Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “parathyroid hormone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,801 records · Page 100Linked to original sources
PubMed1991

Regulation of glycosaminoglycan synthesis by parathyroid hormone and prostaglandin E2 in cultured dental pulp cells.

The effects of parathyroid hormone (PTH) and prostaglandin E2 (PGE2) on glycosaminoglycan (GAG) synthesis in bovine dental pulp cells were studied. Dibutyryl cyclic adenosine 3',5'-monophosphate and isobutyl methylxanthine were used to assess whether their effects were mediated by intracellular cAMP. Glycosaminoglycan synthesis was assayed by measuring [35S]sulfate incorporation into the GAG fraction of dental pulp cells. Glycosaminoglycan synthesis was increased 1.3-fold by PTH (4 units per ml) alone, 1.6-fold by PTH in the presence of isobutyl methylxanthine, 1.2-fold by PGE2 (100 ng per ml) alone, and 1.5-fold by PGE2 in the presence of isobutyl methylxanthine. Dibutyryl cyclic adenosine 3',5'-monophosphate enhanced GAG synthesis in a concentration-dependent manner and mimicked the effects of PTH and PGE2. The effects of these hormones on pulp and gingival cells were compared; addition of PTH, PGE2, and dibutyryl cAMP had no effect on gingival cell GAG synthesis, whereas their addition induced significant increases of GAG in pulp cells. These results indicate that PTH and PGE2 are involved in the differentiation of dental pulp cells and that these effects are mediated by cAMP.

Animals↗
PubMed1978

Effect of parathyroid hormone and insulin on extracellular cyclic adenosine-3',5'-monophosphate in patients with benign and malignant breast tumors.

Basal excretion of cyclic adenosine monophosphate (cAMP) and its basal level in blood plasma in breast cancer (BC) patients and those with fibroadenomatosis did not differ essentially. However, intravenous injection of parathyroid hormone (100 U) and insulin (0.08 U/kg body weight) was followed by a much less rise in urine-cAMP excretion and blood-cAMP levels in BC patients than in benign process in mammary gland. A substantial correlation between changes in plasma cAMP level and the degree of insulin-induced hypoglycemia was not observed. There was a negative correlation between reponse to parathyroid hormone and insulin and body overweight in BC patients. It was suggested that body fat content may influence the peculiarities of metabolism of extracellular cAMP in cancer patients considerably.

Adipose Tissue↗
PubMed1986

Effect of age on parathyroid hormone and forskolin stimulated adenylate cyclase and protein kinase activity in the renal cortex.

The capacity of parathyroid hormone (PTH) to stimulate the renal production of 1,25-dihydroxyvitamin D declines with age. Since the action of PTH in the kidney is mediated by cAMP, we have examined the effect of PTH and forskolin on renal cortical adenylate cyclase in young (3 months), adult (13-15 months), and old (25-27 months) F344 rats. PTH-dependent adenylate cyclase, measured as cAMP accumulation in cortical slices, was reduced in adult and old rats compared to young rats over a PTH concentration range of 0.015-15 units/ml. There was no difference in PTH-dependent adenylate cyclase activity between adult and old rats. Renal plasma membrane preparations demonstrated similar changes in PTH-stimulated adenylate cyclase activity. There was no difference in calcitonin, forskolin, or guanyl-5-ylimidodiphosphate (Gpp(NH)p) stimulation of adenylate cyclase in plasma membranes from each age group, suggesting that the defect lies in the membrane receptor for PTH. The decreased adult sensitivity to PTH could be reversed by thyroparathyroidectomy. PTH stimulation of cytosolic protein kinase activity did not change with age. These results suggest that the decrease in PTH-dependent adenylate cyclase is due to the alterations at the level of PTH receptor. These alterations may be in response to the increase in serum PTH seen in these animals with increasing age.

Adenylyl Cyclases↗
PubMed1992

Long-term effects of parathyroid operation on serum calcium and parathyroid hormone values in sporadic primary hyperparathyroidism.

