The Role of Vitamin D Metabolites in the Management of Bone Abnormalities in Renal Disease

Author(s):  
Hartmut H. Malluche ◽  
Shaul G. Massry
1981 ◽  
Vol 7 (5) ◽  
pp. 294-315 ◽  
Author(s):  
J. A. Kanis ◽  
C. B. Brown ◽  
E. C. Cameron ◽  
T. Cundy ◽  
M. M. Platts ◽  
...  

2012 ◽  
Vol 108 (11) ◽  
pp. 1915-1923 ◽  
Author(s):  
Cherlyn Ding ◽  
Dan Gao ◽  
John Wilding ◽  
Paul Trayhurn ◽  
Chen Bing

Vitamin D deficiency and the rapid increase in the prevalence of obesity are both considered important public health issues. The classical role of vitamin D is in Ca homoeostasis and bone metabolism. Growing evidence suggests that the vitamin D system has a range of physiological functions, with vitamin D deficiency contributing to the pathogenesis of several major diseases, including obesity and the metabolic syndrome. Clinical studies have shown that obese individuals tend to have a low vitamin D status, which may link to the dysregulation of white adipose tissue. Recent studies suggest that adipose tissue may be a direct target of vitamin D. The expression of both the vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes has been shown in murine and human adipocytes. There is evidence that vitamin D affects body fat mass by inhibiting adipogenic transcription factors and lipid accumulation during adipocyte differentiation. Some recent studies demonstrate that vitamin D metabolites also influence adipokine production and the inflammatory response in adipose tissue. Therefore, vitamin D deficiency may compromise the normal metabolic functioning of adipose tissue. Given the importance of the tissue in energy balance, lipid metabolism and inflammation in obesity, understanding the mechanisms of vitamin D action in adipocytes may have a significant impact on the maintenance of metabolic health. In the present review, we focus on the signalling role of vitamin D in adipocytes, particularly the potential mechanisms through which vitamin D may influence adipose tissue development and function.


Author(s):  
O.V. Kalashnikov ◽  
G.V. Gayko ◽  
O.A. Burianov ◽  
V.V. Tymochuk ◽  
D.M. Poluliakh

Summary. At present, there is a need to systematize the data of our own comprehensive research and literature in order to determine the role of active metabolites of vitamin D in the formation of structural and functional disorders (SFD) in osteoarthritis of the hip. Objective: on the basis of our own complex researches and data of literature, to determine the role of the insufficiency of vitamin D metabolites in the development of SFD in coxarthrosis. Materials and Methods. The basis for determining the role of active metabolites of vitamin D in the development of SFN in coxarthrosis was our own comprehensive studies of 506 patients with osteoarthritis of the hip and data from the literature. Results. On the basis of the theory of functional systems, a conceptual model for the development of SFD in coxarthrosis has been developed. The leading factor in the development of SFD in the rapid progression of idiopathic and dysplastic osteoarthritis of the hip is the lack of active metabolites of vitamin D. The presence of undifferentiated connective tissue dysplasia in turn causes a decrease in the absorption of provitamin D in the stomach and intestines. With a slow progression of idiopathic coxarthrosis, the leading factor in the development of these disorders is the excessive load on the hip joint. Factors of violation of biomechanical conditions and injury of the hip joint are factors of the progression of coxarthrosis of dysplastic and post-traumatic genesis. Pathogenic factors lead to functional and structural changes in systems of different levels and their elements with the development of inverted processes in the structures of the hip joint. Conclusions. Insufficiency of vitamin D metabolites on the background of undifferentiated connective tissue dysplasia leads to biochemical changes in articular cartilage and serum, affects both osteo- and chondrogenesis, leads to reduced immune status of patients and the development of clinical manifestations of rapid progression of idiopathic and dysplastic coxarthrosis. With a slow progression of idiopathic coxarthrosis, the main factor leading to the development of the above mentioned disorders is the excessive load on the hip joint. Factors of violation of biomechanical conditions and injury of the hip joint determine the development of SFD in coxarthrosis of dysplastic and post-traumatic genesis.


2020 ◽  
Vol 24 (3) ◽  
pp. 367-373
Author(s):  
Leila Malekmakan ◽  
Zeinab Karimi ◽  
Afshin Mansourian ◽  
Maryam Pakfetrat ◽  
Jamshid Roozbeh ◽  
...  

Bone ◽  
1985 ◽  
Vol 6 (1) ◽  
pp. 55-55
Author(s):  
S. Ralston ◽  
R.A. Cowan ◽  
A.S. Jenkins ◽  
A.G. Robertson ◽  
M.D. Gardner ◽  
...  

1983 ◽  
Vol 244 (6) ◽  
pp. F674-F678 ◽  
Author(s):  
M. M. Friedlaender ◽  
Z. Kornberg ◽  
H. Wald ◽  
M. M. Popovtzer

The effects of 1 alpha (OH)vitamin D3 [1 alpha (OH)D3] and 24,25(OH)2vitamin D3 [24,25(OH)2D3] on the phosphaturic action of parathyroid hormone (PTH) were studied in two groups of parathyroidectomized (PTX) rats. In group 1, PTX PTH-infused rats received intravenous 1 alpha (OH)D3, and in group 2, PTX PTH-infused rats received intravenous 24,25(OH)2D3. PTX PTH-infused rats served as controls. The effects of both vitamin D metabolites on renal PTH-activated adenylate cyclase (AC) were studied in vitro. In group 1, PTH increased fractional excretion of phosphate (CP/CIn) from 0.045 +/- 0.012 (+/- SE) to 0.263 +/- 0.011 (P less than 0.005). 1 alpha (OH)D3 failed to influence this response. In group 2, PTH increased CP/CIn from 0.055 +/- 0.008 to 0.289 +/- 0.027 (P less than 0.005). 24,25(OH)2D3 reduced the PTH-induced rise in CP/CIn from 0.289 +/- 0.027 to 0.192 +/- 0.021 (P less than 0.01) and decreased the urinary excretion of adenosine 3',5'-cyclic monophosphate. In vitro, 24,25(OH)2D3 blunted the PTH-activated AC, whereas 1 alpha (OH)D3 had no effect. These results show that 24,25(OH)D3, similar to two other 25(OH) metabolites of vitamin D-25(OH)vitamin D3 and 1,25(OH)2vitamin D3-suppresses the phosphaturic action of PTH, whereas 1 alpha(OH)D3, which is devoid of a 25(OH) group, lacks this effect. This suggests that a 25(OH) group is a prerequisite for the antiphosphaturic effect of vitamin D, whereas the 1 alpha (OH) group is not essential for this action.


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