Interrelationship of Parathyroid and Adrenocortical Function in Calcium Homeostasis in the Rat

Williams, George C.; Peterson, William C.; Bowser, E. N.; Henderson, W. J.; Hargis, G. K.; Martinez, Norberto J.

doi:10.1210/endo-95-3-707

Cited by 60 publications

(20 citation statements)

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“…Functionally, the present data appear consistent with those obtained in other experimental models where excessive PTH secretion was induced in rats [ Williams et al, 1974] and man [Fucik et al, 1975] after acute or chronic treatment with glucocor- Fig.6, 7. Details of chief cells front triamcinolonetreated baboons.…”

Section: Discussionsupporting

confidence: 92%

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Fine structure of the parathyroid glands in baboons, <i>Papio hamadryas</i> in response to experimental hypercorticoidism

Coleman¹,

Silbermann²,

Bernheim³

1980

Cells Tissues Organs

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Female baboons maintained under laboratory conditions were subjected to a series of 10 weekly injections (4 mg/kg body weight) of the synthetic glucocorticoid, triamcinolone hexacetonide. In response to the treatment, serum immunoreactive parathyroid hormone (PTH) levels were raised, though blood calcium levels remained within normal physiological limits. Light and electron-microscopic studies were made on the parathyroid glands at the end of the experimental period. The baboon parathyroid glands were composed of ‘light’ and ‘dark’ forms of the chief cells in varying ratios from gland to gland even within a single animal. Glucocorticoid-induced parathyroid hyperactivity as measured by circulating PTH levels was not accompanied by cellular hypertrophy, though there was an increase in the relative number of ‘light’ cells. At the ultrastructural level, after treatment, many of the ‘light’ cells were found to contain more free ribosomes, larger profiles of granular endoplasmic reticulum and had better developed mitochondria. Interdigitations between adjacent chief cells were more complex in treated glands. Apart from these features, chief cells of treated glands were basically similar to those of untreated controls. Our study showed that functional parathyroid hyperactivity in baboons is not necessarily accompanied by significant ultrastructural changes in chief cells.

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Section: Discussionsupporting

confidence: 92%

“…The effects of glucocorticoids on parathyroid gland function have now been described in vivo and in vitro [Jee et al, 1972;Williams et al, 1974;Fucik et al, 1975;An, 1976;Kukrejaei al., 1976;Coleman and Silbermann, 1978].…”

Section: Introductionmentioning

confidence: 99%

Fine structure of the parathyroid glands in baboons, <i>Papio hamadryas</i> in response to experimental hypercorticoidism

Coleman¹,

Silbermann²,

Bernheim³

1980

Cells Tissues Organs

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“…Elevated iPTH values in rats (39) and humans (5,40,41) after administration of supraphysiologic doses of glucocorticoids have been reported. In the present study, we found no increase in serum iPTH when euglucocorticoid and hyperglucocorticoid values were compared using a radioimmunoassay system that is highly sensitive to increases in parathyroid gland function (26).3 Inasmuch as PTH regulates 25-OH-D 1-hydroxylase activity (42), the absence of secondary hyperparathyroidism is further evidence against a major reduction in availability of 1,25(OH)2D in hyperglucocorticoidism.…”

Section: Discussionmentioning

confidence: 99%

Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.

