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PubMed1998

Magnesium loading effect on magnesium deficiency in endurance-trained subjects during prolonged restriction of muscular activity.

The aim of this study was to evaluate the effect of magnesium (Mg) loading (10.0 mg Mg/kg body wt) and daily Mg supplements (5.0 mg Mg/kg body wt) on Mg deficiency shown by increased and not by decreased serum Mg concentration during hypokinesia (decreased km number/d). The studies were done during 30 d of prehypokinesia and 364 d of hypokinesia (HK) periods. Forty endurance-trained volunteers aged 22-26 yr with a peak VO2 max of 66.3 mL.kg-1 min-1 and with an average 15.0 km/d running distance were chosen as subjects. They were equally divided into four groups: 1. Unsupplemented ambulatory control subjects (UACS). 2. Unsupplemented hypokinetic subjects (UHKS). 3. Supplemented hypokinetic subjects (SHKS). 4. Supplemented ambulatory control subjects (SACS). The SHKS and SACS groups took daily 5.0 mg elemental Mg/kg body wt and subjected to Mg loading (10.0 mg Mg/kg body wt). Both the SHKS and UHKS groups were maintained under an average running distance of 4.7 km/d, whereas the SACS and UACS groups did not experience any modifications to their normal training routines and diets. During the prehypokinetic and hypokinetic periods, excretion of Mg in feces and urine, concentration of Mg in serum, and Mg balance were measured. Urinary and serum sodium (Na), potassium (K), and calcium (Ca) were also determined. In both SHKS and UHKS groups, fecal Mg loss, urinary excretion of electrolytes, and serum concentrations of electrolytes increased significantly (p < or = 0.05) when compared with the SACS and UACS groups. During Mg loading tests, urinary and fecal Mg excretion was also greater in the SHKS and UHKS groups than in the SACS and UACS groups. Throughout the study, Mg balance was negative in the SHKS and UHKS groups, whereas in the SACS and UACS groups, Mg balance was positive. It was concluded that significant losses of Mg occurred in the presence of negative Mg balance and Mg deficiency in endurance-trained subjects during prolonged exposure to HK, daily mg supplements, and Mg loading tests. This suggests that Mg is not entering or being retaining by the bones and cells of many tissues where most Mg is deposited normally, resulting in Mg deficiency as was shown by the increased serum Mg concentration.

Adult↗
PubMedDate not supplied

Daily magnesium supplementation on serum and urinary magnesium changes in rats during prolonged restriction of motor activity.

The objective of this investigation was to determine whether a plentiful magnesium (Mg2+) supplementation might be used to normalize or prevent Mg deficiency. This is manifested by increased rather than decreased serum Mg2+ concentration as is observed during prolonged hospitalization, which is developed during prolonged hypokinesia (HK) (decreased motor activity). Eighty male Wistar rats with an initial body weight of 370-390 g were used to perform the studies: They were equally divided into four groups: 1. Unsupplemented control animals (UCA); 2. Supplemented control animals (SCA); 3. Unsupplemented hypokinetic animals (UHA); and 4. Supplemented hypokinetic animals (SHA). For the simulation of the hypokinetic effect, the hypokinetic animals were kept in small individual cages made of wood which restricted their movements in all directions without hindering food and water intake. The control and hypokinetic supplemental animals receive 0.9 mg/mL Mg sulfate daily with their drinking water. Prior to and during the experimental period, urinary excretions of Mg, calcium, and phosphate along with their concentrations in serum, water intake, and urine excretion, and body weight were determined in the control and hypokinetic animals. In the supplemental and unsupplemental hypokinetic rats, urinary excretions and serum concentrations of electrolytes increased significantly, whereas serum concentration and urinary excretion thereof remained unchanged in the supplemented and unsupplemented control animals. It was concluded that a daily intake of large amounts of Mg supplementation cannot be used to prevent or normalize Mg deficiency in rats during prolonged exposure to HK.

Analysis of Variance↗
PubMed2005

Erythrocyte magnesium fluxes in mice with nutritionally and genetically low magnesium status.

