A single eggshell contains 2.07 ± 0.18 g of Ca; therefore half an eggshell could provide the amount of Ca needed by adult human beings per day. The best way to use chicken eggshell as Ca dietary supplement is powdered to add to bread, pizza or spaghetti as there were small changes in texture and no changes in flavor.

Changes in luminal pH arising from intestinal alkaline phosphatase activity induced by luminal calcium concentration modulate intestinal calcium absorption.

Yerba mate (Ilex paraguariensis) is a xanthine-containing beverage, which is also rich in caffeine. Because caffeine has a negative impact on bone mineral density (BMD) mainly associated with low calcium (Ca) diets, there would be expected a negative effect of yerba mate on bone. In this study, Sprague-Dawley rats were used and randomly assigned into four groups (n = 6/group): Control + Ca 0.2 g %; Control + Ca 0.9 g %; Yerba + Ca 0.2 g %; Yerba + Ca 0.9 g %. At the end of the experiment, tibias and femurs were obtained for BMD, morphometric, histomorphometric, and biomechanical analyses. While there was no difference in bone parameters between rats with and without yerba mate consumption, a negative effect of low Ca diet was observed in BMD, morphometric, histomorphometric, and biomechanical results. Interaction between Ca content in the diet and yerba mate was only found in trabecular bone volume, which would indicate that the negative effect of low Ca intake on bone volume is reversed in part by yerba mate infusion. However, yerba mate was not able to reverse the negative effect of low Ca content on biomechanical properties and trabecular connectivity. In summary, at least in our study, yerba mate would not have a negative effect on bone and would be safe for the bone health of consumers.

This report deals with the relationships between glucose (G) and insulin on the tubular transport of phosphate (P) in chronically diabetic rats with high plasma levels of parathyroid hormone (PTH). Alloxan-induced diabetes leads to phosphorus depletion of the soft tissues. This phenomenon appears associated with weight loss and negative P balances caused by the increased urinary P excretion. Administration of 2 IU of insulin/100 g body weight (bw) to diabetic rats normalized their P balance and body weight. The effect of parathyroid function on the P metabolism of diabetic rats was investigated with balance experiments. Diabetic rats, intact or thyroparathyroidectomized (TPTX), have a greater urinary excretion of P than their controls. However, in control rats, the ratio intact:TPTX for urinary P is 1.0:0.76, showing the antiphosphaturic effect of parathyroid ablation. For diabetic animals, on the other hand, the ratio is 1.0:1.44. The simultaneous deficit of insulin and PTH thus quadruples the urinary P loss, instead of compensating for each other. The contribution of insulin deficit and hyperglycemia to the defect in tubular reabsorption (TRP) was investigated with clearance experiments (done on anesthetized, perfused rats). Five experimental groups were used: Controls (C), diabetics (D), controls + glucose (C + G), diabetics + insulin (D + I) and diabetics + insulin + glucose (D + I + G). All experimental groups showed a linear relationship between the TRP of P and G. The regression equation for C is significantly different (F = 40.1, P < 0.001) from that of D animals. The slope value measure the number of mumoles of P per mumol of G reabsorbed. For C and D rats, the ratio P:G approximates 1:4 and 1:20, respectively. The increase in P:G ratios represents the competition between both substrates for tubular resorption. Glycemias up to 11 mM (C and D + I) exist concurrent with the P:G ratio 1:4 Glycemias above 25 mM (D, C + G and D + I + G) produce a P:G ratio of 1:20. Fractional excretion of P (FEP) increased significantly in untreated, chronically diabetic rats (0.47 +/- 0.12 vs controls = 0.05 +/- 0.01, P < 0.001). After a single intramuscular injection of insulin, the FEP decreased as a function of insulin levels. To normalize the FEP of diabetic rats in short-term experiments, insulin had to be administered in doses that produce plasma insulin levels 25 times greater than normal. The general information afforded by the present experiments shows that in untreated, chronically diabetic rats, insulin deficit plays an indirect role. The absence of PTH enhances the effect of hyperglycemia. The latter and the concurrent tubular overload of glucose are the cause of hyperphosphaturia in these animals.

Fluoride (F) has a known mitogenic effect on bone cells. The daily administration of 40 micromol NaF per 100 g of body weight (bw) increases bone mass in rats. Nevertheless, the quality and composition of bone formed under F stimulus is still matter of study. The objective of this work was to investigate the effect of sodium fluoride (NaF, CAS 7681-49-4) administration on phosphate metabolism and its impact on bone. Experiments were carried out in female fasted 50-day-old rats. Unless otherwise stated, NaF dose was 40 micromol NaF/day . 100 g bw, administered by gastric tube. Four groups of 4 rats each were given the following daily NaF doses: Group A: 0, B: 20, C: 40 and D: 60 micromol NaF/day x 100 g bw. After 30 days rats were killed saving their femora and plasma. Bone phosphorous contents (BPC) and phosphatemia (mg/dl) were measured. BPC decreased significantly as a function of NaF dose. A: 93.3+/-14.1; B: 78.7+/-15.5; C: 61.1+/-14.7**; D: 59.6+/-8.6 **mg P/g dry bone (** significant difference to group A, p < 0.01). Phosphatemia (mg/dl) increased significantly with a peak at 90 min after NaF dose (basal: 5.34+/-0.06; 90 min: 8.15 +/-0.43, p < 0.001). Phosphaturia (microg/min) increased though differences were not significant (basal: 46.7+/-42.8; 4 h: 1275 +/-757, p > 0.05). In thyroparathyroidectomized rats, plasma phosphate increased continuously for at least 240 min. Renal plasmatic flow, glomerular filtration rate and renal blood flow were not affected by NaF treatment. In isolated perfused rat kidneys, urinary phosphate excretion remained unaffected after NaF administration. Phosphate concentration was measured in the plasma and erythrocytes of rats after one dose of NaF (n = 8). Phosphate content of erythrocyte was not affected by NaF, in spite of the concurrent increase in phosphatemia. It is concluded that the treatment with NaF causes a transitory increase in plasma phosphate levels. Neither renal hemodynamic factors nor the inhibitory effect on parathormone actions appear to be the causes of hyperphosphatemia. Efflux of phosphate from cells might not be the cause of the increase in phosphatemia. The loss of phosphorous from bone appears as the most probable determinant of hyperphosphatemia after fluoride administration.