The metabolism of magnesium and calcium by the rat
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Magnesium deprivation induced interspecific aggressive behaviour (muricidal behaviour) in rats undoubtedly attributable to magnesium deficiency since magnesium chloride, by correcting magnesium deficiency, suppressed it. Inhibition of magnesium deficiency-induced behaviour by various magnesium salts should enable the classification of the therapeutic effects of these salts. Consequently we compared the effects of various magnesium salts used therapeutically on the inhibition of the acute muricidal behaviour induced by magnesium deficiency. All the magnesium salts used (chloride, pidolate, aspartate, gluconate, lactate) suppressed the muricidal behaviour. There was no significant difference in the duration of the treatment needed to inhibit this comportment for each of the salts studied. In contrast, significant differences appeared, concerning the different phases of muricidal behaviour. Magnesium pidolate significantly increased the attack latency (P < 0.05). By repeating the muricidal assays, we showed that magnesium pidolate treated rats had a muricidal behaviour rate which was lower than that of the other magnesium salt-treated rat groups. Consequently, it can be assumed that all the magnesium salts used had an acute anti-muricidal, perhaps anti-stress, effect and that magnesium pidolate presented, on this experimental model the greatest efficacy.
Magnesium deficiency (plants)
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SummaryThe metabolism of calcium was studied in manganese-deficient and zinc-deficient rats by a method combining a kinetic study using 45Ca with a short-term classical balance study. There were no differences in managanese-deficient rats as compared with controls in any of the parameters of calcium metabolism, including pool size, endogenous fecal calcium, urinary clacium, or in the rates of calcium entering or leaving bone. The zinc-deficient animals, however, showed significant decreases, as compared with both ad libitum and restricted-intake controls, in a number of parameters of calcium metabolism. These included the rates of calcium entering and leaving bone, pool size, the rate of slow exhange, and the slowly exchangeable calcium in bone. The results suggest that the skeletal abnormals are not the result of abnormal calcium metabolism. In zinc deficiency, on the other hand, specific effects on calcium metabolism were noted. Thus it appears that zinc, but not manganese, is required for normal metabolism of calcium.
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The concentration of magnesium in muscle was determined and a standardized magnesium load test was performed in 21 patients, who 4 to 10 years previously had undergone intestinal bypass operations for severe obesity. The plasma concentration and 24-h urinary excretion of magnesium were also studied. Basic urinary excretion of magnesium and muscle magnesium were significantly lower in patients compared to healthy controls, while no differences were found in plasma magnesium. A slight negative correlation between muscle magnesium and retained magnesium was demonstrated (r = -0.51, P less than 0.05). Patients with magnesium retention greater than 20 per cent showed a significant decrease of magnesium retention after treatment with magnesium chloride mixture. Four patients with primarily low muscle magnesium all demonstrated an increment in the amount of magnesium in muscle after treatment. The load test described can be applied as a screening test in diagnosing magnesium deficiency.
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