Vitamin D Metabolism and Parathyroid Function in Man

1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)D3 <2.5 nmol/l (10 ng/ml)], serum labelled 1,25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable in vitamin D-replete individuals, who appeared to form labelled 24,25-(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immuno-reactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated molar concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone.

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Adaptation of vitamin D metabolism to calcium challenge: is it dependent on parathyroid hormone?

Acta Endocrinologica ◽

10.1530/acta.0.120s122 ◽

1989 ◽

Vol 120 (3_Suppl) ◽

pp. S122-S123

Author(s):

S. H. SCHARLA ◽

H. W. MINNE ◽

U. G. LEMPERT ◽

C. OSWALD ◽

H. SCHMIDT-GAYK ◽

...

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Vitamin D Metabolism

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Effects of Chlorothiazide Administration and Dietary Calcium Restriction on Parathyroid Function, Vitamin D Metabolism and Intestinal Calcium Absorption in the Rat

Advances in Experimental Medicine and Biology - Regulation of Phosphate and Mineral Metabolism ◽

10.1007/978-1-4684-4259-5_54 ◽

1982 ◽

pp. 501-507

Author(s):

Murray J. Favus ◽

Fredric L. Coe ◽

Satish C. Kathpalia ◽

Asher Porat ◽

Prabir K. Sen ◽

...

Keyword(s):

Vitamin D ◽

Calcium Absorption ◽

Dietary Calcium ◽

Intestinal Calcium Absorption ◽

Vitamin D Metabolism ◽

Parathyroid Function

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Abnormal parathyroid hormone stimulation of 25-hydroxyvitamin D-1 alpha-hydroxylase activity in the hypophosphatemic mouse. Evidence for a generalized defect of vitamin D metabolism.

Journal of Clinical Investigation ◽

10.1172/jci112274 ◽

1986 ◽

Vol 77 (1) ◽

pp. 181-187 ◽

Cited By ~ 51

Author(s):

T Nesbitt ◽

M K Drezner ◽

B Lobaugh

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Hydroxylase Activity ◽

Vitamin D Metabolism ◽

Hormone Stimulation ◽

Hydroxyvitamin D ◽

25 Hydroxyvitamin D ◽

Stimulation Of

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REGULATION OF VITAMIN-D METABOLISM WITHOUT PARATHYROID HORMONE

The Lancet ◽

10.1016/s0140-6736(73)90794-0 ◽

1973 ◽

Vol 302 (7824) ◽

pp. 289-291 ◽

Cited By ~ 43

Author(s):

R.G. Larkins ◽

KayW. Colston ◽

LeonoraS. Galante ◽

S.J. Macauley ◽

ImogenM.A. Evans ◽

...

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Vitamin D Metabolism

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Adaptation of intestinal calcium absorption: Parathyroid hormone and vitamin D metabolism

Archives of Biochemistry and Biophysics ◽

10.1016/0003-9861(78)90368-5 ◽

1978 ◽

Vol 188 (1) ◽

pp. 157-163 ◽

Cited By ~ 10

Author(s):

M.L. Ribovich ◽

H.F. DeLuca

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Calcium Absorption ◽

Intestinal Calcium Absorption ◽

Vitamin D Metabolism

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Bioactive parathyroid hormone in pregnant rats and fetuses

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.258.4.e549 ◽

1990 ◽

Vol 258 (4) ◽

pp. E549-E554 ◽

Cited By ~ 4

Author(s):

A. Bourdeau ◽

G. Manganella ◽

C. L. Thil-Trubert ◽

C. Sachs ◽

G. Cournot

Keyword(s):

Parathyroid Hormone ◽

Plasma Calcium ◽

Ether Anesthesia ◽

Pregnant Rats ◽

Calcium Gradient ◽

Osteoclast Number ◽

Cytochemical Bioassay ◽

Parathyroid Function ◽

Immunoreactive Parathyroid Hormone ◽

Intact Rats

Parathyroid function at the end of gestation (day 21) was investigated by measuring plasma calcium (PCa), immunoreactive parathyroid hormone (iPTH), bioactive parathyroid hormone (bioPTH; cytochemical bioassay), and bone histology in intact and thyroparathyroidectomized (TPTX; day 12, ether anesthesia) rats and their fetuses. In pregnant intact rats, PCa was significantly lower, and iPTH, bioPTH, and osteoclast number were higher than in nonpregnant rats. In fetuses, PCa was higher than maternal PCa and correlated with fetal bioPTH. TPTX suppressed maternal bioPTH and decreased iPTH and osteoclast number, whereas fetal iPTH and bioPTH were decreased with no change in osteoclast number. Fetal PCa was near normal and was correlated with maternal PCa but not with fetal bioPTH. The fetomaternal calcium gradient was maintained and even increased. This study shows that there is maternal physiological hyperparathyroidism and functional fetal parathyroid glands at the end of gestation in the rat. Parathyroid hormone does not seem to be responsible for maintaining the high fetomaternal calcium gradient in TPTX animals.

