Calcium and phosphorus metabolism and nutrition of poultry: are current diets formulated in excess?

2017 ◽  
Vol 57 (11) ◽  
pp. 2304 ◽  
Author(s):  
X. Li ◽  
D. Zhang ◽  
W. L. Bryden

Calcium (Ca) and phosphorus (P) are important nutrients in poultry diet formulations. In the present review, we discuss recent advances in our understanding of the metabolism of Ca and P in poultry. Recent data are provided in support of the proposition that current poultry diets are formulated in excess for Ca and P. The quantities of Ca and P available for metabolism reflect rates of intestinal absorption, bone accretion and resorption, glomerular filtration, renal tubular reabsorption, and intestinal endogenous losses. Ca and P homeostasis is largely under endocrine control. Parathyroid hormone and the hormonal form of vitamin D3 are the two hormones credited with this role. However, a novel hormonal axis involving Fibroblast Growth Factor 23 and Klotho has been recently delineated, which, in conjunction with parathyroid hormone and vitamin D3, tightly regulates Ca and P homeostasis. Recent studies have suggested that current commercial diets for both broilers and layers contain excess Ca and P, the content of which could be reduced without affecting production or bird welfare. The challenge in reducing Ca and P concentrations in poultry diets is the uncertainty about what concentrations of Ca and P can be fed without compromising bird welfare. This is because there are limited data on the available P and Ca concentrations in poultry feedstuffs determined biologically. This is further complicated by the need for agreement on evaluation systems for evaluation of Ca and P bioavailability. We conclude that direct ileal or pre-caecal digestible Ca and P values are preferred.

Metabolism ◽  
1974 ◽  
Vol 23 (8) ◽  
pp. 715-727 ◽  
Author(s):  
Elizabeth M. Short ◽  
Louis J. Elsas ◽  
Leon E. Rosenberg

2019 ◽  
Vol 72 (11) ◽  
pp. 741-747 ◽  
Author(s):  
Jenny Leung ◽  
Martin Crook

Phosphate in both inorganic and organic form is essential for several functions in the body. Plasma phosphate level is maintained by a complex interaction between intestinal absorption, renal tubular reabsorption, and the transcellular movement of phosphate between intracellular fluid and bone storage pools. This homeostasis is regulated by several hormones, principally the parathyroid hormone, 1,25-dihydroxyvitamin D and fibroblast growth factor 23. Abnormalities in phosphate regulation can lead to serious and fatal complications. In this review phosphate homeostasis and the aetiology, pathophysiology, clinical features, investigation and management of hypophosphataemia and hyperphosphataemia will be discussed.


PEDIATRICS ◽  
1972 ◽  
Vol 49 (6) ◽  
pp. 837-840
Author(s):  
Claude Arnaud ◽  
Francis Glorieux ◽  
Charles R. Scriver

The later stages of the vitamin D deficiency syndrome during infancy are associated with impaired renal tubular reabsorption of amino acids, phosphate, and other metabolites. Secondary hyperparathyroidism has been implicated as the cause of the renal abnormality. Serum immunoreactive parathyroid hormone levels are elevated in infants with vitamin D deficiency (60 to 238 µl Eq/ml; normal < 40 µl q/ml). The highest levels were found in the more advanced stages of vitamin D deficiency.


1967 ◽  
Vol 45 (1) ◽  
pp. 103-114 ◽  
Author(s):  
Alfred F. Michael ◽  
Keith N. Drummond

Infusion of certain neutral L-amino acids (alanine, glycine, valine, and tryptophan) into dogs resulted in an inhibition of the renal tubular reabsorption of phosphate and increased phosphate excretion. This was seen in both the parathyroidectomized animal and under conditions of exogenous parathormone infusion, indicating that the phosphaturia induced by amino acids is independent of parathyroid hormone action. This effect was stereospecific and did not occur with D-alanine; no effect was observed after infusion of the basic amino acids L-arginine and L-lysine.


1979 ◽  
Vol 237 (6) ◽  
pp. F415-F423 ◽  
Author(s):  
C. Y. Pak

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25–dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.


