Role of cofactors in the treatment of malnutrition as examplified by magnesium.
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In the absence of appropriate amounts of metabolically important cofactors such as magnesium, replenishment of malnourished patients with protein and carbohydrate will exaggerate the underlying abnormality even though the primary deficiency is corrected. The malnourished patients cannot utilize the food substances provided unless they have within their cells commensurate amounts of all the necessary cofactors required for the metabolism of the food supplied. This therapeutic problem in malnutrition is illustrated by three different examples of clinical deterioration when caloric and vitamin replenishment have been undertaken in the face of magnesium deificiency. (+info)
Administration of the oral antibiotic frenolicin-B selectively alters copper nutriture in male rats.
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The polyketide antibiotic Frenolicin-B (FB) produces anorexia and esophageal epithelial hyperplasia (EH) in rats, findings that are characteristic of zinc deficiency. Because FB also chelates divalent cations in vitro, we conducted studies to determine whether FB modifies blood and organ concentrations of zinc and other essential metals (calcium, copper, iron and magnesium). Groups of male Sprague-Dawley rats ( approximately 250g; n = 20/group) consumed diets with adequate (40 microg/g), deficient (<2 microg/g) or fortified (100 microg/g) zinc concentrations ad libitum for 28 d. Two groups fed either Zn-adequate or Zn-fortified diets also were given 100 mg/(kg. d) of FB in diet, and 2 groups were pair-fed controls. Histopathology or metal analyses were performed on tissues from 10 rats/group. FB caused EH of the nonglandular stomach but not of other tissues. Of the metals evaluated, only copper concentrations were significantly reduced in all tissues examined except kidney. A broad range of kidney copper concentrations was found; these concentrations were associated with plasma copper and proteinaceous deposits within tubules. In rats, FB substantially and selectively depletes Cu in vivo, suggesting that drugs with structures that permit metal chelation should be evaluated for their potential to alter trace metal nutriture. (+info)
Changes in gene expression in rat thymocytes identified by cDNA array support the occurrence of oxidative stress in early magnesium deficiency.
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Magnesium deficiency in experimental animals leads to inflammation, exacerbated immune stress response and a decrease of specific immune response. It also results in a significant increase in free radical species and subsequent tissue injury. An accelerated thymus involution was observed in Mg-deficient rats in relation to enhanced apoptosis and enhanced susceptibility to oxidative stress. To examine the stress-inducing effects of low Mg status on thymocytes, cDNA arrays were used to evaluate changes in gene expression in weaning rats submitted to Mg deficiency of short duration (2 days). Several genes exhibited changes in their expression caused by Mg deficiency before any perceptible modification in cell integrity and functions. The up-regulated genes included cytochrome c oxidase, glutathione transferase, CuZn superoxide dismutase, genes associated with the stress response (HSP70 and HSP84) and a gene involved in DNA synthesis and repair (GADD45). The down-regulated genes included Na/P cotransporter 1. These findings are consistent with altered cell growth, modifications of ion fluxes and oxidative stress described during Mg deficiency. The observation of induction of genes involved in protection and repair in cells from Mg-deficient animals provides additional evidence of the role of oxidative stress in the pathobiology of this deficiency. (+info)
BACKGROUND: Magnesium has been suggested to be beneficial in counteracting all phases of the processes that lead to ischemic heart disease, including terminal events such as arrhythmia and sudden death. OBJECTIVE: We tested the hypothesis that an intake of magnesium considerably below the recommended dietary allowance can produce chemical and physiologic evidence of depletion. DESIGN: Twenty-two postmenopausal women were maintained in a metabolic unit and ate a diet of conventional foods containing less than one-half of or more than the recommended dietary allowance for magnesium (320 mg/d). Dietary assignments were random and double blind in a crossover design. Magnesium concentrations were measured by spectroscopy and ion-specific electrolyte analysis, and Holter electrocardiograms lasting approximate 21 h were recorded. RESULTS: Magnesium concentrations in erythrocytes, serum (total and ultrafilterable), and urine were significantly lower when dietary magnesium was lower. Holter monitors showed a significant increase in both supraventricular and supraventricular plus ventricular beats when the dietary magnesium concentration was low. Hypomagnesemia, hypocalcemia, and hypokalemia were not found. CONCLUSIONS: The magnesium requirement was defined with the use of biochemical and electrophysiologic criteria. The recommended dietary allowance of 320 mg/d seems correct; 130 mg is too little. Persons who live in soft water areas, who use diuretics, or who are predisposed to magnesium loss or ectopic beats may require more dietary magnesium than would others. (+info)
Changes in N-acetyl-beta-D-glucosaminidase activity in the urine and urinary albumin excretion in magnesium deficient rats.
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To discover the details of the effects of magnesium (Mg) deficiency on kidney function, the course of changes in N-acetyl-beta-D-glucosaminidase (NAG) activity in the urine and in urinary albumin excretion were examined in rats fed a Mg-deficient diet. NAG activity in the urine and urinary albumin excretion in rats fed the Mg-deficient diet significantly increased from 7 d until the end of the feeding period. We suggest that Mg-deficient diet rapidly induces kidney function insufficiency. (+info)
Dietary magnesium depletion affects metabolic responses during submaximal exercise in postmenopausal women.
