Métodos para la determinación del estado del magnesio en humanos / Methods of assessment of magnesium status in humans / Métodos para a determinação do estado do magnésio em humanos

En la actualidad, datos epidemiológicos sugieren que, en países occidentales, la ingesta de magnesio no satisface la ingesta recomendada, lo que apoya un riesgo de deficiencia de magnesio latente en estas poblaciones. La evaluación del estado de magnesio sigue siendo un desafío para el laboratorio clínico ya que el magnesio se encuentra distribuido mayoritariamente en el hueso y tejidos blandos. Existe la necesidad de conciliación entre una prueba de fácil acceso, rápida, sensible y representativa del magnesio intracelular. La utilidad de diferentes biomarcadores en sujetos sanos ha sido evaluada; se ha reportado que el magnesio en plasma, eritrocitos y orina parecen ser biomarcadores sensibles a la ingesta dietética y útiles como biomarcadores en la población general. Sin embargo, esto no es concluyente, ya que se resalta que aún se requieren estudios mejor diseñados, que impliquen factores como mayor población empleada, dosis y tiempo de suplementación. El progreso en la genética y la genómica abren perspectivas interesantes en la búsqueda de estos biomarcadores que permitan cuantificar los niveles de magnesio celular así como también las reservas de todo el cuerpo, para poder así establecer recomendaciones dietéticas mejor ajustadas a la población.

Epidemiological studies suggest that dietary magnesium in the Western countries does not meet the recommended intake, supporting a risk of latent magnesium deficiency with Western diet behavior. Assessment of magnesium status remains a major challenge for the clinical laboratory, since, magnesium storage is mostly found in bone and soft tissues. The conciliation between an easy obtained sample, rapid and robust laboratory test, and the parameter representative for intracellular magnesium is extremely difficult to reach. In a current systematic review study, the usefulness of magnesium status biomarkers in healthy subjects has been evaluated. It is proposed that plasma and erythrocyte magnesium, and urinary magnesium excretion which respond to dietary manipulation appear to be useful biomarkers in the general population. However, it is emphasized that well-designed studies of sufficient size with varying doses and duration of magnesium supplementation are still required. The development of specific and sensible biomarkers, making it possible to obtain cell magnesium levels as well as body magnesium pool evaluation, relevant to study individuals, small and large populations, remains a major challenge for the assessment of magnesium status. A progress in genetics and genomics opens new interesting perspectives in the search of these biomarkers.

Na atualidade, dados epidemiológicos sugerem que, nos países ocidentais, a ingestão de magnésio não supre a ingestão recomendada, o que apoia um risco de deficiência de magnésio latente nestas populações. A avaliação do estado do magnésio continua sendo um desafio para o laboratório clínico, visto que o magnésio se encontra distribuído principalmente no osso e nos tecidos moles. Há a necessidade de conciliar evidência facilmente acessível, rápida, sensível e representativa do magnésio intracelular. A utilidade de vários biomarcadores em indivíduos saudáveis foi avaliada, e foi relatado que o magnésio em plasma, eritrócitos e urina parecem ser biomarcadores sensíveis à ingestão dietética e úteis como biomarcadores na população geral. No entanto, esta não é conclusiva, uma vez que se destaca que são requeridos ainda estudos melhor desenhados, envolvendo fatores como utilização de maior população, dosagem e tempo de suplementação. Um avanço na genética e na genômica abre perspectivas interessantes na busca desses biomarcadores para poder quantificar os níveis de magnésio celular bem como as reservas do corpo inteiro, e assim poder estabelecer melhores recomendações na dieta adaptadas à população.

Métodos para la determinación del estado del magnesio en humanos / Methods of assessment of magnesium status in humans / Métodos para a determinaþÒo do estado do magnésio em humanos