1968 ◽  
Vol 40 (4) ◽  
pp. 467-475 ◽  
Author(s):  
P. ADAMS ◽  
T. M. CHALMERS ◽  
B. L. RIGGS ◽  
J. D. JONES

SUMMARY Calcium and phosphorus metabolism were studied in 22 patients with spontaneous primary hypothyroidism. Two patients were found to have hypercalcaemia but the mean serum calcium concentration of the group was significantly less than that of control subjects. The renal tubular reabsorption of phosphate was decreased and could be increased to normal with small calcium infusions. The response to calcium deprivation and to infusions of EDTA was abnormal and suggested an impaired ability to mobilize calcium from bone. There was a significant correlation between the defect in calcium mobilization, as judged from the response to EDTA, and the renal tubular reabsorption of phosphate. In three patients serum parathyroid hormone concentrations, measured by radioimmunoassay, were in the upper part of the normal range. It is suggested that in patients with hypothyroidism the target cells in bone are less responsive to the effects of parathyroid hormone than normal; as a consequence parathyroid hormone secretion may be increased.


1976 ◽  
Vol 51 (4) ◽  
pp. 345-351 ◽  
Author(s):  
R. A. L. Sutton ◽  
N. L. M. Wong ◽  
J. H. Dirks

1. The effect of purified bovine parathyroid hormone on renal tubular reabsorption of sodium and calcium has been studied by micropuncture in intact and recently thyroparathyroidectomized dogs. 2. Parathyroid hormone increased the rejection of sodium and calcium proportionately at the late proximal tubule in both intact and operated dogs. 3. In both groups of dogs, there was increased delivery of sodium and calcium to the distal tubule after the hormone. However, the Ca/Na ratio decreased, suggesting some selective enhancement of calcium reabsorption before the superficial distal puncture site. 4. In the final urine, the Ca/Na ratio decreased highly significantly in both groups of dogs, indicating a further selective effect of parathyroid hormone on calcium reabsorption in or beyond the distal convoluted tubule.


1988 ◽  
Vol 74 (6) ◽  
pp. 607-612 ◽  
Author(s):  
E. V. McCloskey ◽  
A. J. P. Yates ◽  
R. E. S. Gray ◽  
N. A. T. Hamdy ◽  
J. Galloway ◽  
...  

1. The effects of three intravenous diphosphonates (etidronate, clodronate and aminohexane diphosphonate) on phosphate homoeostasis were studied in 30 patients with Paget's disease of bone and in three patients with hypoparathyroidism. 2. In Paget's disease, all three diphosphonates induced significant increases in serum phosphate and renal tubular reabsorption of phosphate. This effect was most marked and persistent after etidronate, whereas in the clodronate- and aminohexane diphosphonate-treated patients the increases were less, of shorter duration and followed thereafter by significant decreases in serum phosphate and renal tubular reabsorption of phosphate. Unlike etidronate, both clodronate and aminohexane diphosphonate caused a significant reduction in serum and urinary calcium, with appropriate homoeostatic increases in immunoassayable parathyroid hormone. 3. Phosphaturic responses to infused parathyroid hormone were observed in two patients with etidronate-induced hyperphosphataemia. 4. In three hypoparathyroid patients, clodronate induced a more marked increase in serum phosphate and renal tubular reabsorption of phosphate than in Paget‘s disease, which was of comparable degree but of shorter duration than that after etidronate in Paget's disease. 5. These findings suggest that all three diphosphonates increase renal tubular reabsorption of phosphate, but that this effect is attenuated with those diphosphonates which induce secondary hyperparathyroidism.


2020 ◽  
Vol 17 (2) ◽  
pp. 220-227
Author(s):  
Anna K. Eremkina ◽  
Svetlana S. Mirnaya ◽  
Anna M. Gorbacheva ◽  
Taras S. Panevin ◽  
Iya A. Voronkova ◽  
...  

Osteomalacia is a systemic bone disease, characterized by an excessive accumulation of non-mineralized osteoid and an imbalance in the organic matrix formation and mineralization. A rare cause of disease is tumor-induced osteomalacia, most often due to phosphaturic mesenchymal tumors (PMT). Usually there are benign small tumors, affecting the soft tissues and bones of any location. The basic pathogenesis of underlying oncogenic osteomalacia is a decreased renal tubular reabsorption of phosphate consequent to hyperproduction of fibroblast growth factor 23 in PMT. Clinical features are nonspecific, the average period from the symptoms onset to diagnosis reaches 3 years and at least 5 years before surgical treatment. Finding the tumour is crucial, as complete removal is curative. We present a clinical case of tumor-induced osteomalacia due to PMT required the complex differential diagnosis with other rare diseases.


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