Inhibition of mouse-killing behaviour in magnesium-deficient rats: effect of pharmacological doses of magnesium pidolate, magnesium aspartate, magnesium lactate, magnesium gluconate and magnesium chloride.
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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.Keywords:
Magnesium deficiency (plants)
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Serum immunoreactive parathyroid hormone (IPTH) was measured in control and in alloxan-induced diabetic rats ingesting a normal calcium diet and in control rats ingesting a low calcium diet. Serum IPTH levels in controls ingesting the low calcium diet were three times those of controls on the normal calcium diet. Serum IPTH in diabetic rats was double that in controls. Therefore,the diabetic rat manifests an appropriate parathyroid response to diminished calcium absorption. The deficiency of duodenal calcium binding protein and the duodenal calcium malabsorption previously observed in diabetic rats are not the result of a defect in PTH regulation of vitamin D metabolism. (En-docrinology95: 749, 1974)
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Abstract Recent studies provide evidence that the GH/IGF-I axis plays a critical role in the regulation of bone accretion that occurs during puberty and that the peak bone mineral density (BMD) is dependent on the amount of dietary calcium intake during the active growth phases. To evaluate whether IGF-I deficiency exaggerates the effect of calcium deficiency on bone accretion during active growth phases, IGF-I knockout (KO) and wild-type (WT) mice were fed with low calcium (0.01%) or normal calcium (0.6%) for 2 wk during the pubertal growth phase and were labeled with tetracycline. The low calcium diet caused significant decreases in endosteal bone formation parameters and a much greater increase in the resorbing surface of both the endosteum and periosteum of the tibia of IGF-I KO mice compared with WT mice. Accordingly, femur BMD measured by dual energy x-ray absorptiometry or peripheral quantitative computed tomography increased significantly in IGF-I WT mice fed the low calcium diet, but not in IGF-I KO mice. IGF-I-deficient mice fed the normal calcium diet showed elevated PTH levels, decreased serum 1,25-dihydroxyvitamin D and serum calcium levels at baseline. Serum calcium changes due to calcium deficiency were greater in IGF-I KO mice compared with WT mice. PTH levels were 7-fold higher in IGF-I KO mice fed normal calcium compared with WT mice, which was further elevated in mice fed the low calcium diet. Treatment of IGF-I-deficient lit/lit mice with GH decreased the serum PTH level by 70% (P < 0.01). Based on these and past findings, we conclude that: 1) IGF-I deficiency exaggerates the negative effects of calcium deficiency on bone accretion; and 2) IGF-I deficiency may lead to 1,25-dihydroxyvitamin D deficiency and elevated PTH levels even under normal calcium diet.
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Lactating rats were compared with nonlactatingcontrols, with regard to the intake andabsorptionof calcium, serum calcium level, and theprotective effect of thyrocalcitonin (TC) against hypereal cemia and hyperphosphatemia. While consuming a commercial diet, intact, nonfastedlactating rats maintained a serum calcium levelof approximately 9 mg/100ml, which was 1 mg/100 ml lower than that of nonlactating controls. The levelrose to that of the controls within one day after removalof the litters from the mother. Comparedwith nonlactating rats, lactating rats had a threefoldhigher calcium intake and a six-fold higher rateof net absorption of calcium. After intragastric calcium (10 mg/100 g body wt)the increase in serum calcium was small (1 mg/100 ml)2 h later in both groups of sham-operated rats butwas markedly increased in th yro pa rath yro idee tomizedgroups, with the lactating rats showing a significantlygreater increase than the nonlactating rats. The injection of a small dose of porcine thyrocalcitonincompletely counteracted this hypercalcemiain lactating rats, but did not have any effecton nonlactating controls. Protection by the thyroidgland against hyperphosphatemia after intragastriccalcium also was significant in both lactating andnonlactating rats. The results show that TC is muchmore effective in lactating than in nonlactating rats,suggesting that TC may be of particular importancein lactation by restricting elevations of serum calciumand phosphorus levels after eating, thereby aidingin conservation of these ions. (Endocrinology99:371, 1976)
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Circadian fluctuations of plasma calcium and immunoassayable calcitonin levels were studied in normal and calcium-deficient 2-month-old rats. The relationship between these parameters was also studied in animals which had been fasted for short periods. The plasma calcium rhythm persisted and was even amplified in rats placed on a 4-week calcium-deficient diet. In these rats, as in normal rats, the plasma calcium concentration diminished during the dark period. Calcitonin levels increased at the onset of the feeding period in normal rats but, in calcium-deficient rats, the pattern changed completely, with a major peak at the end of the light period and remaining at a low level during the dark feeding period. This modification of calcitonin rhythmicity appeared to be dependent on the degree of calcium deficiency. Fasting had little effect on calcitonin rhythms in either normal or calcium-deficient rats. It is concluded that the calcitonin rhythm is relatively independent of feeding per se and that there appears to be no simple relationship between plasma calcium and calcitonin concentrations. It is suggested that the results may best be interpreted as reflecting the presence of rhythmic endogenous phenomena which are intrinsic to calcium metabolism and its regulation in the rat.
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Calcium ionophore A23187 (20 μM) evoked the secretion of somatostatin (SRIF) as well as insulin from isolated rat pancreatic islets in a medium containing a relatively low concentration of calcium (0.9 HIM) and a low concentration of glucose (5.5 mM). A high level of extracellular calcium (7.5 mM) also had a stimulatory effect on SRIF and insulin release. On the other hand, in the presence of high glucose (16.7 mM), A23187 had different effects on D and B cells; insulin release was markedly suppressed by A23187, but SRIF secretion was significantly enhanced. A high concentration of glucose (16.7 mM) did not stimulate SRIF secretion at a low extracellular calcium concentration (0.25 mM), at which level insulin release is significantly enhanced. These findings indicate that calcium may play an important role in the regulation of the secretion of SRIF as well as insulin and suggest that the B and D cells differ in their sensitivity to the calcium ion.
