scholarly journals THE ACTION OF VITAMIN D AND PARATHYROID HORMONE IN VITRO ON CALCIUM UPTAKE AND RELEASE BY KIDNEY MITOCHONDRIA

1962 ◽  
Vol 48 (9) ◽  
pp. 1604-1609 ◽  
Author(s):  
H. F. DeLuca ◽  
G. W. Engstrom ◽  
H. Rasmussen
2006 ◽  
Vol 291 (5) ◽  
pp. R1499-R1506 ◽  
Author(s):  
Juan Fuentes ◽  
Joana Figueiredo ◽  
Deborah M. Power ◽  
Adelino V. M. Canário

Parathyroid hormone-related protein (PTHrP) is a factor associated with normal development and physiology of the nervous, cardiovascular, immune, reproductive, and musculoskeletal systems in higher vertebrates. It also stimulates whole body calcium uptake in sea bream ( Sparus auratus) larvae with an estimated 60% coming from intestinal uptake in seawater. The present study investigated the role of PTHrP in the intestinal calcium transport in the sea bream in vitro. Unidirectional mucosal-to-serosal and serosal-to-mucosal 45Ca fluxes were measured in vitro in duodenum, hindgut, and rectum mounted in Ussing chambers. In symmetric conditions with the same saline, bathing apical and basolateral sides of the preparation addition of piscine PTHrP 1–34 (6 nM) to the serosal surface resulted in an increase in mucosal to serosal calcium fluxes in duodenum and hindgut and a reduction in serosal to mucosal in the rectum, indicating that different mechanisms are responsive to PTHrP along the intestine. In control asymmetric conditions, with serosal normal and mucosal bathed with a saline similar in composition to the intestinal fluid, there was a net increase in calcium uptake in all regions. The addition of 6 nM PTHrP 1–34 increased net calcium uptake two- to threefold in all regions. The stimulatory effect of PTHrP on net intestinal calcium absorption is consistent with a hypercalcemic role for the hormone. The results support the view that PTHrP, alone or in conjunction with recently identified PTH-like peptides, counteracts in vivo the hypocalcemic effects of stanniocalcin.


1997 ◽  
Vol 52 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Günter Klaus ◽  
Tanja May ◽  
Ulrike Hügel ◽  
Barbara Von Eichel ◽  
Julian Rodriguez ◽  
...  

1984 ◽  
Vol 105 (3) ◽  
pp. 354-359 ◽  
Author(s):  
Claes Rudberg ◽  
Göran Åkerström ◽  
Henry Johansson ◽  
Sverker Ljunghall ◽  
Jan Malmaeus ◽  
...  

Abstract. The effects of 125-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2–16 h. There was a gradual suppression of PTH release (5–55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.


2017 ◽  
Vol 45 (1) ◽  
pp. 36-45 ◽  
Author(s):  
T. Greulich ◽  
W. Regner ◽  
M. Branscheidt ◽  
C. Herr ◽  
A. R. Koczulla ◽  
...  

It has been recognised that vitamin D (VitD) has a potential role in the regulation of inflammation and protection from infection. In a prospective clinical observational pilot study, we investigated the serum levels of 25-hydroxyvitamin-D3 (25(OH D3), 1,25-hydroxyvitamin-D3 (1,25(OH)2D3), parathyroid hormone (PTH), and cathelicidin in intensive care unit (ICU) patients with or without systemic inflammatory response syndrome (SIRS). We included 32 patients with SIRS (septic patients), 16 ICU patients without SIRS, and 16 healthy controls. To substantiate the findings of the clinical study, we stimulated monocyte-derived macrophages with microbial patterns and analysed the impact of VitD on release of cytokines and antimicrobial activity. We found that patients with or without SIRS had relatively low levels of 25(OH)D3 and 1,25(OH)2D3. Patients with sepsis had significantly lower levels of 25(OH)D3 as compared to ICU control patients and healthy controls (10.53 ± 11.3 μg/l versus 16.46 ± 12.58 μg/l versus 24.04 ± 12.07 μg/l); the same was true for 1,25(OH)2D3. Serum levels of PTH and cathelicidin were significantly increased in sepsis patients, as compared to the other groups. In vitro, VitD significantly decreased the release of pro-inflammatory cytokines from macrophages and increased the antimicrobial activity of the cells. We concluded that patients with sepsis have significantly lower VitD levels. In vitro, VitD modulates inflammation and increases the antibacterial activity of innate immune cells. These findings suggest that VitD insufficiency is mechanistically related to increased susceptibility to SIRS and sepsis.


