scholarly journals Effect of 24,25-dihydroxyvitamin D3 on 1,25-dihydroxyvitamin D3 metabolism in calcium-deficient rats

1988 ◽  
Vol 250 (3) ◽  
pp. 671-677 ◽  
Author(s):  
T Matsumoto ◽  
K Ikeda ◽  
H Yamato ◽  
K Morita ◽  
I Ezawa ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Water Soluble ◽  
Considerable Proportion ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Urinary Cyclic Amp ◽  
24,25 Dihydroxyvitamin D3

The effect of 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] on 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] metabolism was examined in rats fed on a low-calcium diet. These rats exhibit hypocalcaemia, high urinary cyclic AMP excretion, a markedly elevated serum 1,25(OH)2D concentration and low serum concentrations of both 24,25(OH)2D and 25(OH)D. When the rats are treated orally with 1, 5 or 10 micrograms of 24,25(OH)2D3/100 g every day, there is a dramatic decrease in serum 1,25(OH)2D concentration in a dose-dependent manner concomitant with an increase in serum 24,25(OH)2D concentration. Serum calcium concentration and urinary cyclic AMP excretion are not significantly affected by the 24,25(OH)2D3 treatment, which suggests that parathyroid function is not affected by the 24,25(OH)2D3 treatment. The 25(OH)D3 1 alpha-hydroxylase activity measured in kidney homogenates is markedly elevated in rats on a low-calcium diet but is not affected by any doses of 24,25(OH)2D3. In contrast, recovery of intravenously injected [3H]1,25(OH)2D3 in the serum is decreased in 24,25(OH)2D3-treated rats. Furthermore, when [3H]1,25(OH)2D3 is incubated in vitro with kidney or intestinal homogenates of 24,25(OH)2D3-treated rats there is a decrease in the recovery of radioactivity in the total lipid extract as well as in the 1,25(OH)2D3 fraction along with an increase in the recovery of radioactivity in the water-soluble phase. These results are consistent with the possibility that 24,25(OH)2D3 has an effect on 1,25(OH)2D3 metabolism, namely that of enhancing the degradation of 1,25(OH)2D3. However, because a considerable proportion of the injected 24,25(OH)2D3 is expected to be converted into 1,24,25(OH)3D3 by renal 1 alpha-hydroxylase in 24,25(OH)2D3-treated rats, at least a part of the decrease in serum 1,25(OH)2D concentration may be due to a competitive inhibition by 24,25(OH)2D3 of the synthesis of 1,25(OH)2D3 from 25(OH)D3. Thus the physiological importance of the role of 24,25(OH)2D3 in regulating the serum 1,25(OH)2D concentration as well as the mechanism and metabolic pathway of degradation of 1,25(OH)2D3 remain to be clarified.

scholarly journals Stimulation of 1,25-dihydroxyvitamin D3 production by 1,25-dihydroxyvitamin D3 in the hypocalcaemic rat

1983 ◽  
Vol 214 (3) ◽  
pp. 893-897 ◽  
Author(s):  
Y Tanaka ◽  
H F DeLuca
Keyword(s):  
Vitamin D3 ◽  
Hydroxylase Activity ◽  
Dihydroxyvitamin D3 ◽  
Hydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Low Phosphorus ◽  
25 Hydroxyvitamin D

Serum 1,25-dihydroxyvitamin D3 concentration and renal 25-hydroxyvitamin D 1 alpha-hydroxylase activity were measured in rats fed various levels of calcium, phosphorus and vitamin D3. Both calcium deprivation and phosphorus deprivation greatly increased circulating levels of 1,25-dihydroxyvitamin D3. The circulating level of 1,25-dihydroxyvitamin D3 in rats on a low-calcium diet increased with increasing doses of vitamin D3, whereas it did not change in rats on a low-phosphorus diet given increasing doses of vitamin D3. In concert with these results, the 25-hydroxyvitamin D 1 alpha-hydroxylase activity was markedly increased by vitamin D3 administration to rats on a low-calcium diet, whereas the same treatment of rats on a low-phosphorus diet had no effect and actually suppressed the 1 alpha-hydroxylase in rats fed an adequate-calcium/adequate-phosphorus diet. The administration of 1,25-dihydroxyvitamin D3 to vitamin D-deficient rats on a low-calcium diet also increased the renal 25-hydroxy-vitamin D 1 alpha-hydroxylase activity. These results demonstrate that the regulatory action of 1,25-dihydroxyvitamin D3 on the renal 25-hydroxyvitamin D3 1 alpha-hydroxylase is complex and not simply a suppressant of this system.