En la actualidad, datos epidemiológicos sugieren que, en países occidentales, la ingesta de magnesio no satisface la ingesta recomendada, lo que apoya un riesgo de deficiencia de magnesio latente en estas poblaciones. La evaluación del estado de magnesio sigue siendo un desafío para el laboratorio clínico ya que el magnesio se encuentra distribuido mayoritariamente en el hueso y tejidos blandos. Existe la necesidad de conciliación entre una prueba de fácil acceso, rápida, sensible y representativa del magnesio intracelular. La utilidad de diferentes biomarcadores en sujetos sanos ha sido evaluada; se ha reportado que el magnesio en plasma, eritrocitos y orina parecen ser biomarcadores sensibles a la ingesta dietética y útiles como biomarcadores en la población general. Sin embargo, esto no es concluyente, ya que se resalta que aún se requieren estudios mejor diseñados, que impliquen factores como mayor población empleada, dosis y tiempo de suplementación. El progreso en la genética y la genómica abren perspectivas interesantes en la búsqueda de estos biomarcadores que permitan cuantificar los niveles de magnesio celular así como también las reservas de todo el cuerpo, para poder así establecer recomendaciones dietéticas mejor ajustadas a la población.(AU)

Epidemiological studies suggest that dietary magnesium in the Western countries does not meet the recommended intake, supporting a risk of latent magnesium deficiency with Western diet behavior. Assessment of magnesium status remains a major challenge for the clinical laboratory, since, magnesium storage is mostly found in bone and soft tissues. The conciliation between an easy obtained sample, rapid and robust laboratory test, and the parameter representative for intracellular magnesium is extremely difficult to reach. In a current systematic review study, the usefulness of magnesium status biomarkers in healthy subjects has been evaluated. It is proposed that plasma and erythrocyte magnesium, and urinary magnesium excretion which respond to dietary manipulation appear to be useful biomarkers in the general population. However, it is emphasized that well-designed studies of sufficient size with varying doses and duration of magnesium supplementation are still required. The development of specific and sensible biomarkers, making it possible to obtain cell magnesium levels as well as body magnesium pool evaluation, relevant to study individuals, small and large populations, remains a major challenge for the assessment of magnesium status. A progress in genetics and genomics opens new interesting perspectives in the search of these biomarkers.(AU)

Na atualidade, dados epidemiológicos sugerem que, nos países ocidentais, a ingestÒo de magnésio nÒo supre a ingestÒo recomendada, o que apoia um risco de deficiÛncia de magnésio latente nestas populaþ§es. A avaliaþÒo do estado do magnésio continua sendo um desafio para o laboratório clínico, visto que o magnésio se encontra distribuído principalmente no osso e nos tecidos moles. Há a necessidade de conciliar evidÛncia facilmente acessível, rápida, sensível e representativa do magnésio intracelular. A utilidade de vários biomarcadores em indivíduos saudáveis foi avaliada, e foi relatado que o magnésio em plasma, eritrócitos e urina parecem ser biomarcadores sensíveis O ingestÒo dietética e úteis como biomarcadores na populaþÒo geral. No entanto, esta nÒo é conclusiva, uma vez que se destaca que sÒo requeridos ainda estudos melhor desenhados, envolvendo fatores como utilizaþÒo de maior populaþÒo, dosagem e tempo de suplementaþÒo. Um avanþo na genética e na gen¶mica abre perspectivas interessantes na busca desses biomarcadores para poder quantificar os níveis de magnésio celular bem como as reservas do corpo inteiro, e assim poder estabelecer melhores recomendaþ§es na dieta adaptadas O populaþÒo.(AU)

Magnesium deficiency and metabolic syndrome: stress and inflammation may reflect calcium activation.

Magnesium (Mg) intake is inadequate in the western diet and metabolic syndrome is highly prevalent in populations around the world. Epidemiological studies suggest that high Mg intake may reduce the risk but the possibility of confounding factors exists, given the strong association between Mg and other beneficial nutriments (vegetables, fibers, cereals). The concept that metabolic syndrome is an inflammatory condition may explain the role of Mg.Mg deficiency results in a stress effect and increased susceptibility to physiological damage produced by stress. Stress activates the hypothalamic-pituitary-adrenal axis (HPA) axis and the sympathetic nervous system. The activation of the renin-angiotensin-aldosterone system is a factor in the development of insulin resistance by increasing oxidative stress. In both humans and rats, aldosteronism results in an immunostimulatory state and leads to an inflammatory phenotype. Stress response induces the release of large quantities of excitatory amino acids and activates the nuclear factor NFkappaB, promoting translation of molecules involved in cell regulation, metabolism and apoptosis. The rise in neuropeptides is also well documented. Stress-induced HPA activation has been identified to play an important role in the preferential body fat accumulation but evidence that Mg is involved in body weight regulation is lacking. One of the earliest events in the acute response to stress is endothelial dysfunction. Endothelial cells actively contribute to inflammation by elaborating cytokines, synthesizing chemical mediators and expressing adhesion molecules. Experimental Mg deficiency in rats induces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, synthesis of inflammatory cytokines and acute phase proteins, extensive production of free radicals. An increase in extracellular Mg concentration decreases inflammatory effects, while reduction in extracellular Mg results in cell activation. The effect of Mg deficiency in the development of insulin resistance in the rat model is well documented. Inflammation occurring during experimental Mg deficiency is the mechanism that induces hypertriglyceridemia and pro-atherogenic changes in lipoprotein metabolism. The presence of endothelial dysfunction and dyslipidemia triggers platelet aggregability, thus increasing the risk of thrombotic events. Oxidative stress contributes to the elevation of blood pressure. The inflammatory syndrome induces activation of several factors, which are dependent on cytosolic Ca activation. Recent findings support the hypothesis that the Mg effect on intracellular Ca2+ homeostasis may be a common link between stress, inflammation and a possible relationship to metabolic syndrome.

