THE ANTAGONISM BETWEEN CORTISONE AND VITAMIN D: EXPERIMENTS ON HYPERVITAMINOSIS D IN RATS

1958 ◽  
Vol 17 (1) ◽  
pp. 35-NP ◽  
Author(s):  
E. M. CRUICKSHANK ◽  
E. KODICEK
Keyword(s):  
Vitamin D ◽  
Antagonistic Effect ◽  
Metastatic Calcification ◽  
Clinical Appearance ◽  
Skeletal Tissue ◽  
Phosphorus Excretion ◽  
Hypervitaminosis D ◽  
Bone Ash ◽  
Urinary Phosphorus Excretion ◽  
Dose Levels

SUMMARY Hypervitaminosis was produced in young growing rats and the effect of daily injections of cortisone acetate (CA) was studied on growth, metastatic calcification, urinary phosphorus excretion and bone ash. Cortisone treatment did not ameliorate the weight loss, clinical appearance, histological lesions or the increased urinary phosphorus. excretion of the hypervitaminotic rats. Control rats, treated with CA alone, showed no untoward effects at the dose levels employed. It is concluded that cortisone does not act as a direct antimetabolite towards vitamin D. The antagonistic effect of the hormone observed in man may be due to reversal of the toxic action of vitamin D by an indirect mechanism, affecting the metabolic sites, such as intestinal tissue, kidney tubules and/or skeletal tissue, on which both vitamin D and cortisone appear to act.

scholarly journals Combination treatment with tenapanor and sevelamer synergistically reduces urinary phosphorus excretion in rats

2020 ◽  
Author(s):  
Andrew J. King ◽  
Jill Kohler ◽  
Cyra Fung ◽  
Zhengfeng Jiang ◽  
Allison Quach ◽  
...  
Keyword(s):  
Male Rats ◽  
Phosphate Binders ◽  
Phosphate Absorption ◽  
Phosphorus Excretion ◽  
Sevelamer Carbonate ◽  
Sodium Hydrogen Exchanger ◽  
Intestinal Phosphate Absorption ◽  
Urinary Phosphorus Excretion ◽  
Dose Levels ◽  
Nhe3 Inhibitor

The majority of patients with chronic kidney disease (CKD) receiving dialysis do not reach target serum phosphorus concentrations, despite treatment with phosphate binders. Tenapanor is a non-binder, sodium/hydrogen exchanger isoform 3 (NHE3) inhibitor that reduces paracellular intestinal phosphate absorption. This pre-clinical study evaluated the effect of tenapanor and varying doses of sevelamer carbonate on urinary phosphorus excretion, a direct reflection of intestinal phosphate absorption. We measured 24-hour urinary phosphorus excretion in male rats assigned to groups dosed orally with vehicle or tenapanor (0.3 mg/kg/day) and provided a diet containing varying amounts of sevelamer (0-3% w/w). We also evaluated the effect of the addition of tenapanor or vehicle on 24-hour urinary phosphorus excretion to rats on a stable dose of sevelamer (1.5% w/w). When administered together, tenapanor and sevelamer decreased urinary phosphorus excretion significantly more than either tenapanor or sevelamer alone across all sevelamer dose levels. The Bliss statistical model of independence indicated that the combination was synergistic. A stable sevelamer dose (1.5% w/w) reduced mean (±standard error of the mean) urinary phosphorus excretion by 42±3% compared with vehicle; together, tenapanor and sevelamer reduced residual urinary phosphorus excretion by an additional 37±6% (P < 0.05). While both tenapanor and sevelamer reduce intestinal phosphate absorption individually, administration of tenapanor and sevelamer together results in more pronounced reductions in intestinal phosphate absorption than if either agent is administered alone. Further evaluation of combination tenapanor plus phosphate binder treatment in patients receiving dialysis with hyperphosphatemia is warranted.

Hypervitaminosis D After Prolonged Feeding With a Premature Formula

PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 862-864
Author(s):  
YASUSHI NAKO ◽  
NAOBUMI FUKUSHIMA ◽  
TAKESHI TOMOMASA ◽  
KANJI NAGASHIMA ◽  
TAKAYOSHI KUROUME
Keyword(s):  
Vitamin D ◽  
Premature Infant ◽  
Premature Infants ◽  
Bone Disease ◽  
Calcium Intake ◽  
Metabolic Bone Disease ◽  
Hypervitaminosis D ◽  
Severe Hypercalcemia ◽  
Metabolic Bone ◽  
Prolonged Feeding

Hypervitaminosis D is one of the causes of severe hypercalcemia in children. Most cases of hypervitaminosis D during childhood are due to an excessive supplementation of vitamin D by physicians or parents.1,2 To prevent metabolic bone disease of prematurity (rickets of prematurity), formulas designed for premature infants ("premature formulas"), which contain more calcium and vitamin D than standard formulas, are given to premature infants in addition to human milk.1 In some cases, separate vitamin D products are also given to these infants, although requirements for vitamin D and calcium intake in the premature infant and the formerly premature infant have not been fully estimated.1