BACKGROUND: This study investigates 410 persons (median age, 67 years) who underwent parathyroid operation for sporadic primary hyperparathyroidism 6 to 32 years (mean, 14.2 years) before 1991. METHODS: Patient records and operative specimens were scrutinized, the patients answered a questionnaire, and fasting serum samples were analyzed for calcium, albumin, creatinine, and intact parathyroid hormone (PTH) values. RESULTS: After primary parathyroid operations were performed with a conservative surgical approach, persistent and recurrent hypercalcemia were noticed in 3.7% and 1.7% of patients, respectively, whereas 4.7% of patients required vitamin D substitution or had essentially mild hypocalcemia. The PTH values were generally increased in patients with postoperative hyperparathyroidism, low in those with vitamin D substitution, and normal to elevated in the patients with hypocalcemia and in those with postoperative normocalcemia. The mean serum creatinine concentration was just below the upper reference range and correlated strongly with serum PTH value. No significant differences in serum PTH values were present between the normocalcemic patients and matched control patients after operation (n = 107), but the patients who underwent operation exhibited greater variation in the PTH concentration. CONCLUSIONS: The results substantiate the efficacy of parathyroid operation in sporadic primary hyperparathyroidism. Biochemical derangements compatible with secondary hyperparathyroidism may evolve during long-term follow-up and contribute to decreases in serum calcium values and increases in serum PTH values of these patients.

Adolescent↗
PubMed1996

High-normal calcium (1.35 mmol/l) dialysate in patients on CAPD: efficient and safe long-term control of plasma calcium, phosphate, and parathyroid hormone.

AIM: The aim of the present study was to examine the long-term efficacy and safety of treatment with a high-normal calcium dialysate with a calcium concentration of 1.35 mmol/l in patients on CAPD. This dialysate calcium concentration is close to the high-normal plasma ionized calcium level aimed at in dialysis patients in order to suppress the parathyroid hormone secretion. The end-points of the study were (1) plasma ionized calcium (iCa) and phosphate (P) levels, (2) plasma intact parathyroid hormone (PTH) levels, (3) doses of calcium carbonate and alfacalcidol, (4) requirements of Al-containing phosphate binders, and (5) bone mineral density (BMD). RESULTS: Thirty-seven non-selected patients on CAPD treatment were followed for an average of 10 months after switching from a dialysate Ca of 1.75 to 1.35 mmol/l. After 1 week, a significant decrease of mean iCa from 1.26 +/- 0.01 to 1.23 +/- 0.01 mmol/l (P < 0.05) and an increase of median PTH from 80 to 135 pg/ml (P < 0.01) were seen. From the 2nd week and onwards, however, basal levels of iCa and PTH were restored and remained stable. mean plasma iCa was kept within 1.23-1.31 mmol/l; mean plasma P below 1.65 mmol/l and median PTH within 52-135 pg/ml. Episodes of hypercalcaemia were few (1.2 cases of plasma iCa > 1.45 mmol/l per 100 treatment weeks), and the need for Al-containing P binders low with only five patients requring this treatment for isolated and four patients for repeated episodes of hyperphosphataemia or hypercalcaemia. After switching from a dialysate Ca of 1.75 to 1.35 mmol/l, the doses of calcium carbonate and alfacalcidol could be significantly increased. Furthermore, using the dialysate Ca of 1.35 mmol/l made it possible to induce a controlled increase of PTH levels to 80-100 pg/ml by a temporarily discontinuation of alfacalcidol and/or a reduction of calcium carbonate dosage in the patients where PTH had become suppressed to levels below the upper normal limit. The intention of the treatment was to maintain PTH levels within 1.5-2.5 times the upper normal limit for non-uraemic patients. Pre-study BMD of the vertebral bodies L2-L4 and of the femoral neck were normal and not significantly different from post-study measurements. CONCLUSION: The present study demonstrated that when using a high-normal dialysate Ca concentration of 1.35 mmol/l in non-selected patients on CAPD treatment, high-normal plasma iCa and near-normal plasma P levels could be readily achieved with a minimal risk of incidental hypercalcaemia despite use of calcium carbonate as the main P binder. As a consequence of the tight Ca and P regulation, minimal doses of alfacalcidol were required to keep PTH within acceptable limits. We recommend this dialysate Ca concentration as a first-choice therapy for the majority of patients starting on CAPD treatment.

Adult↗
PubMed2006

The parathyroid hormone family of peptides: structure, tissue distribution, regulation, and potential functional roles in calcium and phosphate balance in fish.