Low intracellular magnesium (Mg) contents may be observed in case of severe Mg insufficient intake or because of genetic regulation. This work was conducted to investigate the influence of intracellular Mg content on erythrocyte Mg(2+) influx and efflux in mice with low nutritionally and genetically (MGL and MGH mice) Mg status. C57BL6 mice were fed for 2 wks a diet containing 1000 mg Mg/kg diet Mg (control group), 100 mg Mg/kg diet (Mg-marginal group) or 30 mg Mg/kg diet (Mg deficient group), while mice with low (MGL) and high (MGH) Mg levels were fed a control diet for 2 wks. The quantification of erythrocyte Mg(2+) influx and efflux was performed using a stable isotope of Mg. Our results showed that erythrocyte Mg(2+) influx and efflux were respectively increased and decreased in nutritional Mg deficiency; while in genetically determined Mg status Mg(2+) fluxes were lower in MGL mice compared to MGH mice. Moreover Mg(2+) efflux was significantly correlated to Mg level in erythrocytes in all the mice studied (p < 0.001). In conclusion, erythrocyte Mg(2+) influx and efflux are modulated by low Mg status, namely decreased Mg(2+) efflux compensate for nutritional Mg deficiency, while the genetic regulation of erythrocyte Mg(2+) content depends on modification of Mg(2+) influx.

Animals↗
PubMed1989

Cardiovascular consequences of magnesium deficiency and loss: pathogenesis, prevalence and manifestations--magnesium and chloride loss in refractory potassium repletion.

Dietary magnesium (Mg) deficiency is more prevalent than generally suspected and can cause cardiovascular lesions leading to disease at all stages of life. The average American diet is deficient in Mg, especially in the young, in alcoholic persons, and in those under stress or with diseases or receiving certain drug therapies, who have increased Mg needs. Otherwise normal, Mg-deficient diets cause arterial and myocardial lesions in all animals studied, and diets that are atherogenic, thrombogenic and cardiovasopathic, as well as Mg-deficient, intensify the cardiovascular lesions, whereas Mg supplementation prevents them. Diuretics and digitalis can intensify an underlying Mg deficiency, leading to cardiac arrhythmias that are refractory unless Mg is added to the regimen. Potassium (K) depletion in diuretic-treated hypertensive patients has been linked to an increased incidence of ventricular ectopy and sudden death. K supplementation alone is not the answer. Mg has been found to be necessary to intracellular K repletion in these patients. Because patients with congestive heart failure and others receiving diuretic therapy are also prone to chloride loss leading to metabolic alkalosis that also interferes with K repletion, the addition of Mg and chloride supplements in addition to the K seems prudent.

Cardiovascular Agents↗
PubMed1998

Intracellular magnesium depletion relates to increased urinary magnesium loss in type I diabetes.

We investigated whether erythrocyte magnesium (Mg) depletion exists in subjects with Type I diabetes. To this end, Mg levels in plasma, erythrocytes and urine were determined in 12 patients with Type I diabetes and compared with 12 healthy control subjects. Mean plasma Mg concentrations were comparable between diabetic patients and control subjects (0.90 +/- 0.29 mmol/l vs 1.04 +/- 0.14 mmol/l, respectively; p = 0.16). Mean erythrocyte Mg concentration was significantly lower in the diabetic group compared with the control group (1.41 +/- 0.56 mmol/l vs. 2.94 +/- 1.13 mmol/l, respectively; p < 0.0001). Mean urine Mg excretion was significantly elevated in the diabetic group with respect to the controls (6.86 +/- 3.5 mmol/g creatinine/24 h vs. 4.03 +/- 1.65 mmol/g creatinine/24 h, respectively; p = 0.02). As to the diabetic group, erythrocyte Mg concentration showed a significant inverse correlation with urine Mg excretion (r = -0.58, p = 0.049). There was no correlation between urine Mg concentration and glycosylated hemoglobin or fasting plasma glucose level. The data suggest that intracellular Mg depletion without significant hypomagnesemia is related to increased urinary Mg loss in patients with Type I diabetes. The urinary Mg loss is not correlated with the degree of metabolic control.

Adult↗
PubMed1984

Magnesium absorption in mature ewes infused intrarumenally with magnesium chloride.

The effects of magnesium supplementation on Mg absorption proximal and distal to the pylorus in ewes maintained on a grass diet were investigated using a combination of balance, digesta flow and electropotential measurements. Three mature ewes each received by intrarumenal infusion a supplement of 0, 1, 2 and 3 g Mg/d in sequence over four 10-d periods. Net Mg absorption distal to the pylorus took place down its electrochemical gradient, although the quantity absorbed remained small during the control and first infusion periods. The bulk of Mg absorption occurred before the pylorus and, during the control and first infusion periods, took place against its electrochemical gradient. The net Mg absorption proximal to the pylorus rose with declining efficiency as Mg intake was increased. It is suggested that saturation of the absorption process at this site was occurring.

