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  • 1
    Electronic Resource
    Electronic Resource
    Dissociation of renal cyclic AMP and phosphate responses to parathyroid hormone in uremia (1979)
    Springer
    Calcified tissue international 29 (1979), S. 147-154 
    Details
    ISSN: 1432-0827
    Keywords: Vitamin D ; Chronic uremia ; Rats ; Renal responsivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Various investigators have shown that chronic uremia is associated with a normal or exaggerated phosphaturic response to parathyroid hormone (PTH). To explore the relationship between progressive uremia, renal tubular cyclic AMP (cAMP), and inorganic phosphate (Pi) response to PTH and acidosis, in vivo and in vitro experiments were designed in rats with experimental uremia of 4–6 weeks’ duration. Both uremic and pair-fed control rats were treated with 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and/or chronic NH4Cl feeding. Urinary Pi and cAMP and plasma immunoreactive PTH (iPTH) were measured as well as PTH- and NaF-stimulated cAMP from isolated renal tubules. Excretion of cAMP decreased by 30% in uremic as compared to control rats despite a 3-fold rise in Pi excretion. Acidosis superimposed on uremia did not further decrease cAMP excretion, nor did it significantly alter the elevated Pi excretion. 1,25(OH)2D3 treatment of uremic rats further lowered cAMP excretion although Pi excretion rose, hypercalcemia occurred, and plasma iPTH fell. In nonuremic control rats, 1,25(OH)2D3 treatment led to hypercalcemia, a progressive decrease in cAMP, and increase in Pi excretion. Isolated renal tubules from uremic or acidotic uremic rats revealed a 50% reduction in both PTH- and NaF-stimulated cAMP generation compared to control rat renal tubules. This observation was unchanged by 1,25(OH)2D3 treatment. Renal tubules of 1,25(OH)2D3-treated control rats demonstrated a decreased cAMP production in response to both PTH and NaF which was inversely related to the calcium content of the renal tubules. Renal tubular calcium levels of uremic rats, initially 3-fold elevated, also increased during 1,25(OH)2D3 treatment. These results are consistent with the hypothesis that progressive uremia results in a dissociation between PTH, urinary cAMP, and Pi excretion which cannot be explained by either metabolic acidosis or 1,25(OH)2D3 deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408070
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Bone maturation in the vitamin D, phosphate deficient rat and the response to acid loading (1979)
    Springer
    Calcified tissue international 27 (1979), S. 233-237 
    Details
    ISSN: 1432-0827
    Keywords: Bone ; Vitamin D ; Acidosis ; Phosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Vitamin D and phosphate deficiency were produced in rats in order (a) to evaluate the degree of bone mineral and matrix maturation using a bromoform/toluene density gradient technique; and (b) to compare the aforementioned bone maturational changes due to vitamin D and phosphate deprivation to those produced with superimposed severe acidosis. Rats were fed a diet deficient in vitamin D and phosphorus (0.2%) from 3 weeks through 7 weeks of age. To examine the additional contribution of dietary calcium, we gave one-half of the animals either a low (0.06%) or high (1.3%) calcium diet. Following the 4 weeks of vitamin D deficiency, one-half of each group was given 1.8% NH4Cl in the drinking water for 4 succeeding days to induce an acute, severe acidosis. The degree of bone maturation was quantitated via bromoformtoulene density gradient fractionation; total mineral and hydroxyproline (collagen) levels were quantitated as well. The vitamin D-deficient rats deprived of adequate dietary phosphate responded by conserving phosphorus, and as a consequence total bone phosphorus levels were maintained within that level for control rats. This conservation was independent of calcium intake but was extremely sensitive to acute acid loading, where a significant reduction in total bone phosphorus was noted. The bone maturational profile obtained from the vitamin D-phosphate deficient rats, however, revealed a significant accumulation of less mature or dense bone collagen and mineral with a corresponding decrease in the most mature or dense moieties. In contrast to the reduction of the total bone phosphorus content by acute acidosis, the skeletal collagen-mineral maturational profile was not significantly affected by the short-term systemic acidosis. The observed retardations in the bone collagen and mineral maturation of the vitamin D-deficient, phosphate-deprived state provide an additional observation which may well relate to the progressive osteopenia documented in states of chronic, mild acidosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02441191
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Altered osteoblast gluconeogenesis in X-linked hypophosphatemic mice is associated with a depressed intracellular pH (1995)
    Springer
    Calcified tissue international 57 (1995), S. 60-63 
    Details
    ISSN: 1432-0827
    Keywords: X-linked hypophosphatemia ; Hyp mouse ; Osteomalacia ; Vitamin D ; Resistant rickets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract We have studied gluconeogenesis and intracellular pH levels in normal (+/Y) and X-linked hypophosphatemic (Hyp/Y) mice. Compared with +/Y littermates, Hyp/Y mouse osteoblasts showed a higher rate of glucose production from fructose (10-fold), glutamine, and malate, but no significant difference when α-ketoglutarate was used as substrate. The activities of the pentose cycle enzymes, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase, were not different in the two osteoblast preparations. Examination of intracellular pH (pHi) using the double excitation of the pH-sensitive dye 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM) revealed a significantly lower pHi in Hyp/Y mouse osteoblasts compared with +/Y mouse osteoblasts (7.01±0.03 n=10 versus 7.15±0.04 n=8, respectively; P〈0.05). These results show for the first time that osteoblasts are capable of glucose production and that glucose production is altered in the Hyp/Y mouse osteoblast. As altered gluconeogenesis has been associated with reduced intracellular pH in other systems, a similar mechanism may be operative in the Hyp/Y mouse osteoblast. The observed defects may be intrinsic to the Hyp phenotype as the alterations in intracellular pH and gluconeogenesis persisted in vitro, or they may represent impressed memory from the in vivo state and the presumed circulating factor that influences phosphate transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00298998
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    Paper (German National Licenses)
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