Parathyroid hormone (PTH) and PTH-related protein (PTHrP) are two factors that share amino acid sequence homology and act via a common receptor. In tetrapods, PTH is the main endocrine factor acting in bone and kidney to regulate calcium and phosphate. PTHrP is an essential paracrine developmental factor present in many tissues and is involved in the regulation of ossification, mammary gland development, muscle relaxation, and other functions. Fish apparently lack an equivalent of the parathyroid gland and were long thought to be devoid of PTH. Only in recent years has the existence of PTH-like peptides and their receptors in fish been firmly established. Two forms of PTH, two of PTHrP, and a protein with intermediate characteristics designated PTH-L are encoded by separate genes in teleost fish. Three receptors encoded by separate genes in fish mediate PTH/PTHrP actions, whereas only two receptors have so far been found in terrestrial vertebrates. PTHrP has been more intensively studied than PTH, from lampreys to advanced teleosts. It is expressed in many tissues and is present in high concentration in fish blood. Administration of this peptide alters calcium metabolism and has marked effects on associated gene expression and enzyme activity in vivo and in vitro. This review provides a comprehensive overview of the physiological roles, distribution, and molecular relationships of the piscine PTH-like peptides.

Animals↗
PubMed2000

A conserved cis-acting element in the parathyroid hormone 3'-untranslated region is sufficient for regulation of RNA stability by calcium and phosphate.

Calcium and phosphate regulate parathyroid hormone (PTH) gene expression post-transcriptionally by changes in protein-PTH mRNA 3'-untranslated region (UTR) interactions, which determine PTH mRNA stability. We have identified the protein binding sequence in the PTH mRNA 3'-UTR and determined its functionality. The protein-binding element was identified by binding, competition, and antisense oligonucleotide interference. The sequence was preserved among species suggesting its importance. To study its functionality in the context of another RNA, a 63-base pair cDNA PTH sequence was fused to the growth hormone (GH) gene. There is no parathyroid (PT) cell line and therefore an in vitro degradation assay was used to determine the stability of transcripts for PTH, GH, and a chimeric GH-PTH 63 nucleotides with PT cytosolic proteins. The full-length PTH transcript was stabilized by PT proteins from rats fed a low calcium diet and destabilized by proteins from rats fed a low phosphate diet, correlating with PTH mRNA levels in vivo. These PT proteins did not affect the native GH transcript. However, the chimeric GH transcript was stabilized by low calcium PT proteins and destabilized by low phosphate PT proteins, similar to the PTH full-length transcript. Therefore, we have identified a PTH RNA-protein binding region and shown that it is sufficient to confer responsiveness to calcium and phosphate in a reporter gene. This defined element in the PTH mRNA 3'-UTR is necessary and sufficient for the regulation of PTH mRNA stability by calcium and phosphate.

3' Untranslated Regions↗
PubMed1979

Plasma cyclic-AMP response to parathyroid hormone in Turner's syndrome and Albright's hereditary osteodystrophy.

Purified bovine parathyroid hormone (BPTH) given by injection to five patients with Turner's syndrome, and seven healthy volunteers produced a significant rise in plasma cyclic AMP reacing a maximum within 10 min. In a pseudohypoparathyroid patient there was no increase. Urinary excretion of cyclic AMP exceeded the normal in three out of four patients with Turner's syndrome. Thus, if there is a relationship between Turner's syndrome and Albright's osteodystrophy it is with the incomplete form known as pseudo-pseudohypoparathyroidism.

Adult↗
PubMed1994

Single-dose cholecalciferol suppresses the winter increase in parathyroid hormone concentrations in healthy older men and women: a randomized trial.

A randomized double-blind controlled trial of a single oral dose of 2.5 mg (100,000 IU) cholecalciferol (vitamin D3) was conducted in the winter in 189 healthy free-living men and women aged 63-76 y. The mean baseline serum concentration for 25-hydroxyvitamin D was 34.5 nmol/L and for parathyroid hormone 3.18 pmol/L. After 5 wk, mean serum 25-hydroxyvitamin D concentrations were 60% higher in the treated than in the placebo group (P < 0.001). There was a 12% difference in parathyroid hormone concentrations in the treated compared with the placebo group (P < 0.001). No differences in serum calcium were seen. Findings suggest that 25-hydroxyvitamin D has a physiological role in the regulation of parathyroid secretion independent of serum calcium in healthy elderly people. Parathyroid concentrations rise and 25-hydroxyvitamin D concentrations decline with age. These results may have implications for the prevention of osteoporotic fractures that occur with increased frequency in winter and in elderly people.