Phagocyte priming by low magnesium status: input to the enhanced inflammatory and oxidative stress responses.

Epidemiological and experimental studies underline the role of magnesium in inflammation. Several data indicate an enhanced response of phagocytes (granulocytes, macrophages) derived from magnesium-deficient animals or cultured under low magnesium conditions to the inflammatory mediators' stimulation. On the contrary, it was pointed out that high extracellular Mg2+ concentration might partially attenuate the activation of phagocyte leukocytes. Thus, it is likely that magnesium-deficient conditions lead to the priming (pre-activation) of phagocytic cells. Magnesium status is an important modulator of the phagocyte response to immune stimuli and consequently could be implicated in a wide range of pathophysiological issues, e.g. those related to the production of radical oxygen species (ROS). It is likely that magnesium directly modulates phagocyte priming by its calcium antagonism and indirectly by its effect on the immunoinflammatory processes, the source of the priming mediators.

High-magnesium concentration and cytokine production in human whole blood model.

The potential influence of magnesium (Mg) on inflammatory responses was assessed using an ex vivo model--human whole blood incubated with and without lipopolysaccharide (LPS). Addition of LPS leads to higher levels of cytokines including TNF-alpha and IL-6. No significant effect of Mg was observed following LPS stimulation whereas high concentration of Mg inhibited the baseline level (without LPS) of TNF-alpha and IL-6 production. This observation contrasts with that of a previous one on Mg-deficient animals. Therefore, the weak efficiency of increasing Mg concentration in this study on the whole blood from healthy volunteers suggests that the efficiency of Mg supplementation on cytokine production induced by endotoxin challenge depends on Mg status.

Vascular function of MGH and MGL mice, two strains which differ by a genetic variation of magnesium metabolism.

Mg deficiency is considered as a risk factor of cardiovascular disorders like hypertension and atherosclerosis. MGH and MGL mice, selected for high and low Mg status, are animal models which present variations of Mg metabolism of genetic origin. The cardiovascular functions of these mice have never been studied. In this study, the arterial blood pressure of MGH and MGL strains was measured by plethysmography. Morphology and reactivity to vasoconstrictor agents were also investigated by a pressurized and perfused system in mesenteric resistance artery. It is shown that: (1) MGH mice presented a higher plasma Mg concentration than MGL; (2) arterial blood pressure and heart rates were similar between the two groups; (3) media thickness, media cross-sectional area, and internal and external diameters were smaller in pressurized mesenteric resistance arteries from MGH mice than in those from MGL mice; (4) the vasoconstriction induced by vasopressin (but not norepinephrine) was higher in the mesenteric arteries from MGH mice than in those from MGL ones. In summary, MGH mice as compared to MGL mice present differences in arterial geometry and higher reactivity to vasopressin without repercussions on arterial blood pressure. The real repercussion of these observations on the cardiovascular system of the MGH and MGL models is at present unknown. More experiments are needed to clarify the influence of differences in Mg metabolism of genetic origin on cardiovascular function.

Lipid metabolism and antioxidant status in sucrose vs. potato-fed rats.