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Weanling Sherman rats were pair-fed for 8 days on a control or a magnesium deficient diet containing 70.5% sucrose. After a 12-hour fast, the rats were injected intraperitoneally with glucose (250 mg/100 g body weight) and arterial blood was drawn at 0, 15, 30, 60, 90 minutes after injection. Before glucose loading, in magnesium deficient rats, plasma magnesium levels were significantly increased. The plasma triglyceride concentration was significantly higher in magnesium deficient rats compared to controls. After glucose loading, in the control group, the plasma insulin concentrations increased to 67.9 +/- 5.8 microU/ml at 15 minutes and returned to pretreatment levels by 30 minutes; in the magnesium-deficient rats, the plasma insulin levels were significantly lower at 15 minutes 32.9 +/- 5.6 microU/ml (P less than 0.01) and returned more slowly to the pre-challenge level. No significant differences were observed in plasma glucose levels between the two groups of rats.
Weanling
Magnesium deficiency (plants)
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Plasma Parathyroid Hormone Levels and Intestinal Calcium Binding Protein in Magnesium Deficient Rats
Rats were pair fed a magnesium deficient or control diet. Plasma parathyroid hormone (PTH) was estimated by radioimmunoassay using synthetic 1-34 PTH and intestinal calcium-binding protein (CaBP) was quantified directly by RIA in proximal duodenum, distal ileum and medium jejunum. In magnesium depleted rats, plasma magnesium levels were significantly decreased, a fall in plasma phosphate paralleled the decrease in plasma magnesium and plasma calcium levels were significantly increased after 14 days of magnesium deficiency. A significant rise in plasma PTH was observed on day 7 and 14 after magnesium deficiency. This increase disappeared on day 20. During the whole experimental period, no significant differences in CaBP levels were observed between the two groups of rats. Thus it is difficult to postulate an increase in vitamin D-dependent calcium absorption to explain the hypercalcemia found in magnesium deficient rats. Neither can the hypercalcemia be readily explained by an increased bone calcium mobilisation due to transient PTH increase since previous results have reported decreased bone resorption in magnesium deficient rats under similar experimental conditions.
Jejunum
Magnesium deficiency (plants)
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Regulation of prepro-PTH and vitamin D receptor (VDR) mRNAs in the parathyroid glands was studied in chickens in vivo. The birds were raised to 21 days of age on a vitamin D-deficient diet with 1% calcium and 0.65% phosphorous. At the end of this period, the chicks exhibited marked hypocalcemia and enlarged parathyroid glands. In three separate trials, the birds were repleted for 6 days with vitamin D and different dietary calcium and phosphate concentrations, with 2 micrograms/kg 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and different dietary calcium concentrations (0.5%, 1.0%, or 1.8%), or with 2 or 10 micrograms/kg 1,25-(OH)2D3 and 0.6% or 1.9% calcium or were kept vitamin D3 deficient and fed 0.5%, 1.0%, or 1.8% dietary calcium. Vitamin D treatment when combined with a high level of dietary calcium resulted in an increase in plasma calcium from 6 mg/dl to greater than 10 mg/dl, a decrease in PTH mRNA of 65%, and a 6- to 8-fold increase in VDR mRNA. In another experiment in which no vitamin D source was given and the diets contained increasing levels of dietary calcium, plasma calcium increased significantly (5.5 vs. 7 mg/dl), while PTH mRNA decreased by 40% and VDR mRNA increased by 60%. Neither parathyroid gland weight nor total RNA was significantly affected. When chicks were repleted with 1,25-(OH)2D3, the increase in plasma calcium and VDR mRNA and the decrease in PTH mRNA were considerably more pronounced than those in the absence of the vitamin D source. Furthermore, in the presence of the hormone, parathyroid weight and total RNA decreased significantly with increasing concentrations of dietary calcium. When the chicks were repleted, respectively, with the two levels of 1,25-(OH)2D3, a marked positive interaction was evident between the hormone and dietary calcium in affecting levels of PTH and VDR mRNA. These results suggest that both 1,25-(OH)2D3 and calcium participate in the regulation of PTH and VDR gene transcription in the avian parathyroid gland. Whereas the action of 1,25-(OH)2D3 requires a minimal level of dietary calcium, calcium affects PTH and VDR gene transcription even in the absence of any vitamin D source.
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Control and magnesium-deficient synthetic diets were fed ad libitum to intact, to adrenalectomized and to hypophysectomized male rats for 8, 15 and 22 days. The course and sequence of the appearance of magnesium-deficiency symptoms were recorded. In the intact and the adrenalectomized rats fed the deficient diet, the growth rate was depressed, whereas the hypophysectomized deficient rats showed no significant difference in weight gain compared to their controls. Rats in each of the three groups on the deficient diet developed hyperemia, leucocytosis (especially eosinophilia) and renal lesions in the distal convoluted tubules coincident with the initial depletion of serum magnesium. In the intact and the adrenalectomized rats these magnesium-deficiency symptoms appeared during the first week on the experimental diet, but in the hypophysectomized rats the onset of the symptoms was significantly delayed to the third week. Although the kidney lesions were similar to those described for the potassium-deficient rats, they appeared to be due to magnesium deficiency per se in these animals. The data also suggested a possible pituitary-kidney axis for the control of serum magnesium level.
Magnesium deficiency (plants)
Potassium deficiency
Hypophysectomy
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