2019 ◽  
pp. 76-77 ◽  
Author(s):  
Milind N Dudhane ◽  
Umesh Pareek

Background: Vitamin D is a secosteroid hormone and well-known for its classical actions in the maintenance of calcium uptake and bone metabolism. Recently, numerous in vitro experiments demonstrated that 1,25-(OH)2D3, the active form of vitamin D, inhibited the growth and differentiation of human prostate cancer cells. Aim:To estimate vitamin D level in prostate cancer patients along with increasing risk. Material & Methods : 100 samples along with control were analysed by cobas e-411 for Vitamin D and PSA. Results: we have found Higher risk of prostate cancer who having low vitamin D. Conclusion:it's time to aware people for supplementation of Vitamin D, so we can prevent for the same


Development ◽  
1986 ◽  
Vol 97 (1) ◽  
pp. 63-74
Author(s):  
Rocky S. Tuan ◽  
Tamao Ono

During development, the chick embryo mobilizes the calcium it needs from two extraembryonic sources, first the yolk and then the eggshell. Since previous studies have strongly suggested that vitamins D and K may regulate chick embryonic calcium metabolism, we have examined here how these vitamins might be involved in regulating the calcium mobilization processes. We used as our experimental system chick embryos which were maintained in longterm in vitro culture in the absence of the eggshell. Our results showed that exogenous vitamin D3, in the form of the active 1,25-dihydroxylated metabolite, was hypercalcaemic in both control embryos and the calcium-deficient, shell-less embryos. Since the eggshell was absent in the latter, the vitamin D-induced hypercalcaemia must involve mobilization of calcium from the yolk and, or, the embryonic skeleton. The latter was unlikely since concomitant hyperphosphataemia was not observed. By radiolabelling the yolk with 45Ca2+ and subsequently monitoring its distribution, we showed that vitamin D3 stimulated yolk calcium mobilization. However, exogenous vitamin D3 did not appear to influence the calcium uptake activity of the chorioallantoic membrane (CAM), the tissue responsible for translocating eggshell calcium. On the other hand, when embryos were rendered vitamin K deficient by the administration of its antagonist, Warfarin, CAM calcium activity was significantly depressed, an effect which was remedied by vitamin K supplementation. We conclude that, during normal chick embryonic development, vitamin D is primarily involved in regulating yolk calcium mobilization whereas vitamin K is required for eggshell calcium translocation by the CAM.


Endocrinology ◽  
2021 ◽  
Author(s):  
Jianping Mao ◽  
Mengjing Wang ◽  
Li Ni ◽  
Wen Gong ◽  
Xinxin Jiang ◽  
...  

Abstract Secondary hyperparathyroidism (SHPT) in uremic patients characterizes by parathyroid gland (PTG) hyperplasia and parathyroid hormone (PTH) elevation. Previously, we demonstrated that NF-κB activation contributed to parathyroid cell proliferation in chronic kidney disease (CKD) rats. Although vitamin D inhibits inflammation and ameliorates SHPT, the contribution of vitamin D deficiency to SHPT via local NF-κB activation remains to be clarified. PTGs collected from 10 uremic patients with advanced SHPT were used to test the expressions of vitamin D receptor (VDR), NF-κB, and proliferating cell nuclear antigen (PCNA). Freshly excised PTG tissues were incubated for 24 h in vitro with VDR activator (VDRA) calcitriol or NF-κB inhibitor Pyrrolidine Thiocarbamate (PDTC). Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to investigate the regulation of PTH transcription by NF-κB. We found higher levels of activated NF-κB and lower expression of VDR in nodular hyperplastic PTGs than in diffuse hyperplasia. In cultured PTG tissues, treatment with VDRA or PDTC inhibited NF-κB activation and PCNA expression, and downregulated preproPTH mRNA and intact PTH levels. ChIP assays demonstrated the presence of NF-κB binding sites in PTH promoter. Furthermore, in luciferase reporter assays, addition of exogenous p65 significantly increased PTH-luciferase activity by 2.4-fold (p<0.01), while mutation of NF-κB binding site at position –908 of the PTH promoter suppressed p65-induced PTH reporter activity (p<0.01). In summary, local NF-κB activation contributes to SHPT and mediates the transcriptional activation of PTH directly in uremic patients. Vitamin D deficiency may be involved in SHPT via the activation of NF-κB pathway.


1983 ◽  
Vol 244 (4) ◽  
pp. E421-E424
Author(s):  
P. H. Stern ◽  
B. P. Halloran ◽  
H. F. DeLuca ◽  
T. J. Hefley

Radii and ulnae from 19-day fetal rats from normal or vitamin D-deficient mothers were treated with 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, or parathyroid hormone in vitro. Both sets of bones resorbed in response to all three agents. Statistical analysis indicated a purely additive model for the effects of vitamin D status and the bone-resorbing agents, with no evidence for interaction. The results suggest that the impaired calcemic response to parathyroid hormone seen in vitamin D-deficient animals in vivo is not the result of a specific unresponsiveness of vitamin D-deficient bone to parathyroid hormone.


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