Animals↗
PubMed1989

Determination of intracellular free magnesium by nuclear magnetic resonance in human magnesium deficiency.

Magnesium (Mg) deficiency is a common clinical problem. As Mg is predominantly an intracellular cation and Mg deficiency may exist despite normal serum Mg (sMg) concentrations, we have utilized nuclear magnetic resonance (NMR) techniques in an attempt to measure intracellular free Mg (Mg2+) in red blood cells (RBC). Twenty normal subjects, 22 hypomagnesemic patients, and 17 normomagnesemic alcoholic patients were studied. Mean RBC Mg2+ in normal subjects (178 +/- 6.3 microM) was significantly greater than in hypomagnesemic patients (146 +/- 7.1 microM, p less than 0.002). RBC Mg2+ correlated with sMg concentration (r = 0.54, p less than 0.001). In addition, four normal subjects were given a low Mg diet for 3 weeks. There was a progressive fall in both the sMg concentration and RBC Mg2+ during Mg depletion, with a concomitant rise in retention of a parenterally administered Mg load. These data suggest that the determination of intracellular Mg2+ by NMR may be a useful research tool in assessing the effect of changes in Mg2+ on intracellular processes. Its utility in the clinical evaluation of disorders of Mg deficiency remains to be determined.

Erythrocytes↗
PubMed1999

Magnesium-manganese interactions caused by magnesium deficiency in rats.

OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the nutritive utilization and tissue distribution of manganese (Mn). METHODS: Wistar rats were fed a Mg-deficient diet (56 mg/kg) for 70 day. Absorbed Mn, Mn balance and Mn content in plasma, whole blood, skeletal muscle, heart, kidney, liver, femoral bone and sternum were determined after 21, 35 and 70 days. RESULTS: The Mg-deficient diet significantly increased Mn apparent absorption and Mn balance from week five until the end of the experimental period. This effect was accompanied by a significant increase in the concentration of Mn in heart at all three time points. Whole blood, skeletal muscle and kidney Mn were significantly increased from day 35, and femur Mn content was increased only at the end of the study (day 70). However, Mn concentration in the sternum decreased significantly from day 35. No changes were found in liver Mn content. CONCLUSION: Mg deficiency increased Mn absorbed, and this favored the deposition of Mn in all tissues studied except the liver and trabecular bone. The lack of response by the liver to increased Mn absorption may have led to the redistribution of this ion to other tissues.

Absorption↗
PubMed2000

Magnesium status and parameters of the oxidant-antioxidant balance in patients with chronic fatigue: effects of supplementation with magnesium.

OBJECTIVE: Magnesium deficiency and oxidative stress have both been identified as pathogenic factors in aging and in several age-related diseases. The link between these two factors is unclear in humans although, in experimental animals, severe Mg deficiency has been shown to lead to increased oxidative stress. METHODS: The relationship between Mg body stores, dietary intakes and supplements on the one hand and parameters of the oxidant-antioxidant balance on the other was investigated in human subjects. RESULTS: The study population consisted of 93 patients with unexplained chronic fatigue (median age 38 years, 25% male, 16% smokers and 54% with Chronic Fatigue Syndrome (CFS). Mg deficient patients (47%) had lower total antioxidant capacity in plasma (p=0.007) which was related to serum albumin. Mg deficient patients whose Mg body stores did not improve after oral supplementation with Mg (10 mg/kg/day) had persistently lower blood glutathione levels (p=0.003). In vitro production of thiobarbituric acid reactive substances (TBARS) by non-HDL lipoproteins incubated with copper was related to serum cholesterol (p<0.001) but not to Mg or antioxidants and did not improve after Mg supplementation. In contrast, velocity of formation of fluorescent products of peroxidation (slope) correlated with serum vitamin E (p<0.001), which was, in turn, related to Mg dietary intakes. Both slope and serum vitamin E improved after Mg supplementation (p<0.001). CONCLUSIONS: These results show that the lower antioxidant capacity found in moderate Mg deficiency was not due to a deficit in Mg dietary intakes and was not accompanied by increased lipid susceptibility to in vitro peroxidation. Nevertheless, Mg supplementation was followed by an improvement in Mg body stores, in serum vitamin E and its interrelated stage of lipid peroxidation.

