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  • 24,25-Dihydroxyvitamin D3  (1)
  • Bone turnover  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Surgically induced uremia in rats II: Osseous PTH-susceptible signaling systems as predictors of bone resorption (1994)
    Springer
    Calcified tissue international 55 (1994), S. 281-287 
    Details
    ISSN: 1432-0827
    Keywords: Renal osteodystrophy ; Hyperparathyroidism ; Adenylate cyclase ; Phospholipase C ; 1,25-Dihydroxyvitamin D3 ; Bone turnover ; Histomorphometry ; Rat model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract Predicting the course of parathormone (PTH)-elicited bone turnover in both humans and experimental rat models with moderate chronic uremia, using only standard clinical chemistry analyses, is often difficult. Consequently, rat bone from 1+2/3 nephrectomized animals, after 230 days of progressive renal failure, was examined for PTH-stimulated adenylate cyclase (AC) and phospholipase C (PLC) activities. Correlations to biological parameters related to the function of bone and kidney were made. Reduced renal function was demonstrated by increased serum creatinine; circulating 1,25 dihydroxyvitamin D3 below detection level; diminished renal PTH-elicited AC activity; and decreased urinary cAMP excretion. PTH-activated renal PL-C was also reduced. However, no significant differences were seen in urine creatinine, calcium, phosphate, and hydroxyproline, nor in serum PTH, alkaline phosphatase, calcium, and phosphate. Notwithstanding, renal osteodystrophy developed as estimated by increased plasticity of the long bones, as well as reduction of the diaphyseal (Dd) and inner femoral midshaft (Di) diameters. Femoral cancellous bone exhibited a substantial elevation of both eroded surface (ES) and osteoid surface (OS) as well as a marked reduction in trabecular bone volume (TBV). Calvarial PTH-activated AC was enhanced, whereas corresponding PL-C was markedly reduced. PTH-enhanced AC correlated positively with ES and negatively with Di, respectively. PTH-enhanced PL-C, however, correlated positively with bone calcium content and negatively with ES. Our results indicate that bone modeling and remodeling are to a large extent related to PTH-elicited signaling systems, and cannot easily be predicted by standard clinical chemistry analyses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310407
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  • 2
    Electronic Resource
    Electronic Resource
    Vitamin D3 analogs and salmon calcitonin partially reverse the development of renal osteodystrophy in rats (1995)
    Springer
    Calcified tissue international 57 (1995), S. 385-391 
    Details
    ISSN: 1432-0827
    Keywords: Kenal osteodystrophy ; Osteomalacia ; Bone dimensions-strength ; Histomorphometry ; Adenylate cyclase ; Phospholipase C ; 1,25-Dihydroxyvitamin D3 ; 24,25-Dihydroxyvitamin D3 ; Calcitonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract We have previously established an uremic rat model which is suitable for investigating the effect of various treatment modalities on the progression of renal osteodystrophy [1]. Four months subsequent to 5/6 nephrectomy, animals were treated three times a week for 3 months with either vehicle, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], 1,25(OH)2D3+24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25(OH)2D3+calcitonin (CT), or 1,25(OH)2D3+ 24,25(OH)2D3+CT. At termination of the study, clinical chemistry, chemical composition, and mechanical properties of femurs, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC), and phospholipase C (PL-C) activities, femoral cross-sectional area, and bone histomorphometry were analyzed. The main findings were that 1,25(OH)2D3±24,25(OH)2D3 treatment enhanced elasticity as well as time to fracture at the femoral metaphysis. CT potentiated the increase in elasticity obtained by 1,25(OH)2D3±24,25(OH)2D3 treatment. Only 24,25(OH)2D3 administration rectified the supernormal PTH-stimulated uremic bone AC, and only 1,25(OH)2D3 medication normalized the diminished CT-elicited AC. The obliterated uremic bone PTH-sensitive PL-C was fully normalized by all drug regimens. Femoral shaft inner zone diameter was enhanced by uremia, however, all drug treatments normalized it. Ditto effect was registered with either drug treatment on the subnormal outer and inner zone widths. Histomorphometrical analyses showed that 1,25(OH)2D3 administration reduced both eroded and osteoid surfaces. Most prominently, adjuvant 24,25(OH)2D3 or CT administration potentiated the beneficial effect of 1,25(OH)2D3 on fibrosis and osteomalacia. We assert that vitamin D3 treatment markedly reverses the development of renal osteodystrophy, and CT potentiates the effect of vitamin D3.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00302075
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