scholarly journals Urinary Hydroxyproline Excretion in Male and Female Chickens

1985 ◽  
Vol 64 (6) ◽  
pp. 1216-1218
Author(s):  
INMACULADA DIEZ PRIETO ◽  
FELIPE PRIETO MONTAÑA ◽  
PAULINO GARCIA PARTIDA
1964 ◽  
Vol 115 (1) ◽  
pp. 85-87 ◽  
Author(s):  
C. R. Jones ◽  
M. W. Bergman ◽  
P. J. Kittner ◽  
W. W. Pigman

1978 ◽  
Vol 54 (1) ◽  
pp. 69-74 ◽  
Author(s):  
R. Wootton ◽  
J. Reeve ◽  
E. Spellacy ◽  
M. Tellez-Yudilevich

1. Blood flow to the skeleton was measured by the 18F clearance method of Wootton, Reeve & Veall (1976) in 24 patients with untreated Paget's disease. In every patient but one, resting skeletal blood flow was increased. There was a significant positive correlation between skeletal blood flow and serum alkaline phosphatase and between skeletal blood flow and urinary total hydroxyproline excretion. 2. Fourteen patients were re-studied after they had received short-term (7 days or less) or long-term (7 weeks or more) calcitonin. Skeletal blood flow, alkaline phosphatase and urinary hydroxyproline excretion fell towards normal in every case. There was some evidence from the short-term studies that calcitonin produced a more rapid fall in skeletal blood flow than in alkaline phosphatase. 3. Glomerular filtration rate appeared to increase transiently in response to calcitonin.


1975 ◽  
Vol 48 (6) ◽  
pp. 537-540 ◽  
Author(s):  
W. A. Crosbie ◽  
S. M. Mohamedally ◽  
N. J. Y. Woodhouse

1. Twelve patients with symptomatic Paget's disease were studied before starting treatment with salmon calcitonin (12.5 μg) subcutaneously twice daily. Eleven of them were studied again after 3 months on this therapy. 2. Although pretreatment values for urinary total hydroxyproline excretion and cardiac output were considerably increased in some patients, there was no correlation between these two variables in the group as a whole. 3. Treatment resulted in a striking reduction in disease activity; the mean urinary hydroxyproline decreased 67%. 4. There was, however, no significant fall in cardiac output or change in oxygen transport during treatment. 5. Of the eight patients with bone pain who received treatment, five claimed complete pain relief.


1966 ◽  
Vol 96 (4) ◽  
pp. 570-572 ◽  
Author(s):  
Mark Immergut ◽  
C.D. Nordschow ◽  
A.R. Tammes ◽  
R.H. Flocks

1972 ◽  
Vol 55 (2) ◽  
pp. 245-252 ◽  
Author(s):  
D. N. KALU ◽  
CARMEL HILLYARD ◽  
G. V. FOSTER

SUMMARY The effect of glucagon on bone was studied in rats. Urinary hydroxyproline excretion and incorporation of [3H]proline into bone hydroxyproline were used as indices of bone collagen breakdown and formation respectively. Parathyroid extract (15 USP units/rat/h, i.v.), infused into thyroparathyroidectomized animals, increased urinary hydroxyproline excretion. This increase was nullified by simultaneous administration of glucagon (50 μg/rat/h, i.v.). Rats treated with glucagon for 12 days (30 μg/100 g/day, s.c.) excreted slightly less hydroxyproline in their urine than controls. In both intact and thyroparathyroidectomized rats, glucagon (10 μg/100 g/h, s.c.) decreased incorporation of [3H]proline into bone. Similar results were obtained in nephrectomized rats, evidence that changes produced by glucagon were not solely due to alterations in proline pool size caused by increased renal excretion. From these data it is concluded that: (1) glucagon can inhibit bone resorption (the effect being slight in normal rats, but easily demonstrable in parathyroid hormone-treated thyroparathyroidectomized rats), (2) release of endogenous calcitonin is not required to produce this effect, (3) parathyroid hormone and glucagon may act on the same target cell in bone, (4) inhibition of skeletal resorption may contribute to glucagon-induced hypocalcaemia, and (5) the hormone possibly decreases bone formation. Since pharmacological doses of glucagon were used in our studies, the relationship of the observations made to the physiological role of glucagon is unknown.


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