Adolescent↗
PubMed1986

Effects of calcium, fluoride and magnesium supplementations on tissue mineralization in calcium- and magnesium-deficient rats.

There is considerable uncertainty about the interrelated effects of calcium (Ca), magnesium (Mg) and fluoride (F) on hypocalcification of the skeleton and Ca accumulation in vital soft tissues. This paper describes experiments with rats fed a diet deficient in Ca and Mg, the latter deficiency being accentuated by a low potassium content. For different groups the drinking water was supplemented with Ca, Mg, F, Ca + F or Mg + F; Ca and F were supplied as chemically compatible compounds. At the end of the 54-d experiment, plasma Ca was strongly reduced in the Ca-deficient groups. Plasma Mg was reduced particularly in the test groups supplied with Ca, without any influence of F supply or varying plasma F. Ca accumulation was much more pronounced in the kidneys than in the heart or aorta, but was mitigated by both Mg and F supplementation. Bone mineralization disturbance due to the dietary imbalance was preventable only by Ca or Ca + F supplementation, and was less in alveolar bone than in femur. However, the Ca supplement was associated with the highest aorta and heart Ca contents, and Ca + F was associated with marked renal Ca accumulation; adequate Mg supply may be essential with Ca + F administration against osteoporosis.

Animals↗
PubMed1994

Role of magnesium and calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P-NMR, spectroscopy and a unique magnesium ion-selective electrode.

It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg), alcohol is now known to be the most notorious cause of Mg-wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg2+ ([Mg2+]i), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2+) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators. Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and cellular Ca2+ concomitant with a progressive reduction in Mg content. Use of 31P-NMR spectroscopy coupled with optical-backscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose-dependent deficits in phosphocreatine (PCr), the [PCr]/[ATP] ratio, intracellular pH (pHi), oxyhemoglobin, and the mitochondrial level of oxidized cytochrome oxidase aa3 concomitant with a rise in brain-blood volume and inorganic phosphate. Temporal studies performed in vivo, on the intact brain, indicate that [Mg2+]i is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg2+ prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag-fura-2, on single-cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration-dependent depletion of [Mg2+]i. These cellular deficits in [Mg2+]i seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to Ca2+ overload and ischemia. A role for ethanol-induced alterations in [Mg2+]i should also be considered in the well-known behavioral actions of alcohol.

Alcoholism↗
PubMed2003

The effects of systemic magnesium sulfate infusion on brain magnesium concentrations and energy state during hypoxia-ischemia in newborn miniswine.

The mechanism of neuroprotection associated with systemically administered magnesium remains unclear. This investigation examined the acute effects of systemically administered MgSO4 on brain extracellular ([Mg]ecf) and intracellular ([Mg]i) fluid Mg concentrations, specific brain phosphorylated metabolites, and brain intracellular pH. Miniswine were studied with P-31 magnetic resonance spectra, to derive [Mg]i, and brain microdialysis probes, to measure [Mg]ecf. Animals were infused with MgSO4 (n = 5, 275 mg/kg over 30 min followed by 100 mg/kg over 30 min, designated MgHI) or Na2SO4 (n = 5, designated NaHI), and both groups underwent hypoxia-ischemia (HI) over the last 15 min of the infusions. Groups differed in plasma [Mg] at the completion of HI (9.1 +/- 1.5 versus 1.1 +/- 0.6 mM for MgHI and NaHI, respectively, p < 0.05). MgHI had elevations of [Mg]ecf (0.23 +/- 0.11 and 0.40 +/- 0.14 mM at control and completion of HI, respectively), and [Mg]ecf was unchanged for NaHI (p < 0.05 versus MgHI). At the completion of HI, MgHI had greater decreases in nucleoside triphosphate (NTP) (48 +/- 6% of control), and more brain acidosis after HI (6.01 +/- 0.07) compared with NaHI (NTP, 70 +/- 3% of control; brain pH, 6.51 +/- 0.14, both p < 0.05 versus MgHI). [Mg]i increased to elevated values during HI in both MgHI and NaHI (p < 0.05 versus control of each group) and remained higher in MgHI over the next 25 min (p < 0.05 versus NaHI). There were inverse correlations during HI between [Mg]i and brain NTP (r2 = 0.73 and 0.59 for MgHI and NaHI, respectively), and brain acidosis (r2 = 0.85 and 0.85 for MgHI and NaHI, respectively) in each group. These findings indicate complex effects of Mg on the brain. Elevation of [Mg]ecf may be beneficial with regards to excitatory neurotransmitters. However, greater disturbance of brain NTP concentration, more acidosis, and the increase in [Mg]i may offset any benefit. The results warrant further investigation using indicators of neuronal injury to determine whether Mg supplementation provides neuroprotection.

