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
1980 ◽  
Vol 239 (4) ◽  
pp. G261-G265
Author(s):  
C. F. Cramer ◽  
J. McMillan

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.


1975 ◽  
Vol 9 (11) ◽  
pp. 857
Author(s):  
M. Vainsel ◽  
Th. Manderlier ◽  
J. Otten

1982 ◽  
Vol 62 (4) ◽  
pp. 381-387 ◽  
Author(s):  
I. G. Lewin ◽  
S. E. Papapoulos ◽  
G. N. Hendy ◽  
S. Tomlinson ◽  
J. L. H. O'riordan

1. The response to exogenous parathyroid hormone (PTH) was tested in normal subjects and patients with osteomalacia due to vitamin D deficiency; 200 MRC units of bovine PTH were administered intravenously. 2. The rise in plasma adenosine 3′:5′-cyclic monophosphate (cyclic AMP) and the increase in urinary excretion of cyclic AMP were reduced in the patients with vitamin D deficiency. After treatment with vitamin D the responses returned to normal. 3. It is suggested that this reversible resistance is due to the secondary hyperparathyroidism associated with vitamin D deficiency.


2011 ◽  
Vol 44 (14) ◽  
pp. 22
Author(s):  
WILLIAM E. GOLDEN ◽  
ROBERT H. HOPKINS

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