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  • 1
    ISSN: 1432-0827
    Keywords: Calcium ; Intestine ; Growth ; Cortisol ; Hydroxyproline ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary This paper reports the effects of cortisol on intestinal management of calcium and on related changes on bone metabolism. Five groups of 12 rats each fed a standard diet (0.8% Ca) received 2, 6, 16, 32, and 128 mg/kg/day of cortisol hemisuccinate, subcutaneously. After 16 days, intestinal absorption and excretion of Ca were measured with the aid of45Ca. True Ca absorption increased as a function of dose up to 16 mg/kg/day and remained high with the larger doses. Endogenous fecal Ca excretion increased exponentially as a function of the dose from 16 mg/kg/day onwards. Therefore, a dual effect was observed: (a) an increase in true Ca absorption at low cortisol doses (which increased net Ca absorption); and (b) an increase in endogenous fecal Ca excretion at high doses (which reduced net Ca absorption). In no case was a depression of true Ca absorption observed. Growth rate and food conversion efficiency were depressed only with a cortisol dose of 128 mg/kg/day. The urinary excretion of hydroxyproline, pyrophosphate, and aminopolysaccharides decreased with low doses and increased above normal levels with the highest dose. When animals treated with 128 mg/kg/day of cortisol were fed Ca-enriched diets, net Ca absorption improved. Simultaneously, growth rate and food conversion efficiency approached normal values. In these experiments, net absorption of Ca was found to be inversely related to urinary excretion of hydroxyproline. The urinary rate of excretion of hydroxyproline is suggested as an indicator of the effect of a Ca supplement on cortisol affected connective tissue turnover.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 14 (1974), S. 169-175 
    ISSN: 1432-0827
    Keywords: Galactose ; Glucose-6-phosphate ; Resorption ; Pyrophosphate ; Hydroxyproline ; Alkaline phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Description / Table of Contents: Résumé L'effet du galactose sur le métabolisme osseux est étudié en soumettant de jeunes rats à un régime semi-synthétique contenant 35% de ce monosaccharide. Les animaux témoins reçoivent le même régime sans galactose, avec du glucose. L'effet d'une consommation de Ca−P, normal et faible, est étudié chez les témoins et les groupes soumis au galactose. La glucose-6-phosphate deshydrogénase osseuse est inhibée lorsque le galactose s'accumule dans les tissues. L'excrétion urinaire de calcium, pyrophosphate, aminopolysaccharides, hydroxyproline en phosphatase alcaline plasmatique (isoenzyme osseuse) est augmentée de façon significative par rapport aux témoins. Les animaux, recevant du galactose avec un régime faible en Ca et P, présentent une balance négative en Ca, due surtout à un excretion fécale plus élevée que les apports. Un rapport inverse est observé entre la balance calcique et l'ingestion alimentaire. L'effet nocif du galactose sur le métabolisme du calcium pourrait agir par l'intermédiaire d'une action sur les cellules osseuses et les fonctions rénales et intestinales, en rapport, peut-être, avec un trouble inconnu du métabolisme hydro-carboné.
    Abstract: Zusammenfassung Die Wirkung von Galaktose auf den Knochenstoffwechsel junger Ratten wurde untersucht, indem diese eine semisynthetische Nahrung erhielten, welche 35% dieses Monosaccharids enthielt. Kontrolltiere erhielten dieselbe Nahrung ohne Galaktose, aber mit Glukose. Die Kontrollgruppe und die Gruppe mit Galaktosenahrung erhielten eine niedrige und eine normal Ca−P-Einnahme. Die Glukose-6-Phosphat-Dehydrogenase des Knochens wurde gehemmt, wenn Galaktose im Gewebe zunahm. Die Urinausscheidung von Calcium, Pyrophosphat, Aminopolysacchariden, Hydroxyprolin und alkalischer Phosphatase des Plasmas (Knochen-Isoenzym) war signifikant höher als bei den Kontrollen. Die Tiere mit Galaktosezusatz und niedriger Ca−P-Aufnahme zeigten eine negative Calciumbilanz, die hauptsächlich durch eine fäkale Ausscheidung bedingt war, welche höher war als die Einnahme. Es wurde eine umgekehrt proportionale Beziehung zwischen Calciumbilanz und Nahrungseinnahme beobachtet. Die nachteilige Wirkung von Galaktose auf den Calciumstoffwechsel mag von einer Wirkung auf die Knochenzellen und auf die Nieren- und Darmfunktion herrühren, vielleicht im Zusammenhang mit einer noch unbestimmten Störung des Kohlenhydratstoffwechsels.
    Notes: Abstract The effect of galactose on bone metabolism was studied by feeding young rats a semisynthetic diet containing 35% of this monosaccharide. Control animals received the same diet without galactose but with glucose. Both a low, and a normal, Ca−P intake were studied in the control and galactose fed groups. Bone glucose-6-phosphate dehydrogenase was inhibited as galactose accumulated in the tissue. Urinary excretion of calcium, pyrophosphate, aminopolysaccharides, hydroxyproline and plasma alkaline phosphatase (bone isoenzyme) were significantly increased above control levels. Galactose fed animals on a low Ca and P diet showed a negative Ca balance, primarily due to a fecal excretion which was greater than intake. An inverse relationship between calcium balance and food intake was observed. The adverse effect of galactose on calcium metabolism may be mediated by an effect on bone cells and on renal and intestinal function, related perhaps to an as yet non-defined disturbance of carbohydrate metabolism.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0827
    Keywords: Respiratory alkalosis ; Ionized calcium ; 1,25 Dihydroxycholecalciferol ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The daily administration of supraphysiological doses of 1,25 dihydroxycholecalciferol (0.1–2.5 µg/d/100 g body weight) to rats, produced respiratory alkalosis. With the doses of 0.1–0.2 µg/d/100 g and feeding a diet with 0.7% of calcium, calcemias did not exceed 2.75 mM, and significantly reduced plasma ionized calcium levels were measured. The latter phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium content, and polyuria with hypostenuria, all known effects of parathyroid hormone. These effects were absent in thyroparathyroidectomized rats treated in the same fashion. Present results suggest that the stimulus of low levels of plasma ionized calcium overcomes the probably inhibitory effect of the steroid on parathyroid hormone secretion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-5233
    Keywords: Key words Phosphaturia ; Glomerular filtration ; Tubular reabsorption ; Parathyroid hormone ; Thyroparathyroidectomy ; Fractional excretion of phosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 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 µmoles of P per µmol 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.
    Type of Medium: Electronic Resource
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