Phosphorus adaptation in rats in absence of vitamin D or parathyroid glands

1980 ◽  
Vol 239 (4) ◽  
pp. G261-G265
Author(s):  
C. F. Cramer ◽  
J. McMillan
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Vitamin D Deficiency ◽  
Intestinal Absorption ◽  
Control Diet ◽  
Inorganic Phosphorus ◽  
Parathyroid Glands ◽  
Intestinal Excretion ◽  
Growing Rats ◽  
Pi Deficiency

Growing rats even when vitamin D deficient became adapted to inorganic phosphorus (Pi) deficiency by increasing absorption and minimizing excretion. Feeding low-Pi diet for 3 wk reduced urinary Pi by 80% (P < 0.001), and urinary 32P by 50% (P < 0.001). Low-Pi regimen increased 32p absorption from a 32P-labeled meal by 50% (P < 0.001), even when the animals were vitamin D deficient or thyroparathyroidectomized. The marked increase in retention of 32P in phosphorus-deficient rats could not be accounted for by decreased endogenous intestinal excretion plus increased kidney reabsorption; increased intestinal absorption played a part. 32P absorption was significantly reduced (P < 0.001) by vitamin D deficiency in rats fed either control diet (.6%) Pi or low-Pi diet (0.03%). Endogenous intestinal or urinary excretion of 32P was unaltered by vitamin D deficiency. The evidence supports the hypothesis that there are two mechanisms for phosphorus adaptation: kidney retention not requiring vitamin D, and inreased intestinal absorption of Pi not requiring parathyroids, thyroids, or vitamin D.

scholarly journals URINARY EXCRETION OF ADENOSINE 3'5' MONOPHOSPHATE IN VITAMIN D DEFICIENCY

1975 ◽  
Vol 9 (11) ◽  
pp. 857-857
Author(s):  
M Vainsel ◽  
Th Manderlier ◽  
J Otten
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Vitamin D Deficiency

scholarly journals The effect of disodium ethane-1-hydroxy-1,1-diphosphonate on the metabolism of calcitriol in chicks

1987 ◽  
Vol 243 (1) ◽  
pp. 75-78 ◽  
Author(s):  
C Lidor ◽  
M S Meyer ◽  
R H Wasserman ◽  
S Edelstein
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Binding Protein ◽  
Sole Source ◽  
Treated Group ◽  
Response To Treatment ◽  
Vitamin D Metabolism ◽  
Calbindin D28k ◽  
25 Hydroxycholecalciferol

Decreased intestinal absorption of Ca2+ occurs in response to treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). The effect is due to decreased 1-hydroxylation of calcidiol (25-hydroxycholecalciferol) in the kidney. In an attempt to establish whether impairment of vitamin D metabolism at steps beyond kidney hydroxylation occurs due to treatment with EHDP, chicks were depleted of vitamin D and were treated with calcitriol (1,25-dihydroxycholecalciferol) as their sole source of the vitamin. The chicks were then divided into two groups, one being treated with EHDP while the second group served as control. Intestinal absorption of Ca2+ in the EHDP-treated group was found to be impaired, along with decreases in concentrations of calbindin D28K (the 28,000-Mr vitamin D-dependent Ca2+-binding protein). When the chicks were dosed with [3H]calcitriol, significantly lower concentrations of the sterol were detected in the duodena of EHDP-treated birds. Measurement of levels of receptors for calcitriol in duodena showed no difference between groups, but levels of calcitriol in sera were considerably lower in the EHDP-treated group along with the elevated biliary and urinary excretion of glucuronidated conjugates. It is therefore concluded that treatment with EHDP results in increased catabolism of calcitriol in addition to the known suppression of the renal production of the hormone.

scholarly journals Response of diamine oxidase and other plasma copper biomarkers to various dietary copper intakes in the rat and evaluation of copper absorption with a stable isotope