Kumar²,

et al. 1980

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A B S T R A C T The decreasedl intestinal absorption of calcium and accelerated l)one loss associate(l with chronic glucocorticoid excess may be mediated by changes in vitamin D metabolism, leading to dlecreased availability of circulating 1,25-dihydroxyvitamin D. This hypothesis was examined in 14 patients with either endogenous or exogenous glucocorticoid excess. Analysis of paired serum samples (mean ±SE) in 13 patients duiring euglucocorticoidlisml-and dutring hyperglucocorticoidism showed that glucocorticoid excess resulted in small decreases of plasma 25-hydroxyvitamin D concentrations (22+2-18±2 ng/ml; P < 0.05) lbut no significant chaniges in plasmiia 1,25-dihydroxyvitamini D (32 ± 8-23±+46 pg/ml) or serum immunoreactive parathyroi(l hormone (21±2-18±2 ,uleq/ml). Additionally, we studied plasmna kinetics of[3H] 1 ,25-dihydroxyvitamin D3 after intravenotus bolus administration in 10 hyperglucocorticoid patients and in 14 normal controls. Assessmiient with a threecompartment model showe(d no significant abnormalities in production rates (hyperglucocorticoid patients 1.2±0.3 ,g/d, controls 1.5±0.2 ,ugld) or metabolic clearance rates (hyperglucocorticoid patients, 32 ± 3 ml/ min; controls 31+3 ml/min). Moreover, there were no significant differences in ciumulative excretion of radioactivity in urine (hyperglutcocorticoid patieints 18±2%; controls, 14±2%) or f'eces (hyperglucocorticoid patients, 60±9%, controls, 54+6%). We conclude that glucocorticoid excess does not effect plasma levels, production, or degradation of 1,25(OH)2D in hunIans. Thus, other mechanisms mutst be postulated to explain satisfactorily the abnormialities of bone structure and intestinal calciumn absorption that maiy occur after chronic glucocoi-ticoidl therapy.

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“…Parathyroid hyperplasia and increased PTH levels with the administration of cortisone acetate have been demonstrated in experimental studies on animals (19) and in patients with Cushing's syndrome (20). More recently, Karmali et al (21) suggested that the action of gluco-PTH secretion in endogenous hypercortisolism corticoids on the parathyroids may be caused by a reduction of the number of 1,25-dihydroxyvitamin D receptors, thus reducing the inhibitory activity of 1,25-dihydroxyvitamin D on this gland.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid hormone secretion in chronic human endogenous hypercortisolism

Lanna

Paula

Montenegro

et al. 2002

Braz J Med Biol Res

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Osteoporosis is a common manifestation of Cushing's syndrome, but the mechanisms responsible for this abnormality have not been defined. With the objective of analyzing parathyroid hormone (PTH) secretion in chronic hypercortisolism (CH), we evaluated 11 healthy subjects and 8 patients with CH, 6 with Cushing's disease and 2 with adrenal adenoma. These volunteers were submitted to tests of PTH stimulation through hypocalcemia (EDTA), PTH suppression through hypercalcemia (iv and oral calcium), and evaluation of bone mineral density (BMD) by DEXA. During the test of PTH stimulation, the calcium and magnesium concentrations of the normal and CH groups were similar. Patients with CH showed an increased PTH response to the hypocalcemic stimulus compared to controls. PTH values were significantly higher in the CH group at 70 (17.5 ± 3.5 vs 10.2 ± 1.3 pmol/l, P = 0.04), and 120 min (26.1 ± 5.9 vs 11.3 ± 1.9 pmol/l, P = 0.008) of EDTA infusion. The area under the curve for PTH during EDTA infusion was also significantly higher in patients with CH than in normal subjects (1867 ± 453 and 805 ± 148 pmol l -1 2 h -1 , P = 0.02). During the test of PTH suppression, calcium, magnesium and PTH levels of the patients with hypercortisolism and controls were similar. BMD was decreased in patients with hypercortisolism in the spine (0.977 ± 0.052 vs 1.205 ± 0.038 g/cm 2 in controls, P<0.01). In conclusion, our results show that subjects with CH present decreased bone mass mainly in trabecular bone. The use of dynamic tests permitted the detection of increased PTH secretion in response to a hypocalcemic stimulus in CH patients that may probably be involved in the occurrence of osteoporosis in this state.

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Interrelationship of Parathyroid and Adrenocortical Function in Calcium Homeostasis in the Rat

Cited by 60 publications

References 0 publications

Fine structure of the parathyroid glands in baboons, <i>Papio hamadryas</i> in response to experimental hypercorticoidism

Fine structure of the parathyroid glands in baboons, <i>Papio hamadryas</i> in response to experimental hypercorticoidism

Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.

Parathyroid hormone secretion in chronic human endogenous hypercortisolism

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