Age and gender effects on 1,25-dihydroxyvitamin D3-regulated gene expression☆
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Cited by (34)
New developments in our understanding of vitamin metabolism, action and treatment
2019, Metabolism: Clinical and ExperimentalCitation Excerpt :With age there is a decline in the ability of the kidney to hydroxylate 25(OH)D3 to 1,25(OH)2D3 [17]. An increase in renal CYP24A1 expression as well as an increase in the clearance of 1,25(OH)2D3 with aging have also been reported [17–20]. Thus the combined effect of a decline in the ability of the kidney to synthesize 1,25(OH)2D3 and an increase in the catabolism of 1,25(OH)2D3 by CYP24A1 may contribute to age related bone loss.
Changes in vitamin D endocrinology during aging in adults
2017, Molecular and Cellular EndocrinologyCitation Excerpt :With aging, there is a decrease in renal production of 1,25(OH)2D by the kidney associated with the decline in renal function (Reichel et al., 1991; Tsai et al., 1984). Studies in rats show that CYP27B1 activity decreases and CYP24A1 activity increases with aging leading to less availability of 1,25(OH)2D (Johnson et al., 1995; Armbrecht et al., 1980). Animal studies have also shown that the stimulatory effect of PTH or low phosphate diet on CYP27B1 expression is blunted in older rats as compared to younger ones (Chau et al., 2005; Armbrecht et al., 1987).
Sex disparities in melanoma outcomes: The role of biology
2014, Archives of Biochemistry and BiophysicsCitation Excerpt :Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2 D3], has been suggested to have a protective effect on melanoma outcomes [88]. There are sex differences in vitamin D plasma levels, with the level in young adult and older female rats significantly lower than males of the same ages [89], and estrogens modulate 1,25(OH)2 D3 activity by upregulating vitamin D receptor (VDR) expression in several cell types and by causing translocation of the VDR from the cytoplasm to the nucleus, shown in cultured human fibroblasts [90–92]. The vitamin D receptor is expressed at a variety of levels on cultured human melanoma cell lines and 1,25(OH)2 D3 inhibited both DNA synthesis and cell growth and induced apoptosis in many but not all melanoma cell lines [93–98].
Novel mechanism of negative regulation of 1,25-dihydroxyvitamin D<inf>3</inf>-induced 25-hydroxyvitamin D<inf>3</inf> 24-hydroxylase (Cyp24a1) transcription: Epigenetic modification involving cross-talk between protein-arginine methyltransferase 5 and the SWI/SNF complex
2014, Journal of Biological ChemistryCitation Excerpt :This mechanism of negative regulation may be important to prevent catabolism of 1,25(OH)2D3 at times when protection against hypercalcemia is not needed. We and others have noted that renal Cyp24a1 increases with age and have suggested that increased catabolism of 1,25(OH)2D3 contributes to age-related bone loss (57, 58). Recent studies have shown an age-dependent decrease in renal PRMT5 (59).
Is the metabolism of 25-hydroxyvitamin D<inf>3</inf> age-dependent in dairy cows?
2013, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :As no impact of the more pronounced hypocalcemia in older cows and the corresponding stronger hormonal response to this challenge could be found, the longer plasma half-life of 25-OHD3 in younger animals is most probably caused by an age-dependent slower rate of degradation of 25-OHD3. This could involve a lower expression and/or activity of the 24-hydroxylase of younger animals in comparison to older individuals which has already been demonstrated in the rat [4]. Although this assumption is supported by the positive correlation between the calculated plasma-half life postpartum and the basal concentrations of 25-OHD3 prepartum when 1,25-(OH)2D3 levels were low, further studies are needed to prove this hypothesis.
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Current address: Nephrology Research Unit, Mayo Clinic, 911A Guggenheim Building, 200 First Street, S.W., Rochester, MN 55901
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Current address: Department of Biochemistry, University of Wisconsin, Madison, WI 53706