2000 ◽  
Vol 83 (5) ◽  
pp. 561-568 ◽  
Author(s):  
C. Feillet-Coudray ◽  
C. Coudray ◽  
D. Bayle ◽  
E. Rock ◽  
Y. Rayssiguier ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Diamine Oxidase ◽  
Control Diet ◽  
The Other ◽  
Control Group ◽  
Deficient Diet ◽  
Apparent Absorption ◽  
Cu Deficiency ◽  
Cu Isotope

There is a lack of agreement on index of Cu status and reliable and sensitive biomarkers are still required. The purpose of this present work was to assess in rats the sensitivity of diamine oxidase (DAO) activity, a recently proposed biomarker, to modifications in dietary Cu intake in comparison with other plasma biomarkers of Cu status. We also evaluated the effect of Cu dietary level on Cu and Zn intestinal absorption. Results showed that plasma Cu and plasma caeruloplasmin were significantly decreased at day 8 compared with the control group (7·4 mg Cu/kg diet) while DAO activity was significantly decreased at day 12 of the deficient diet (0·61 mg Cu/kg diet). Cu supplementation (35 mg Cu/kg diet) had no effect on any of the studied biomarkers of Cu status. In Cu-deficient rats plasma Cu and DAO activities were normalized 4 d after return to the control diet while caeruloplasmin was normalized later, at day 11. Apparent absorption values (%) of total Cu or65Cu isotope were significantly increased in the Cu-deficient rats compared with the other groups and similar in the control and the Cu-supplemented groups. The urinary excretion of total Cu or65Cu isotope were increased in the Cu-supplemented group compared with the other two groups. Both apparent absorption and urinary excretion of total Zn or67Zn isotope remained unchanged in the three experimental groups. In conclusion, DAO activity seemed to be less sensitive to Cu deficiency than plasma Cu or caeruloplasmin concentrations. The present study also showed a significant increase in Cu intestinal absorption with dietary Cu restriction but no decrease with Cu supplementation in the rat.

scholarly journals Characterization of the vitamin D-dependent Ca2+-binding sites in rat intestinal Golgi-enriched membrane fractions

1984 ◽  
Vol 218 (2) ◽  
pp. 347-354 ◽  
Author(s):  
J R F Walters ◽  
M M Weiser
Keyword(s):  
Vitamin D ◽  
Ionic Strength ◽  
Vitamin D Deficiency ◽  
Binding Sites ◽  
Control Diet ◽  
Specific Protein ◽  
High Affinity ◽  
Equilibrium Binding ◽  
Number Of Binding Sites

Rat intestinal Golgi-enriched membrane fractions take up Ca2+ by a vitamin D-dependent process that has been shown to recover within 15 min of repletion of vitamin D-deficient animals with intravenous 1,25-dihydroxycholecalciferol. The present paper reports studies characterizing the Ca2+-binding sites of these membrane fractions. Equilibrium binding of Ca2+ at concentrations between 5 and 400 microM showed significant decreases at all concentrations in membranes derived from vitamin D-deficient animals when compared with normal control-diet-fed animals. The predominant class of binding sites had a relatively high affinity for Ca2+ (KD approx. 3 microM). Vitamin D-deficiency did not change the affinity of this class of site, but decreased the number from 347 +/- 26 to 168 +/- 50 nmol of Ca2+ bound/mg of protein (means +/- S.D.). Mg2+ inhibited binding only at low Ca2+ concentrations, and the characteristics of this binding suggested positive co-operativity between two binding sites. Equimolar concentrations of Zn2+, La3+, Pb2+ and Mn2+ inhibited Ca2+ binding by over 50%. Increased ionic strength decreased Ca2+ binding by no more than half. Binding was maximal at pH 7.5 and half-maximal at pH 6.3. The large number of binding sites with relatively high affinity for Ca2+ suggests that it is unlikely that this binding is to any specific protein or to non-specific sites present on many proteins, and that the most likely sites are lipid molecules.