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Prolactin stimulation of parathyroid hormone secretion in bovine parathyroid cells

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1984.247.5.e675 ◽

1984 ◽

Vol 247 (5) ◽

pp. E675-E680 ◽

Cited By ~ 1

Author(s):

L. Magliola ◽

L. R. Forte

Keyword(s):

Parathyroid Hormone ◽

Hormone Secretion ◽

Vitamin D Metabolism ◽

Parathyroid Function ◽

Wide Range ◽

Camp Levels ◽

Bovine Species ◽

Ca Homeostasis

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.

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Role of prolactin in vitamin D metabolism and calcium absorption during lactation in the rat

Journal of Endocrinology ◽

10.1677/joe.0.0940443 ◽

1982 ◽

Vol 94 (3) ◽

pp. 443-453 ◽

Cited By ~ 53

Author(s):

C. J. Robinson ◽

E. Spanos ◽

M. F. James ◽

J. W. Pike ◽

M. R. Haussler ◽

...

Keyword(s):

Vitamin D ◽

Alkaline Phosphatase ◽

Parathyroid Hormone ◽

Alkaline Phosphatase Activity ◽

Plasma Levels ◽

Calcium Absorption ◽

High Plasma ◽

Intestinal Calcium Absorption ◽

Vitamin D Metabolism

Intestinal calcium absorption and plasma levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were measured in lactating and non-lactating rats and the effects of bromocriptine and exogenous prolactin treatment were evaluated. In lactating rats calcium absorption and plasma levels of parathyroid hormone, 1,25(OH)2D3 and alkaline phosphatase activity were significantly increased. Bromocriptine treatment significantly reduced the enhanced calcium absorption and levels of plasma 1,25(OH)2D3 and alkaline phosphatase but had no significant effect on plasma levels of parathyroid hormone. Prolactin administered with bromocriptine to lactating animals prevented all the changes observed with bromocriptine treatment alone. It was concluded that the increased plasma levels of prolactin during lactation lead to high plasma levels of 1,25(OH)2D3 which are responsible for the enhanced intestinal calcium absorption.

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REGULATORY HYPERPARATHYROIDISM IN A PIG BREED WITH VITAMIN D DEPENDENCY RICKETS

Acta Endocrinologica ◽

10.1530/acta.0.0920295 ◽

1979 ◽

Vol 92 (2) ◽

pp. 295-308 ◽

Cited By ~ 12

Author(s):

R. Wilke ◽

J. Harmeyer ◽

C. von Grabe ◽

R. Hehrmann ◽

R. D. Hesch

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Binding Assay ◽

Clinical Symptoms ◽

Plasma Concentrations ◽

Fold Increase ◽

Protein Binding Assay ◽

Deficiency Rickets ◽

Clinical Healing ◽

Immunoreactive Parathyroid Hormone

ABSTRACT A radioimmunoassay for porcine parathyroid hormone has been developed and applied to measure immunoreactive parathyroid hormone (PTH) in plasma of pigs with hereditary vitamin D dependency rickets (VDDR) (pseudovitamin D deficiency rickets). Levels of 25-hydroxycholecalciferol (25-(OH)-D3) in plasma were measured by a protein binding assay. Both plasma concentrations of PTH and 25-(OH)-D3 showed an approximately 4-fold increase compared to normal pigs. PTH levels increased with duration of the disease. Daily dosing of the animals with 1–4 μg of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) reduced PTH concentrations and resulted in clinical healing. Iv administration of 10 μg of 25-(OH)-D3/day did not alter PTH concentrations nor the clinical symptoms. The results suggest that these animals suffer from regulatory hyperparathyroidism. The metabolic defect could be due to a failure of the kidney to convert 25-(OH)-D3 to 1,25-(OH)2-D3.

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