Animals↗
PubMed1987

Renal magnesium wasting in a patient with short bowel syndrome with magnesium deficiency: effect of 1 alpha-hydroxyvitamin D3 treatment.

We studied a patient with severe hypomagnesemia due to small bowel resection who had marked renal magnesium (Mg) loss in response to iv Mg infusion. She had an undetectable serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] level before treatment. Although Mg infusion increased her serum Mg levels and enhanced renal PTH action, as evidenced by an elevation in nephrogenous cAMP, the serum 1,25-(OH)2D level remained low. After the administration of 1 alpha-hydroxyvitamin D3, her serum 1,25-(OH)2D level increased, and fractional excretion of Mg decreased. With the elevation in serum 1,25-(OH)2D, serum Mg levels could be maintained without Mg infusion, although they were still subnormal. These results are consistent with the assumption that patients with the short bowel syndrome and Mg deficiency have reduced renal tubular Mg reabsorption which causes renal Mg loss, and that impaired tubular Mg reabsorption is due at least in part to deficient renal action of 1,25-(OH)2D. Because depressed serum 1,25-(OH)2D levels cannot be corrected rapidly by Mg infusion, administration of 1 alpha-hydroxyvitamin D3 or 1,25-(OH)2D3 appears to be the treatment of choice for Mg deficiency in patients with short bowel syndrome.

Adult↗
PubMed1995

Systemic magnesium deficiency disclosed by magnesium loading test in patients with essential hypertension.

The present study was designed to determine whether magnesium (Mg) deficiency is present in patients with essential hypertension. We measured the retention of an intravenously administered Mg load (0.2 mmol/kg MgSO4 over 4 h), and serum and erythrocyte Mg concentrations in 17 inpatients with essential hypertension and in 15 normotensive controls. There was no significant difference between the two groups in erythrocyte Mg concentration (normotensives vs., hypertensives: 2.0 +/- 0.5 vs. 2.1 +/- 0.4 mmol/l cells), serum Mg concentration (normotensives vs. hypertensive: 2.1 +/- 0.2 vs. 2.1 +/- 0.2 mg/dl), or in urinary Mg excretion (normotensives vs. hypertensives: 65.8 +/- 25.5 vs. 73.7 +/- 26.7 mg/day). However, Mg retention was significantly higher in hypertensives than in normotensives (normotensives vs. hypertensives: 31.8 +/- 12.1 vs. 41.9 +/- 13.3%). These results suggest that a systemic Mg deficiency, which is undectectable by serum or erythrocyte Mg determination, may exist in patients with essential hypertension.

Adult↗
PubMed1992

Mononuclear cell magnesium and retention of magnesium after intravenous loading in patients with acute myocardial infarction.

A magnesium (Mg++) retention test was performed in 19 patients with acute myocardial infarction (AMI) 4-11 days after admission to the coronary care unit. The retention of Mg++ was 45 +/- 23% of the 30 mmol given intravenously. It has been proposed that a retention of more than 20% represents Mg++ deficiency. The mononuclear cell Mg++ concentration before the retention test was on an average slightly higher in the AMI patients than in 25 healthy volunteers (72.5 +/- 24.2 vs. 62.9 +/- 9.2 mumol g-1 protein) indicating no Mg++ depletion in the first group. The reason why patients during the phase of AMI show an increased retention of Mg++ is unknown, but changes in concentrations of several hormones and a reduction in blood glucose could be of importance. Serum concentrations of Mg++ were lower on admission than after 4-11 days. These initial reductions are probably due to increased concentrations of circulating catecholamines during the early hours of AMI.

Adult↗
PubMed1990

Lactational responses to and in vitro ruminal solubility of magnesium oxide or magnesium chelate.

