Lack of influence of 24,25-dihydroxyvitamin D3 on parathyroid hormone secretion from normal or hyperplastic glands

1983 ◽  
Vol 35 (1) ◽  
pp. 449-454 ◽  
Author(s):  
Marcos Rothstein ◽  
Klaus Olgaard ◽  
Mario Arbelaez ◽  
Delmar Finco ◽  
Saulo Klahr ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Dihydroxyvitamin D3 ◽  
24,25 Dihydroxyvitamin D3

Effect of vitamin D3, 25-hydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 on parathyroid hormone secretion

1987 ◽  
Vol 41 (1) ◽  
pp. 48-51 ◽  
Author(s):  
Larry K. Cantley ◽  
John B. Russell ◽  
Deborah S. Lettieri ◽  
Louis M. Sherwood
Keyword(s):  
Parathyroid Hormone ◽  
Vitamin D3 ◽  
Hormone Secretion ◽  
Dihydroxyvitamin D3 ◽  
24,25 Dihydroxyvitamin D3

Regulation of parathyroid hormone secretion by plasma calcium in aging rats

1991 ◽  
Vol 260 (2) ◽  
pp. E220-E225 ◽  
Author(s):  
J. Fox
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Fold Increase ◽  
Male Rats ◽  
Aged Rats ◽  
Adult Rats ◽  
Dihydroxyvitamin D3 ◽  
Set Point ◽  
Skeletal Resistance ◽  
Immunoreactive Parathyroid Hormone

Plasma immunoreactive parathyroid hormone (irPTH) levels increase with aging. This study determined 1) whether NH2-terminal irPTH secretory responses to induced hypocalcemia differ between adult (6-mo-old) and aged (24- to 26-mo-old) male rats and 2) whether a higher set point for irPTH release by Ca is responsible for the elevated irPTH levels with aging. Basal irPTH levels were 68% higher and 1,25-dihydroxyvitamin D3 levels were 44% lower in aged rats. An acutely induced, constant hypocalcemic stimulus [0.32 mM decrement in ionized Ca (Ca2+) for 2 h] was developed in catheterized conscious adult and aged rats by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) infusion using the Ca clamp technique. The initial irPTH secretory response to acute hypocalcemia (5-10 min) was reduced in aged rats (1.9- vs. 3.1-fold increase), suggesting reduced hormone stores. However, higher sustained irPTH levels (30 min to 2 h) were maintained in aged rats, indicating increased irPTH synthesis and release. The EGTA infusion rate necessary to maintain constant hypocalcemia was less in aged rats, suggesting skeletal resistance to PTH. Slow EGTA and Ca infusions were used to determine irPTH secretion at plasma Ca2+ levels from 0.7 to 1.5 mM. In aged rats, irPTH levels were higher at all Ca2+ concentrations, but the set point for irPTH release by Ca2+ was the same as in adult rats. Thus the elevated irPTH secretion in aged rats is not caused by a change in the set point for irPTH release but does result in decreased irPTH stores.

Interaction of 24,25-Dihydroxyvitamin D3 and parathyroid hormone on bone enzymes in vitro

1979 ◽  
Vol 27 (1) ◽  
pp. 47-52 ◽  
Author(s):  
M. Lieberherr ◽  
M. Garabédian ◽  
H. Guillozo ◽  
M. Bailly du Bois ◽  
S. Balsan
Keyword(s):  
Parathyroid Hormone ◽  
Dihydroxyvitamin D3 ◽  
24,25 Dihydroxyvitamin D3

Influence of estrogen on renal vitamin D hydroxylases and serum 1alpha,25-(OH)2D3 in chicks.

1978 ◽  
Vol 235 (3) ◽  
pp. E338 ◽  
Author(s):  
J W Pike ◽  
E Spanos ◽  
K W Colston ◽  
I MacIntyre ◽  
M R Haussler
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Vitamin D3 ◽  
Steroid Treatment ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Chick Kidney ◽  
24,25 Dihydroxyvitamin D3

The influence of estrogen on the metabolism of 25-hydroxyvitamin D3 was studied in 2- to 5-wk-old chicks. Single injections of at least 500 microgram diethylstibestrol (DES) increased the conversion of 25-hydroxyvitamin D3 to 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) and suppressed the production of 24,25-dihydroxyvitamin D3 in chick kidney homogenates. Acute (one 5-mg) injections of testosterone or progesterone did not enhance the 25-hydroxyvitamin D3-1alpha-hydroxylase, indicating specificity. However, chronic pretreatment with DES appeared to allow the potentiation of previously unstimulatory steroids such as progesterone and testosterone. In addition, the hormonal metabolite of vitamin D3, 1alpha,25-(OH)2D3, was measured in 4- to 6-wk chick plasma after steroid treatment. Greater than 1 mg DES per day for 5 days was necessary to enhance the circulating level of 1alpha,25-(OH)2D3; testosterone alone had no effect. This elevation was rapid, occurring within 12--24 h after injection. These data suggest that estrogen (as evidenced by DES treatment) is a modulator of vitamin D metabolism along with other known regulators such as parathyroid hormone, phosphate, and 1alpha,25-(OH)2D3. The mechanism of the regulation is as yet unknown.

Idiopathic Hypoparathyroidism: A Case Study on the Interactions Between Exogenous, Parathyroid Hormone Infusion and 1,25-Dihydroxyvitamin D

PEDIATRICS ◽  
1986 ◽  
Vol 78 (6) ◽  
pp. 1139-1141
Author(s):  
FERNANDO SANTOS ◽  
JAMES C. M. CHAN
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Calcium Excretion ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Hormone Administration ◽  
Urine Calcium Excretion

Idiopathic hypoparathyroidism is a rare entity which is clinically characterized by episodes of hypocalcemia and hyperphosphatemia with deficient endogenous parathyroid hormone secretion.1,2 Exogenous parathyroid hormone administration elicits the appropriate renal phosphaturic response,3,4 and no associated endocrinopathies have been reported.1,2 Treatment with 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is currently recommended.1,2,5 Responses to exogenous parathyroid hormone infusion consist not only of an increase in urine phosphate excretion but, more definitively, an increase in nephrogenous cyclic adenosine monophosphate (cAMP) production.6 Studies of these parameters in pediatric patients have been reported,3 but little is known about the influence of parathyroid hormone administration on the urine calcium excretion of hypoparathyroidism in children and how the renal response to parathyroid hormone may be modified by the 1,25-(OH)2D3 therapy.

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