OBJECTIVE: Consumption of high levels of simple carbohydrates is associated with several metabolic disorders in humans and in laboratory animals, including symptoms of an early stage of metabolic syndrome (syndrome X). This disorder has several cardiovascular risk factors, such as hypertriglyceridemia, and is associated with an increase in oxidative stress. In contrast to sucrose, potato, a source of complex carbohydrates and antioxidant micronutrients, was thought to improve lipid metabolism and antioxidant protection. METHODS: We investigated the effects of diets containing i) complex dietary carbohydrates and antioxidant micronutrients (potato Solanum tuberosum L.), ii) complex carbohydrates (starch) and iii) a simple carbohydrate (sucrose) on lipid metabolism and antioxidant status in rats. RESULTS: An increase in short chain fatty acid (SCFA) pools was observed in the cecum of rats fed a potato-based diet, resulting from an increase in all SCFAs, especially propionate (+360%, P < 0.0001). Feeding rats a potato-based diet for 3 weeks led to a decrease in cholesterol (-37%, potato vs. control and -32%, potato vs. sucrose) and triglycerides (-31%, potato vs. control and -43%, potato vs. sucrose) concentrations in triglyceride-rich lipoproteins (TGRLP) fractions. The antioxidant status was decreased by sucrose consumption and improved by potato consumption. CONCLUSIONS: Our present results suggest that consumption of complex carbohydrates (provided as cooked potatoes), in combination with different antioxidant micronutrients, may enhance the antioxidant defences and improve lipid metabolism, when compared with starch (complex carbohydrates) and to sucrose consumption (source of simple sugar). These effects limit oxidative stress and reduce the risk of developing the associated degenerative diseases, including cardiovascular disease, and could have potential in cardiovascular disease prevention.

Relationship between low magnesium status and TRPM6 expression in the kidney and large intestine.

The body maintains Mg(2+) homeostasis by renal and intestinal (re)absorption. However, the molecular mechanisms that mediate transepithelial Mg(2+) transport are largely unknown. Transient receptor potential melastatin 6 (TRPM6) was recently identified and shown to function in active epithelial Mg(2+) transport in intestine and kidney. To define the relationship between Mg(2+) status and TRPM6 expression, we used two models of hypomagnesemia: 1) C57BL/6J mice fed a mildly or severely Mg(2+)-deficient diet, and 2) mice selected for either low (MgL) or high (MgH) erythrocyte and plasma Mg(2+) status. In addition, the mice were subjected to a severely Mg(2+)-deficient diet. Our results show that C57BL/6J mice fed a severely Mg(2+)-deficient diet developed hypomagnesemia and hypomagnesuria and showed increased TRPM6 expression in kidney and intestine. When fed a Mg(2+)-adequate diet, MgL mice presented hypomagnesemia and hypermagnesuria, and lower kidney and intestinal TRPM6 expression, compared with MgH mice. A severely Mg(2+)-deficient diet led to hypomagnesemia and hypomagnesuria in both strains. Furthermore, this diet induced kidney TRPM6 expression in MgL mice, but not in MgH mice. In conclusion, as shown in C57BL/6J mice, dietary Mg(2+)-restriction results in increased Mg(2+) (re)absorption, which is correlated with increased TRPM6 expression. In MgL and MgH mice, the inherited Mg(2+) status is linked to different TRPM6 expression. The MgL and MgH mice respond differently to a low-Mg(2+) diet with regard to TRPM6 expression in the kidney, consistent with genetic factors contributing to the regulation of cellular Mg(2+) levels. Further studies of these mice strains could improve our understanding of the genetics of Mg(2+) homeostasis.

Inulin supplementation prevents high fructose diet-induced hypertension in rats.

BACKGROUND & AIMS: The aim of this experiment was to evaluate the potential beneficial effect of supplementation with different inulin-type fructan fractions against common features of the metabolic syndrome in a rat model of this syndrome (fructose-fed rat). METHODS: Forty Wistar rats were randomly divided into five groups and the animals received for 4 weeks either a semi-purified starch or fructose-based diet, or diets in which fructose was partially substituted with various fructans: 10 g/100 g of long-chain inulin or oligofructose, or an oligofructose-enriched inulin. After this period, blood pressure was measured and samples of blood and tissues were collected for selected biochemical analyses. RESULTS: As compared to the starch-fed group, the fructose-fed rats presented: hypertriglyceridemia, hypertension, increased susceptibility to heart peroxidation and renal damages. Long-chain inulin and oligofructose-enriched inulin supplementation prevented fructose induced elevated blood pressure, susceptibility to heart peroxidation and renal damages. All inulin-type fructans containing diets prevented fructose induced hypertriglyceridemia. CONCLUSIONS: These results suggest that supplementation with inulin-type fructans is efficient against fructose induced hypertension and that effects are most pronounced for long-chain inulin and oligofructose-enriched inulin. We hypothesize that the anti-hypertensive effect of inulin could be explained by the reduction of the high fructose induced oxidative stress.