Thirty-six midlactation Holstein cows were used in a randomized incomplete block design to evaluate lactational responses to varying dietary concentrations of Mg supplemented by MgO or Mg chelate. Basal diet was 41:4:55 corn silage:cottonseed hulls:concentrate (.21% total Mg). Magnesium oxide was added to the basal diet to give .32, .37, and .43% total dietary Mg, and Mg chelate was added to provide .23, .25, and .27% Mg, DM basis. Dietary treatments were formulated to supply equal concentrations of bioavailable Mg from either Mg source. Dry matter intake and milk yield were greater by cows fed MgO-supplemented than Mg chelate-supplemented treatments. Milk fat percentages were not affected. Milk protein percentages increased with Mg chelate compared with protein percentages with MgO. Treatments did not affect gross efficiency (4% FCM/DM intake) or body weight change. Lack of response to Mg chelate suggested that either the bioavailability was not as high as assumed or that sufficient total bioavailable Mg was not provided in those treatments. A companion in vitro experiment showed that MgO-supplemented concentrates, with more total supplemental Mg, supplied two to three times more soluble Mg than Mg chelate-supplemented concentrates.

Animal Feed↗
PubMed1994

Effects of fructooligosaccharides on the absorption of magnesium in the magnesium-deficient rat model.

Magnesium (Mg) is an essential dietary element that plays important roles, acting as a cofactor of many enzymes. Rats fed a Mg-deficient diet have been reported to exhibit auricular and facial peripheral hyperemia and hemorrhage. Moreover, increased intake of calcium (Ca) or phosphorus (P) has been reported to impair apparent absorption of Mg. We tried to induce such typical inflammation in Mg-deficient rats by feeding low-Mg, high-Ca, and high-P diets. Increasing concentrations of Ca or P in the experimental diets significantly decreased the apparent absorption of Mg. And all rats fed the low-Mg (0.25 mg/g diet), high-Ca (10.4 mg/g diet), and high-P (12.0 mg/g diet) diet exhibited auricular and facial peripheral-hyperemia and hemorrhage. Then, we used the low-Mg, high-Ca, and high-P diet to investigate the effects of the fructooligosaccharides (FO) on absorption of Mg and skin inflammation. In the rats fed FO-containing (1 or 5%) diet, apparent absorption of Mg was significantly increased as compared with that of the control (FO 0%) group. In the rats fed a 5% FO-containing diet and sufficient Mg (0.50 mg/g), auricular and facial peripheral hyperemia and hemorrhage were significantly reduced. We concluded that FO increased the Mg absorption in rats fed a low-Mg, high-Ca, and high-P diet. Moreover, FO reduced inflammation in Mg-deficient rats, such as peripheral hyperemia and hemorrhage.

Animals↗
PubMed1999

Effect of magnesium-deficient diet on serum and urine magnesium concentrations in healthy cats.

OBJECTIVE: To evaluate the efficacy of using serum total and ionized magnesium (Mg) concentrations and urine Mg concentrations to identify Mg deficiency in cats. ANIMALS: 6 healthy castrated male cats. PROCEDURE: A Mg-replete diet was fed for 37 days, followed by a Mg-deficient diet for 37 days. On days 1, 3, and 7 of the last week of each diet, serum ionized and total Mg concentrations were determined; in addition, urine Mg concentration was determined each day of the last week. Serum total and ionized Mg concentrations were compared with urine Mg concentration, amount of Mg excreted during 24 hours (24-hour urine Mg excretion), ratio of urine Mg concentration to urine creatinine concentration (Umg:Ucr), and urinary fractional excretion of Mg (FEmg) to determine which variable best predicted Mg status. RESULTS: Cats fed Mg-deficient diets had significantly lower serum total and ionized Mg concentrations and 24-hour urine Mg excretion values, compared with cats fed Mg-replete diets. Serum total Mg concentration was the best predictor of Mg status. Twenty-four-hour urine Mg excretion was a repeatable, reliable measurement and had the best correlation with serum total Mg concentration. Serum total Mg concentration also correlated with urine Mg concentration, Umg:Ucr, and FEmg. CONCLUSIONS AND CLINICAL RELEVANCE: Serum total and ionized Mg concentrations can be used to identify cats with dietary-induced Mg deficiencies. Twenty-four-hour urine Mg excretion and urine Mg concentration correlated best with serum total Mg concentration and, therefore, may be the most useful urine variables for identifying Mg deficiency.

Animal Feed↗