intake - (fecal Mg + urine Mg)

Statistical analyses.

Values are given as means ± SD; the significance of differences between means was determined by ANOVA and multiple range comparisons by Fisher’s least significant difference procedures. ANOVA assumes that the data are sampled from populations that follow Gaussian distribution. This assumption was tested using the method of Kolmogorov and Smirnov. ANOVA assumes that the data are sampled from population with identical SD. This assumption was tested using the method of Bartlett. Simple linear correlation analyses were used to assess the relationship between dietary Mg intake and true and apparent Mg absorption and between dietary Mg intake and endogenous Mg excretion. Differences with P < 0.05 were considered significant.

	RESULTS

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Effects of dietary Mg intake on body growth, food efficiency and Mg status.

The growth rate of the rats was not affected by the low dietary Mg intake at any time point of the study. Weight gain (g/d, 4.04 ± 0.94; 4.72 ± 1.01; 3.98 ± 0.60) and food efficiency (g weight gain/g food, 0.25 ± 0.10; 0.32 ± 0.09; 0.28 ± 0.07) did not differ among the 150, 300 and 600 mg Mg/kg diet groups, respectively.

On d 4, plasma Mg concentrations differed among the three groups (Table 2 ). The urinary Mg excretions were not different in the groups receiving the two low dietary Mg levels, but were significantly less than in the control group. At the end of the experiment, plasma Mg level and urinary Mg excretion differed among the three experimental groups. However, erythrocyte and bone Mg levels were lower only in the rats fed the Mg-deficient diet (150 mg Mg/kg) compared with the other two groups.

Results at both time points were generally the same. Food consumption and feces weight did not differ among the three groups at the first absorption test (Table 3 ). Hence, the ingested amounts of Mg were directly proportional to the level of Mg in the experimental diets. Fecal levels of Mg and intestinal Mg absorption (mg/d) were directly proportional to the levels of Mg in the three diets (Table 3 , Fig. 1 ). Consequently, the fractional apparent intestinal absorption of Mg (%) did not differ among the three groups. In line with this are the results obtained with stable isotope monitoring, which showed that the fractional true intestinal absorption of ²⁵ Mg (%) also did not differ among the three groups. The fecal endogenous excretion of Mg (mg/d) was directly proportional to dietary Mg intake (Fig. 1) . The endogenous excretion percentage was rather high even in rats fed 150 mg Mg/kg in their diets. Mg balance did not differ among the groups (Table 3) .

View larger version (34K): [in this window] [in a new window]   FIGURE 1 Relationships among graded dietary Mg intakes, true and apparent intestinal Mg absorptions and endogenous Mg excretion in rats, after 2 (panels A–C) or 24 d (panels D–E) intakes of the diets. Simple linear correlation analyses were used to assess the relationship between dietary Mg intake and true and apparent Mg absorption and between dietary Mg intake and endogenous Mg excretion. Some of the reported correlations may be spurious because they are based on three clusters of data rather than a continuum of data points. A solid line indicates linear regression and a dotted line the 95% confidence interval.

	DISCUSSION

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The apparent intestinal absorption was determined by the chemical balance technique, i.e., Mg intake minus fecal Mg excretion. The true intestinal absorption of Mg was measured by stable isotope fecal monitoring (19 ). The typical protocol for intestinal Mg absorption measurement in rats using stable isotope consists of collecting feces for four consecutive days. We applied such a protocol to determine Mg absorption in the chronic exposure trial. In the acute exposure trial, we restricted the fecal collection period to only 2 d to minimize the eventual effect of Mg status modification on the intestinal absorption measurement. The determination of intestinal Mg absorption by administration of isotope by gavage is based on the fact that the administered isotope will be mixed with the dietary Mg and follow the same metabolism processes of the dietary Mg in the digestive tract (19 ,22 ). To ensure valid results, increased amounts of Mg stable isotope (²⁵Mg), directly proportional to dietary Mg intakes, were given by gavage in this study. Apparent and true intestinal absorption of Mg (mg/d) were directly proportional to the dietary Mg intake at the beginning and end of the study. This clearly indicates that fractional intestinal Mg absorption (%) was not increased when Mg intake was acutely lowered or after a period of adaptation. However, Mg balance was not different at either test period among the three experimental groups, indicating that renal adaptation to graded dietary Mg is the homeostatic mechanism operational under the conditions in this study.