Dietary inulin in mice stimulates Mg2+ absorption and modulates TRPM6 and TRPM7 expression in large intestine and kidney.

Complex fermentable carbohydrates, such as inulin-type fructans have been shown to improve Mg2+ absorption in the hindgut and body stores. The mechanisms for this are not well understood. The newly identified transient receptor potential melastatin 6 and 7 (TRPM6 and TRPM7) channels have been shown to function in active epithelial Mg2+ transport in the apical membrane of epithelial cells, the kidney and intestine and to be regulated by dietary intake. To determine the modulation of TRPM6 and TRPM7 expression in kidney and large intestine by long-chain inulin ingestion, C57B16J mice were fed a control or a long-chain inulin enriched diet (65 g of inulin/kg diet) for two weeks. Our results show that the inulin-enriched diet ameliorated Mg2+ absorption and Mg2+ bone stores. These features were accompanied by increased TRPM6 and TRPM7 expression in the hindgut. Downregulation of TRPM6 in the kidney of inulin fed mice could be related to reduced Mg2+ reabsorption and supports the beneficial effect of dietary fibers on Mg2+ absorption and stores. Inulin ingestion also modulates TRPM6 and TRPM7 expression in the large intestine. The origin and role of this modulation is not known. Changes in Mg2+ fluxes, lower pH of the digestive content and increased cell proliferation may be involved.

Inflammation interferes with the assessment of vitamin A status in magnesium deficiency.

Hyporetinemia is observed in several pathological conditions including a primary deficiency of vitamin A and has also been reported to accompany inflammatory diseases. Experimental magnesium (Mg) deficiency in rodents is accompanied by an inflammatory syndrome. The present study was designed to determine whether the acute phase response in Mg-deficient rats can modify vitamin A status. Clinical symptoms of acute phase response were observed in Mg-deficient rats and were accompanied by a reduction in plasma retinol and of plasma retinol binding protein (RBP). Mg deficiency in rats resulted in hyporetinemia without a significant decrease in liver retinol reserves. Consequently, the data strongly suggest that the decrease in plasma retinol concentration, resulting from the level of its binding protein, is related to the inflammatory effect of Mg deficiency. These results point to the possible interference of Mg deficiency on the use of plasma retinol as an indicator of vitamin A status.

Magnesium and the inflammatory response: potential physiopathological implications.

The purpose of this review is to summarize experimental findings showing that magnesium modulates cellular events involved in inflammation. Experimental magnesium deficiency in the rat induces after a few days a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines and acute phase proteins, excessive production of free radicals. Increase in extracellular magnesium concentration, decreases inflammatory response while reduction in the extracellular magnesium results in cell activation. Because magnesium acts as a natural calcium antagonist, the molecular basis for inflammatory response is probably the result of modulation of intracellular calcium concentration. The priming of phagocytic cells, the opening calcium channel and activation of N-methyl-d-aspartate (NMDA) receptors, the activation of nuclear factor-kappa B (NFkappaB) have been considered as potential mechanisms. Moreover, magnesium deficiency induces a systemic stress response by activation of neuro endocrinological pathways. As nervous and immune systems interact bidirectionally, the roles of neuromediators have also been considered. Magnesium deficiency contributes to an exaggerated response to immune stress and oxidative stress is the consequence of the inflammatory response. Inflammation contributes to the pro-atherogenic changes in lipoprotein metabolism, endothelial dysfunction, thrombosis, hypertension and explains the aggravating effect of magnesium deficiency on the development of metabolic syndrome. Further studies are still needed to assess more accurately the role of magnesium in immune response in humans, but these experimental findings in animal models suggest that inflammation is the missing link to explain the role of magnesium in many pathological conditions.

The effect of aging on intestinal absorption and status of calcium, magnesium, zinc, and copper in rats: a stable isotope study.