Four Cases of Hypervitaminosis D Following Treatment for Vitamin D Deficiency

2011 ◽  
pp. P2-117-P2-117
Author(s):  
Michelle Beth Vanstone ◽  
Sharon E Oberfield ◽  
Thomas Oliver Carpenter
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Hypervitaminosis D

scholarly journals Effect of RenaGel(R), a non-absorbable, cross-linked, polymeric phosphate binder, on urinary phosphorus excretion in rats

1997 ◽  
Vol 12 (5) ◽  
pp. 961-964 ◽  
Author(s):  
D. Rosenbaum ◽  
S. Holmes-Farley ◽  
W. Mandeville ◽  
M. Pitruzzello ◽  
D. Goldberg
Keyword(s):  
Phosphate Binder ◽  
Phosphorus Excretion ◽  
Urinary Phosphorus Excretion

scholarly journals Normocalcemia in the Face of Marked Hypervitaminosis D: The Utility of Vitamin D Metabolite Profiling

2019 ◽  
Vol 4 (2) ◽  
pp. 264-269
Author(s):  
Tomás P Griffin ◽  
Hannah Murray ◽  
Liam Blake ◽  
Damian G Griffin ◽  
Marcia Bell ◽  
...  
Keyword(s):  
Vitamin D ◽  
Metabolite Profiling ◽  
Hypervitaminosis D ◽  
The Face

The importance of the salivary glands in the maintenance of phosphorus homeostasis in the sheep

1973 ◽  
Vol 24 (6) ◽  
pp. 913 ◽  
Author(s):  
RC Clark ◽  
OE Budtz-Olsen ◽  
RB Cross ◽  
P Finnamore ◽  
PA Bauert
Keyword(s):  
Salivary Glands ◽  
Potassium Dihydrogen Phosphate ◽  
Phosphorus Loading ◽  
Dihydrogen Phosphate ◽  
Short Term ◽  
Potassium Dihydrogen ◽  
Phosphorus Excretion ◽  
Phosphorus Absorption ◽  
Term Basis ◽  
Urinary Phosphorus Excretion

Urinary and faecal phosphorus excretion were measured in five sheep for 4 days after acute intravenous infusion of 3.38 g of phosphorus as potassium dihydrogen phosphate. Urinary phosphorus excretion was increased for 12 hr after the infusion, but urinary phosphorus output was small compared with the marked increase in faecal phosphorus output. The increase in faecal phosphorus excretion coincided with and followed the appearance in the faeces of Cr-EDTA, which had been introduced into the rumen as a marker at the time of the phosphate infusion. This suggests that secretion of phosphorus into gut regions below the reticulo-rumen is not quantitatively altered in response to intravenous phosphorus loading, and that phosphorus absorption is also unaffected (at least not on a short-term basis). The additional phosphorus entered the alimentary canal at the level of the reticulo-rumen, and it was deduced that this occurred predominantly via the salivary glands. Persistence of the increase in faecal phosphorus excretion for some time after the Cr-EDTA marker had been cleared emphasizes the importance of the phosphorus recirculation system to ruminants like the sheep.

Effect of fasting on tubular phosphorus reabsorption

1979 ◽  
Vol 237 (3) ◽  
pp. F241-F246 ◽  
Author(s):  
N. Beck ◽  
S. K. Webster ◽  
H. J. Reineck
Keyword(s):  
Metabolic Acidosis ◽  
Cyclic Amp ◽  
Partial Resistance ◽  
Tubular Reabsorption ◽  
The Other ◽  
Partial Reduction ◽  
Phosphorus Excretion ◽  
Urinary Phosphorus Excretion

In the thyroparathyroidectomized (TPTX) rat, fasting increased urinary phosphorus excretion by decreasing the tubular reabsorption of P1 (TRP) and resulted in hypophosphatemia. The administration of either sucrose or NaHCO3 prevented the metabolic acidosis associated with fasting and decreased the phosphaturia, indicating that the phosphaturia in fasting is in part due to metabolic acidosis. In rats on partial reduction of P1 intake selectively, the phosphaturic response to parathyroid hormone (PTH) was completely suppressed. On the other hand, the fasting rat partially retained the phosphaturic response to PTH, although dietary P1 intake was totally absent. These findings suggest that the renal P1 wasting in fasting may take place by dual mechanisms: a) the PTH-independent decrease in TRP, and b) an inability to totally suppress the response to PTH. Cyclic AMP generation in response to PTH, determined both in vivo and in vitro, was not measurably altered in fasting. However, the phosphaturic response to cyclic AMP was decreased in fasting, suggesting that the mechanism of partial resistance to PTH is probably not at but after cyclic AMP generation.

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