Vitamin D deficiency enhances expression of autophagy-regulating miR-142-3p in mouse and 'involved' IBD patient intestinal tissues

2021 ◽  
Author(s):  
Laurel McGillis ◽  
Dana M. Bronte-Tinkew ◽  
Frances Dang ◽  
Mariana Capurro ◽  
Akriti Prashar ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Control Diet ◽  
Adaptor Protein ◽  
Paneth Cells ◽  
Deficient Diet ◽  
Vitamin D Levels ◽  
Treatment Naïve ◽  
Potential Link ◽  
Vitamin D Signaling

Vitamin D deficiency is an environmental factor involved in the pathogenesis of inflammatory bowel disease (IBD), however, the mechanisms surrounding its role remain unclear. Previous studies conducted in an intestinal epithelial-specific vitamin D receptor (VDR) knockout model suggest that a lack of vitamin D signaling causes a reduction in intestinal autophagy. A potential link between vitamin D deficiency and dysregulated autophagy is microRNA (miR)-142-3p, which suppresses autophagy. In this study, we found that wildtype C57BL/6 mice fed a vitamin D deficient diet for 5 weeks had increased miR-142-3p expression in ileal tissues compared to mice fed a matched control diet. Interestingly, there was no difference in expression of key autophagy markers ATG16L1 and LC3II in the ileum whole tissue. However, Paneth cells of vitamin D deficient mice were morphologically abnormal and had an accumulation of the autophagy adaptor protein p62 which was not present in the total crypt epithelium. These findings suggest that Paneth cells exhibit early markers of autophagy dysregulation within the intestinal epithelium in response to vitamin D deficiency and enhanced miR-142-3p expression. Finally, we demonstrated that treatment-naïve IBD patients with low levels of vitamin D have an increase in miR-142-3p expression in colonic tissues procured from 'involved' areas of disease. Taken together, our findings demonstrate that insufficient vitamin D levels alter expression of autophagy-regulating miR-142-3p in intestinal tissues of mice and IBD patients, providing insight into the mechanisms by which vitamin D deficiency modulates IBD pathogenesis.

MAGNESIUM STUDIES IN RELATION TO VITAMIN D-RESISTANT RICKETS

PEDIATRICS ◽  
1967 ◽  
Vol 40 (3) ◽  
pp. 425-435
Author(s):  
Constantine S. Anast
Keyword(s):  
Vitamin D ◽  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Serum Magnesium ◽  
Age Groups ◽  
Disease Process ◽  
The Body ◽  
Magnesium Metabolism ◽  
Vitamin D Resistant Rickets ◽  
Resistant Rickets

Magnesium metabolism was found to be unaltered in a 4-year-old boy with untreated vitamin D-resistant rickets who manifested abnormalities of calcium and phosphorous metabolism commonly found in this disease. This is at variance with the previously reported finding of altered magnesium metabolism in a patient with resistant rickets acquired at adolescence. The possibility that this difference may reflect either a variation in the underlying disease process in the two age groups or a difference in the severity of the disease process is discussed. It is of significance that the gastrointestinal absorption of calcium was decreased while that of magnesium was normal in our untreated patient. This suggests that the mechanisms involved in intestinal transport of these two minerals are not identical. Treatment with 200,000 to 300,000 I.U. of vitamin D per day resulted in a decrease in the serum magnesium levels with no consistent changes in the urinary excretion, intestinal absorption, or retention of magnesium; during this time, however, the intestinal absorption, urinary excretion, and retention of calcium were all increased. The administration of 350,000 I.U. of vitamin D per day was associated with an increase in both the urinary excretion and intestinal absorption of magnesium. At this dose the retention of magnesium initially increased and subsequently decreased as the increase in urinary magnesium offset the increased intestinal absorption of this mineral. It is not known if the effects of vitamin D on the intestinal absorption and urinary excretion of magnesium represent primary actions of this vitamin on the kidney and gastrointestinal tract or whether they are secondary to changes in calcium and phosphorous metabolism. The fact that vitamin D administration resulted in a lowering of the serum magnesium level before there were any consistent alterations in fecal and urinary magnesium is in keeping with previously reported animal studies which indicate that vitamin D acts to cause a redistribution of magnesium in the body.

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