Many investigators have reported changes in mineral status with age but conflicting observations were done concerning mineral absorption. This study was conducted to clarify the effect of aging on intestinal absorption and status of minerals, using a stable isotope approach. To do so, 40 rats of different ages: 9, 22, 44, and 88 weeks were fed with a semi-purified diet for a total of 30 days. At the beginning of the 4th week, the rats received a stable isotope solution containing (44)Ca, (25)Mg, (67)Zn, and (65)Cu. Individual feces and urine were then collected during 4 consecutive days in order to measure stable isotopes by inductively coupled plasma/mass spectrometry (ICP/MS) and blood and tissues were sampled for mineral status determination. Intestinal absorption of (44)Ca and (67)Zn considerably decreased with age, whereas intestinal (25)Mg absorption decreased only moderately and intestinal (65)Cu absorption was unaffected. Plasma and bone calcium (Ca) were not modified with age whereas urinary Ca excretion considerably increased. Plasma and erythrocyte magnesium (Mg) levels were unaffected with age whereas urinary Mg excretion and Mg bone level decreased. Plasma zinc (Zn) level decreased and bone Zn level increased with age whereas red blood cell and liver Zn level and urinary Zn excretion remained unchanged. Plasma Cu level increased with age whereas liver and bone Cu levels and urinary Cu excretion remained unchanged. These results show that the effect of aging on the intestinal mineral absorption and status differ largely according to the mineral considered. Further studies are required under different nutritional conditions to explore the underlying mechanisms during aging and to adjust a better nutrition of the elderly.

In vivo antioxidant activity of procyanidin-rich extracts from grape seed and pine (Pinus maritima) bark in rats.

BACKGROUND: In vitro evidence exists for the potential antioxidant benefits of procyanidin-rich extracts, but in vivo studies are scarce. We have evaluated the effects of selected procyanidin-rich extracts on oxidative stress in rats in condition of prolonged consumption of these compounds and also after single administration i.e. in postprandial conditions. METHODS: Rats were fed for 8 weeks with diets supplemented with either a grape seed extract (GE), a pine bark extract (PE), or a high-degree polymerized pine bark extract (HPE). An additional study was performed in order to assess the postprandial effect of these extracts on plasma antioxidant capacity. The ferric-reducing antioxidant power (FRAP) and thiobarbituric acid-reactive substances (TBARS) were determined in plasma. For lipid peroxidation study of heart tissue, homogenates were prepared and TBARS were measured after lipid peroxidation induced by FeSO4-ascorbate. RESULTS: After 8 weeks of dietary treatment, total antioxidant capacity in plasma was significantly higher in the GE and PE groups as compared with the other two groups. Plasma TBARS concentrations and heart susceptibility to peroxidation were not significantly different between the groups. In the postprandial state, by comparing plasma antioxidant capacity 2 hours after ingestion of the different procyanidin-rich extracts (500 mg/kg body weight), we observed that FRAP values were higher in the procyanidin-rich extracts groups as compared with the control group. Moreover, plasma FRAP concentration was significantly higher in the GE group as compared with the other groups. CONCLUSION: The results of the present experiment constitute positive evidence for an in vivo antioxidant effect at the plasma level of procyanidin-containing plant extracts.

Dietary inulin intake and age can significantly affect absorption of the faecal marker dysprosium in rats.

It is believed that rare earth elements are not absorbed, and thus they are generally used in some mineral absorption studies as a faecal marker. The aim of the present study was to determine the effect of inulin intake and age on dysprosium (Dy) absorption in rats. Eighty male Wistar rats of four different ages (2, 5, 10 and 20 months) were randomised into either a control group or a group receiving 3.75 % inulin in their diet for 4 d and then 7.5 % inulin until the end of the study. The animals were fed fresh food and water ad libitum for 30 d. The intestinal absorption of Dy was determined from a 4 d (day 21 to day 25) balance study. Mean faecal Dy recovery (%) in the eight groups (3 months control, 3 months inulin, 6 months control, 6 months inulin, 11 months control, 11 months inulin, 21 months control, 21 months inulin) was 94.0 (sd 8.6), 64.8 (sd 10.1), 95.8 (sd 9.4), 81.5 (sd 12.1), 98.4 (sd 9.8), 87.8 (sd 9.5), 97.8 (sd 6.2) and 84.9 (sd 10.9), respectively. Our results showed clearly that dietary inulin intake decreased faecal Dy recovery in all four rat groups, and faecal Dy recovery was significantly higher in the old rats (10 and 20 months) than in the young and adult rats. These results show that the faecal recovery (or intestinal absorption) of Dy may vary greatly with nutritional or physiological states such as inulin intake or age. The use of rare earth elements as a faecal marker should be thus validated under each nutritional or physiological state before being employed in mineral absorption studies.