The first study of the intestinal absorption of Mg was conducted after 4 d of consumption of the experimental diets. The purpose of this study was to test whether a reduction in the dietary intake of Mg increased the intestinal absorption of this cation. At d 4 of the experiment, the consumption of the diets with low levels of Mg lowered plasma Mg concentration and reduced the urinary excretion of Mg. However, at this stage, low dietary Mg did not increase the intestinal absorption of Mg. The second study of the intestinal absorption of Mg was conducted after 4 wk to determine whether a more pronounced modification in Mg status might lead to long-term modification of the intestinal absorption of Mg, a mechanism requiring a long adaptation period. In rats fed the diet with insufficient Mg, blood and bone Mg contents were affected, reflecting a more pronounced Mg deficiency (17 ), and even under these conditions, intestinal absorption of Mg was not affected. These results show that the active absorption mechanism of Mg is likely important only under conditions of extremely low dietary Mg intake, e.g., 50 mg/d in humans. This represents < 15% of dietary recommended allowances for Mg (23 –25 ).

True intestinal Mg absorption was correlated with the dietary intake of Mg [r = 0.989; P < 0.0001 (acute study) and r = 0.979; P < 0.0001 (after adaptation)]. Apparent intestinal Mg absorption and dietary intake of Mg also were correlated [r = 0.860; P < 0.0001 (acute study) and r = 0.874; P < 0.0001 (after adaptation)]. However, the true intestinal absorption of Mg was much more closely correlated with the Mg intakes than was apparent intestinal absorption. The low correlations observed between apparent intestinal absorption and Mg intake may be due to the low accuracy in measuring apparent intestinal absorption using the error-prone classic balance technique (26 ). It is also likely due to the wide variability of endogenous excretion of Mg, which may affect the values of the apparent absorption of Mg.

There are different approaches to measuring endogenous excretion of minerals. One of these approaches uses a tracer that is infused parenterally and then measured in the feces for a timed duration (27 ). However, this approach measures only the mineral eliminated in the intestinal secretions and fails to measure the minerals eliminated with intestinal cell desquamation, which may represent the major part of endogenous mineral excretion. The most often reported approach is that based on the difference between apparent and true intestinal absorptions (19 ,28 –30 ). This approach was applied in this work. The endogenous excretion of Mg passes into the lumen of the gut through exocrine pancreatic secretions, bile, sloughed cells, mucus and mucosal Mg secretions. Radioactive or stable isotopes of Mg have often been used to determine true Mg absorption in humans and animals (19 ,29 ) The endogenous excretion of Mg was rather high in the rats of this study, representing 30% of the dietary Mg intake. Other studies reported an endogenous excretion of Mg between 15 and 25% (28 ,30 ). This difference may be due to any of several reasons such as diet composition or age of animals. The endogenous excretion (mg/d) was directly proportional to the dietary Mg intakes at both periods studied (Fig. 1) . Thus, there was a marked decrease in endogenous excretion of Mg when dietary Mg intake was decreased. This reduction may help limit the Mg loss from the body during insufficient intake of Mg. However, the relative endogenous excretion of Mg (%) was significantly higher at the beginning of the study in the Mg-deficient group compared with the control group. This may also be due to the fact that the previous high dietary Mg, when the rats consumed the control diet, interferes with the endogenous excretion of Mg obtained at that early period.

Another possibility is that the commercial pellets fed to the rats before the study were responsible for this relatively high endogenous excretion of Mg (%) in the Mg-deficient rats. This diet is very rich in Mg (2000 mg/kg) and is also rich in fermentable fiber. The high Mg level in the diet may be responsible for the high level of Mg in the sloughed intestinal cells, which contribute to endogenous Mg excretion. One of the consequences of fermentable fiber in diets is an increase in the turnover of epithelial cells (31 ), which may also be responsible for the increase in endogenous Mg excretion. In line with this hypothesis is the fact that the endogenous Mg excretion was higher at the beginning of the study (d 4, acute test) than at the end of the study for all experimental groups (d 28, chronic test).

In conclusion, there is no evidence for any compensatory adaptative rise in the fraction of Mg absorbed as Mg intake is lowered. Absorbed Mg amounts and Mg dietary intake, over a wide intake range, were strongly and positively correlated. This clearly indicates that the passive paracellular transport of Mg is the predominant component of intestinal Mg absorption in rats. Further studies are still necessary to emphasize the possible role of endogenous Mg excretion in the homeostatic mechanisms of Mg. Finally, these animal results require confirmation in human studies before extrapolation to human nutrition.

	ACKNOWLEDGMENTS

 
The authors thank Claudine Lab and Annie Bellanger for technical assistance.

	FOOTNOTES

 
¹ Presented as an oral communication at the 7th Congress of Magnesium held September 2001 in Saragosse, Spain.

Manuscript received 10 December 2001. Initial review completed 10 January 2002. Revision accepted 14 April 2002.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS Calculations RESULTS DISCUSSION LITERATURE CITED

 

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