Effects of metabolic acidosis on PTH and 1,25(OH)2D3 response to low calcium diet

1982 ◽  
Vol 243 (6) ◽  
pp. F570-F575 ◽  
Author(s):  
D. A. Bushinsky ◽  
M. J. Favus ◽  
A. B. Schneider ◽  
P. K. Sen ◽  
L. M. Sherwood ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Ionized Calcium ◽  
Total Serum ◽  
Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Total Serum Calcium ◽  
Camp Generation ◽  
Immunoreactive Parathyroid Hormone

To study the effects of chronic metabolic acidosis on the metabolism of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] rats were given either a low calcium diet (LCD) (0.002% calcium) or chow (1.2% calcium); ammonium chloride (NH4Cl) was added (1 or 1.5%) to the drinking water of some rats eating LCD or chow while others served as nonacidotic controls. LCD increased circulating 1,25(OH)2D3 levels from 46 +/- 14 to 204 +/- 24 pg/ml (P less than 0.001) in the absence of NH4Cl; 1.5% NH4Cl prevented the increase in 1,25(OH)2D3 (25 +/- 6 vs. 27 +/- 8 pg/ml (P, NS) but 1% NH4Cl did not (50 +/- 12 vs. 161 +/- 23 pg/ml; P less than 0.001). Acidosis suppressed neither serum immunoreactive parathyroid hormone (PTH) nor urine cAMP response to LCD. Although total serum calcium and phosphorus showed no regular changes with NH4Cl, acidosis raised blood ionized calcium in rats fed either chow or LCD, and serum 1,25(OH)2D3 levels were inversely correlated with ionized calcium (r = 0.714; P less than 0.001) during LCD. Chronic NH4Cl acidosis prevented serum 1,25(OH)2D3 from rising during LCD, independent of changes in PTH secretion, cAMP generation, or serum phosphorus. The absence of a 1,25(OH)2D3 response may be due to increased ionized calcium produced by acidosis.

Calcium transport in the ileum of uremic rats

1982 ◽  
Vol 242 (2) ◽  
pp. G128-G134
Author(s):  
M. Koller ◽  
U. Binswanger
Keyword(s):  
Renal Failure ◽  
Calcium Transport ◽  
Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Unidirectional Fluxes ◽  
Small Intestinal ◽  
Normal Calcium

Duodenal and ileal calcium transport was studied by 45Ca uptake and estimation of unidirectional fluxes in vitro in kidney-intact and 5/6-nephrectomized rats. After normal-calcium diet, calcium transport was impaired by uremia in the duodenum but not in the ileum. However, 5/6-nephrectomized rats on low-calcium diet showed, in concert with impaired growth, a reduced calcium transport both in duodenum and ileum. Comparing data after normal- and low-calcium diets, the ileal adaptation to low-calcium diet was intact in mild renal failure but abolished in severe uremia (urea less than 100 mg/dl). These results suggest that ileal calcium transport after normal-calcium diet is mainly passive. Taking into account reduced food intake as an additional factor, the active ileal calcium transport after low-calcium diet declines with progressive renal failure according to decreasing levels of 1,25-dihydroxyvitamin D3. A suspected enhancement of the distal small intestinal calcium transport by parathyroid hormone in uremic rats as compensation for proximally impaired absorption could not be demonstrated.

scholarly journals Icariin protects against cage layer osteoporosis by intervening in steroid biosynthesis and glycerophospholipid metabolism

2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Zhengwang Yu ◽  
Jie Huang ◽  
Zhongxin Zhou
Keyword(s):  
Metabolic Diseases ◽  
Chinese Herb ◽  
Therapeutic Effects ◽  
Mineral Density ◽  
Steroid Biosynthesis ◽  
Metabolic Pathway Analysis ◽  
Effective Prevention ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

AbstractCage layer osteoporosis (CLO) is a common bone metabolism disease in the breeding industry of China. However, effective prevention for CLO has not been developed. Icariin (ICA), the main bioactive component of the Chinese herb Epimedium, has been shown to have good therapeutic effects on bone-related diseases. In this study, the effects of ICA were further evaluated in a low-calcium diet-induced CLO, and a serum metabolomics assay was performed to understand the underlying mechanisms. A total of 144 31-wk-old Lohmann pink-shell laying hens were randomly allocated to 4 groups with 6 replicates of 6 hens per replicate. The 4 dietary treatment groups consisted of a basal diet (3.5% calcium), a low-calcium diet (2.0% calcium), and a low-calcium diet supplemented with 0.5 or 2.0 g/kg ICA. The results showed that ICA exerted good osteoprotective effects on low-calcium diet-induced CLO. ICA significantly increased femur bone mineral density, improved bone microstructure, decreased bone metabolic level, and upregulated mRNA expression of bone formation genes in femoral bone tissue. Serum untargeted metabolomics analysis showed that 8 metabolite levels were significantly changed after ICA treatment, including increased contents of 7-dehydrocholesterol, 7-oxocholesterol, desmosterol, PC (18:1(9Z)/18:1(9Z)), PS (18:0/18:1(9Z)), N,N-dimethylaniline and 2-hydroxy-butanoic acid and decreased N2,N2-dimethylguanosine. Metabolic pathway analysis based on the above 8 metabolites indicated that ICA mainly perturbed steroid biosynthesis and glycerophospholipid metabolism. These findings suggest that ICA can effectively prevent bone loss in low-calcium diet-induced CLO by mediating steroid biosynthesis and glycerophospholipid metabolism and provide new information for the regulation of bone metabolic diseases.

Sign in / Sign up

Export Citation Format

Share Document