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Magnesium is an essential mineral that is required for optimal biological function including energy metabolism. Although national nutritional surveys indicate that usual magnesium intakes do not meet recommendations, particularly among older women, diet-induced magnesium depletion is considered rare among humans without concurrent illness. We examined the effects of dietary magnesium restriction on biochemical measures of magnesium nutriture and physiologic responses during submaximal exercise in 10 postmenopausal women, 45-71 y old, not receiving hormone replacement therapy. The women consumed diets containing conventional foods with varying magnesium content totaling 112 mg/8.4 MJ (2000 kcal) supplemented with 200 mg magnesium daily for 35d (control), then 112 mg/8.4 MJ for 93d (depletion) followed by 112 mg/8.4 MJ supplemented with 200 mg magnesium/d for 49d (repletion) in a depletion-repletion experiment. RBC magnesium concentration (P < 0.05), magnesium retention (P < 0.05) and skeletal muscle magnesium concentration (P < 0.05) decreased when dietary magnesium was restricted. Peak oxygen uptake, total and cumulative net oxygen uptake determined by using indirect calorimetry and peak heart rate increased (P < 0.05) during standardized submaximal work with restricted compared with adequate dietary magnesium. These findings indicate that dietary magnesium depletion can be induced in otherwise healthy women; it results in increased energy needs and adversely affects cardiovascular function during submaximal work. This may also explain previous observations of increased energy cost during standardized exercise in physically active men and women considered to have reduced magnesium nutriture. (+info)
Dietary magnesium intake in type 2 diabetes.
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BACKGROUND: Magnesium deficiency is common in type 2 diabetes and may have a negative impact on glucose homeostasis and insulin resistance, as well as on the evolution of complications such as retinopathy, thrombosis and hypertension. OBJECTIVE: To assess the dietary magnesium intake of patients with type 2 diabetes in Zurich, Switzerland and to compare the magnesium intake of diabetic and non-diabetic subjects. DESIGN: The magnesium intake of 97 randomly selected patients with type 2 diabetes and 100 healthy, non-diabetic controls matched for age and sex was estimated using a diet history method. During winter and summer periods, mean daily magnesium intakes were calculated from detailed information given by the test subjects about their eating habits over the previous 2 months. The calculations were performed using EBIS, a computer program based on a German nutrient data base (BLS 2.3), with food items specific to Switzerland added or directly analysed when necessary. RESULTS: The mean+/-s.d. daily magnesium intake of the male diabetic and male control subjects was 423.2+/-103.1 and 421.1+/-111.0 mg, respectively. The mean daily magnesium intake of the female diabetic and female control subjects was 419.1+/-109.7 and 383.5+/-109.7 mg, respectively. There were no significant differences in daily magnesium intake between the diabetic and the non-diabetic subjects and mean intakes in both groups exceeded Swiss recommended dietary intakes. CONCLUSIONS: Dietary intake of magnesium appears sufficient in Swiss adults with type 2 diabetes and is unlikely to contribute to the aetiology of magnesium deficiency. SPONSORSHIP: The Swiss Federal Institute of Technology, Zurich, Switzerland. (+info)
Synergistic effect of ofloxacin and magnesium deficiency on joint cartilage in immature rats.
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Single high oral doses of fluoroquinolones (e.g., 1,200 mg of ofloxacin/kg of body weight) are chondrotoxic in juvenile rats. Characteristic cartilage lesions are detectable as early as 12 h after treatment. Since this dosing regimen does not reflect the therapeutic situation, we studied the effects of a 5- or 7-day treatment with ofloxacin at lower oral doses (10, 30, and 100 mg/kg twice a day [b.i.d.]) on joint cartilage in 4-week-old rats. We additionally investigated whether the effects of ofloxacin under these conditions are enhanced in animals kept on a magnesium-deficient diet during treatment. Knee joints were examined histologically. The concentrations of ofloxacin and magnesium were determined in plasma and cartilage. The lowest ofloxacin dose at which cartilage lesions occurred in animals on a standard diet was 100 mg/kg b.i.d. for 5 days. Peak plasma ofloxacin levels were approximately 10 mg/liter in these rats and thus were in the same range as the levels in the plasma of humans during therapy with high doses of ofloxacin. Treatment with 30 mg of ofloxacin/kg b.i.d. for 7 days caused no cartilage lesions in rats on a standard diet, but lesions did occur in 10 of 12 rats that were simultaneously fed a magnesium-deficient diet. Magnesium concentrations in bone, plasma, and cartilage from animals on an Mg(2+)-deficient diet were significantly lower than those in the controls. The concentration in plasma from animals on an Mg(2+)-deficient diet was 0.27 +/- 0.03 mmol/liter, whereas it was 0.88 +/- 0.08 mmol/liter in plasma from rats on a standard diet (means +/- standard deviations). Ofloxacin treatment did not change the total magnesium concentrations in tissues, as determined with ashed samples. The incidence of ofloxacin-induced lesions was higher in the magnesium-deficient animals, suggesting a synergistic effect. These results must be taken into account for a benefit-risk evaluation if ofloxacin is considered for use in the pediatric population. (+info)