Dietary inulin intake and age can affect intestinal absorption of zinc and copper in rats.

Nondigestible inulin-type fructan intake can stimulate intestinal mineral absorption in both humans and animals. However, this stimulatory effect may depend on experimental conditions such as the duration of the experience, mineral levels in the diet, and the animal's physiological status. The aim of this study was to determine the effect of inulin intake on Zn and Cu absorption in rats at different ages. Male Wistar rats (n = 80) of 4 different ages (2,5, 10, and 20 mo) were randomly assigned to a control group or a group administered 3.75% inulin in their diet for 4 d followed by 7.5% inulin for 26 d. Absorption of Zn67 and Cu65 was determined on d 21 of the experiment by fecal monitoring using Zn67 and Cu65 isotopes. Zn and Cu status was also assessed. Absorption of Zn67 and Cu65 was significantly lower in 11- and 21-mo-old rats than in 3- and 6 mo-old-rats. Moreover, inulin intake significantly increased Zn67 and Cu65 absorption. In conclusion, age and dietary inulin intake can significantly affect intestinal absorption of zinc and copper in rats. Further studies are required to explore this effect over longer periods of inulin intake and to test the effects of inulin in humans.

Dietary inulin intake and age can significantly affect intestinal absorption of calcium and magnesium in rats: a stable isotope approach.

BACKGROUND: previous studies have shown that non-digestible inulin-type fructan intake can increase intestinal mineral absorption in both humans and animals. However, this stimulatory effect on intestinal absorption may depend on experimental conditions such as duration of fermentable fiber intake, mineral diet levels and animals' physiological status, in particular their age. OBJECTIVES: the aim of this study was to determine the effect of inulin intake on Ca and Mg absorption in rats at different age stages. METHODS: eighty male Wistar rats of four different ages (2, 5, 10 and 20 months) were randomized into either a control group or a group receiving 3.75% inulin in their diet for 4 days and then 7.5% inulin for three weeks. The animals were fed fresh food and water ad libitum for the duration of the experiment. Intestinal absorption of Ca and Mg was determined by fecal monitoring using stable isotopic tracers. Ca and Mg status was also assessed. RESULTS: absorption of Ca and Mg was significantly lower in the aged rats (10 and 20 mo) than in the young and adult rat groups. As expected, inulin intake increased Ca and Mg absorption in all four rat groups. However, inulin had a numerically greater effect on Ca absorption in aged rats than in younger rats whereas its effect on Mg absorption remained similar across all four rat age groups. CONCLUSION: the extent of the stimulatory effect of inulin on absorption of Ca may differ according to animal ages. Further studies are required to explore this effect over longer inulin intake periods, and to confirm these results in humans.

Stable isotopes in studies of intestinal absorption, exchangeable pools and mineral status: the example of magnesium.

Magnesium (Mg) is a biologically essential mineral and Mg deficiency is known to lead to severe biochemical and symptomatic disorders. Radioactive isotopes and, more recently, stable isotopes have been used as research tools to determine intestinal Mg absorption in humans and animals under different nutritional and physiological conditions. Mg isotopes are given orally or orally plus intravenously and analysed in faeces and/or in plasma and urine in order to calculate intestinal Mg absorption and possibly endogenous Mg excretion. Mg isotopes have been used to assess exchangeable pools of Mg under nutritional and physiopathological conditions. Mg isotopes are given intravenously and are analysed in plasma and urine to calculate the size and half-life of the various Mg exchangeable pools. More recently, in vitro isotopic tests have been developed to study the need of cells for Mg in different nutritional and genetic conditions. Whole blood is incubated with Mg isotopes and isotopic blood cell enrichment is measured, which reflects the avidity of cells for Mg and thus its initial status. This paper is a report on the use of stable Mg isotopes and their advantages in these different fields of Mg absorption and metabolism. The studies available have clearly demonstrated that stable isotopes provide a useful research tool for determining intestinal Mg absorption, and represent a precious research tool for the study of Mg metabolism and the assessment of Mg status.