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Results for “PHOSPHORUS METABOLISM”

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At least 19 recordsLinked to original sources
PubMed1997

[Bone metabolism and phosphorus metabolism in patients with prostate cancer: paracrine and endocrine effects produced by prostate neoplasm].

We examined whether paracrine factors produced by prostate cancer cells can modulate bone metabolism in proportion to the volume of cancer cells in bone metastasis. Endocrine factors produced by prostate cancer cells affect both phosphate and 1,25-dihydroxyvitamin D metabolisms. Levels of urine pyridinoline (U-Pyr) excretion and serum carboxy-terminal propeptide of type 1 procollagen (P1CP) in patients with bone metastasis were significantly higher than those in patients without bone metastasis (P < 0.05). In patients with bone metastasis (n = 17), serum prostate-specific antigen (PSA) levels were significantly correlated with the levels of U-Pyr and urine deoxypyridinoline (U-dPyr) excretion, serum cross-linked carboxyterminal telopeptide of type 1 collagen (1CTP), and P1CP levels (p < 0.05). However, serum PSA levels were not correlated with U-Pyr, U-dPyr excretions, serum 1CTP and P1CP levels in patients without bone metastasis. Therefore, prostate cancer cells appear to have some paracrine effects on bone cells. In controls (n = 15), serum 1,25-dihydroxyvitamin D levels (1,25-(OH)2D) were inversely correlated with serum phosphorus levels (P < 0.01). In prostate cancer patients with bone metastasis, the ability to regulate the serum 1,25-(OH)2D levels in response to serum phosphorus levels is lost. These results suggest that endocrine factors produced by prostate cancer cells disturb the regulation of serum 1,25-(OH)2D in response to serum phosphorus levels.

Aged↗
PubMedDate not supplied

[The characteristics of histocompatibility antigen distribution in urolithiasis patients with a phosphorus metabolic disorder].

Phosphorus metabolic disturbances play a great role in the occurrence of urolithiasis. This study covered 150 patients with urolithiasis to establish correlations between the frequency of histocompatibility antigens and the increase in blood and urinary phosphorus levels. The HLA antigens were identified by the routine microlymphocytotoxic method involving a histotyping serum panel. The ABO antigens and rhesus were determined by the agglutination method by using reference sera. The study revealed specific distribution of histocompatibility antigens in urolithiasis patients with disturbed phosphorus metabolism. Hyperphosphatemia correlated with the higher frequency of HLA-B35 (chi 2 = 9.89) and E/E system rhesus (chi 2 = 8.63); hyperphosphaturia showed a negative association with the HLA-A28 antigens (chi 2 = 9.7), as well as with E/e (chi 2 = 14.69) and e/e (chi 2 = 39.36) and a positive association with HLA-B13 (chi 2 = 5.98) and B35 (chi 2 = 36.58). The highest relative risk for hyperphosphatemia associated with the B27 and B35 antigens was observed with genetic predisposition, being 3.63 and 7.13, respectively. B12- and B35-positive individuals were at higher risk for hyperphosphaturia up to 11.25. There were significant differences in antigen frequency, and sex, genetic predisposition to urolithiasis, association of phosphorus metabolic disturbances with other metabolic disorders, and their effects of parathyroid lesions, etc. The findings reveal the immunogenetically induced risk for the occurrence and development of urolithiasis with disturbed phosphorus metabolism to make goal-oriented prophylactic measures.

ABO Blood-Group System↗
PubMed1987

Clinical disorders of phosphorus metabolism.

Deranged phosphorus metabolism is commonly encountered in clinical medicine. Disturbances in phosphate intake, excretion and transcellular shift account for the abnormal serum levels. As a result of the essential role played by phosphate in intracellular metabolism, the clinical manifestations of hypophosphatemia and hyperphosphatemia are extensive. An understanding of the pathophysiology of various phosphate disorders is helpful in guiding therapeutic decisions.

Humans↗
PubMed1999

Psr1, a nuclear localized protein that regulates phosphorus metabolism in Chlamydomonas.

Understanding the ways in which phosphorus metabolism is regulated in photosynthetic eukaryotes is critical for optimizing crop productivity and managing aquatic ecosystems in which phosphorus can be a major source of pollution. Here we describe a gene encoding a regulator of phosphorus metabolism, designated Psr1 (phosphorus starvation response), from a photosynthetic eukaryote. The Psr1 protein is critical for acclimation of the unicellular green alga Chlamydomonas reinhardtii to phosphorus starvation. The N-terminal half of Psr1 contains a region similar to myb DNA-binding domains and the C-terminal half possesses glutamine-rich sequences characteristic of transcriptional activators. The level of Psr1 increases at least 10-fold upon phosphate starvation, and immunocytochemical studies demonstrate that this protein is nuclear-localized under both nutrient-replete and phosphorus-starvation conditions. Finally, Psr1 and angiosperm proteins have domains that are similar, suggesting a possible role for Psr1 homologs in the control of phosphorus metabolism in vascular plants. With the identification of regulators such as Psr1 it may become possible to engineer photosynthetic organisms for more efficient utilization of phosphorus and to establish better practices for the management of agricultural lands and natural ecosystems.

Adaptation, Physiological↗
PubMed1984

Role of change in vitamin D metabolism with age in calcium and phosphorus metabolism in normal human subjects.

This study describes the age-related changes of vitamin D metabolism and its related hormones, immunoreactive PTH (iPTH) and calcitonin (CT) in normal human subjects. The objective was to assess their roles in the changes in metabolism of calcium and phosphorus with age. Serum calcium and phosphorus levels declined linearly with age from newborn infants to older adults (r = -0.385, P less than 0.01; r = -0.568, P less than 0.01). The serum calcium and phosphorus levels in adults of 51 yr of age or more were significantly lower than those in children and younger adults of 50 yr of age or less (P less than 0.025, P less than 0.01), whereas the calcium and phosphorus levels in cord blood were significantly higher than those in children and younger adults (P less than 0.025, P less than 0.01). The serum concentration of 1 alpha,25-dihydroxyvitamin D (1 alpha,25-(OH)2-Vit D) did not change in children and younger adults, being 42.0 +/- 1.4 (SE) pg/ml, but it significantly decreased to 31.4 +/- 1.9 pg/ml in older adults (P less than 0.01). There were no significant age-related changes in the serum concentrations of 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, or vitamin D-binding protein (DBP) among children, younger adults and older adults. The concentrations of all vitamin D metabolites and DBP in cord serum were significantly lower than those in children and younger adults (P less than 0.01). Serum iPTH levels were higher in older adults (P less than 0.05) and lower in cord blood (P less than 0.1), compared with those in children and younger adults, whereas the serum CT level was higher in cord serum (P less than 0.01). No sex differences were found in the serum concentrations of calcium, phosphorus, vitamin D metabolites, DBP, iPTH, and CT. The serum concentration of calcium or phosphorus did not correlate significantly with that of 1 alpha 25-(OH)2-Vit D by simple correlation analysis. Multivariate analysis, however, showed that the change in the serum concentration of 1 alpha,25-(OH)2-Vit D, as well as iPTH and CT, contributed to their correlation with the change in the serum concentrations of calcium and phosphorus. These data indicate that change in vitamin D metabolism might play some role in the age-related change of serum calcium and phosphorus levels in children and adults, but that calcium and phosphorus metabolism in the fetus might be regulated by some mechanisms other than vitamin D metabolism.

Adolescent↗