Aged↗
PubMed1997

Reconstitution of calcium-regulated parathyroid hormone secretion from streptolysin-O-permeabilized parathyroid cells by guanosine 5'-O-(thio)triphosphate.

Intracellular Ca2+ levels determine the amount of PTH secretion from parathyroid cells. Dissociated calf parathyroid cells were permeabilized with streptolysin-O (SLO) to provide an in vitro model system to examine Ca(2+)-dependent regulation of hormone secretion. PTH release from these cells was energy dependent and increased by cytosolic cofactors. Guanosine 5'-O-(thio)triphosphate (GTP gamma S) increased PTH secretion from SLO-permeabilized cells in a dose-dependent manner from 0.1-100 microM. In the absence of GTP gamma S there was no relationship between the ambient Ca2+ concentration and the rate of PTH secretion. However, in the presence of GTP gamma S, intracellular Ca2+ inhibited PTH secretion with an EC50 of approximately 0.1 microM, corresponding to physiological intracellular Ca2+ levels. Thus, the addition of GTP gamma S to SLO-permeabilized parathyroid cells reconstituted the inverse relationship between extracellular Ca2+ and PTH secretion that is observed in vivo and in intact cells. The data indicate that this effect is mediated at least in part by heterotrimeric guanosine triphosphatases. In addition, calcium/calmodulin-dependent protein kinase II appears to mediate low Ca(2+)-dependent PTH secretion from these cells.

Animals↗
PubMed1994

Production of human parathyroid hormone by recombinant Escherichia coli TG1 on synthetic medium.

Production of human parathyroid hormone (hPTH) by Escherichia coli TG1:I52cIts was studied. The hPTH is expressed as a fusion protein under control of the bacteriophage lambda pR promoter. The organism grows on glucose/mineral salt medium and the expression of the gene product was investigated under variation of temperature and growth rate prior to and after induction. hPTH formation largely depends on cultivation temperature and is optimal for a temperature shift from 30 to 38 degrees C. Product expression is growth coupled and specific hPTH concentration is independent of growth rate. The results are compared with a previous study on E. coli N4830:pEX-PPTH grown on complex media.

Culture Media↗
PubMed1984

Photoaffinity labeling of parathyroid hormone receptors: comparison of receptors across species and target tissues and after desensitization to hormone.

Cells derived from human giant cell tumors of bone and fibroblasts derived from human neonatal foreskin respond to parathyroid hormone (PTH) by increasing the intracellular and extracellular levels of adenosine cyclic 3',5'-phosphate (cAMP). Using photoaffinity labeling methods, we examined these cells for the presence of a PTH receptor or a binding subunit of a receptor complex. A previously designed biologically active and photolabile radioligand analogue of PTH was reacted with these intact cells. After photolysis, the cells were extracted, and the proteins were denatured, reduced, and separated by electrophoresis on sodium dodecyl sulfate (Na-DodSO4)-polyacrylamide gels followed by autoradiography. A single membrane component, Mr 70 000, was labeled specifically in intact cells cultured from skeletal and dermal tissue. By mixing, in pairs, photolabeled proteins from (a) intact human cells derived from giant cell tumors of bone, (b) intact human fibroblasts, and (c) canine renal cortical membranes, the receptors (or their binding subunits) for PTH were compared directly and found to be identical in terms of molecular size (as determined by the migration position on NaDod-SO4-polyacrylamide gels) across species (dog and human) and target tissue (bone, skin, and kidney). Preincubation of cells cultured from giant cell tumors of bone with PTH resulted in loss of the PTH-induced cAMP response (desensitization). Preincubation with PTH was accompanied by a marked decrease in photoaffinity labeling of the PTH binding component and suggests that the loss of hormone response in cells preincubated with PTH was related to a decrease in the number or availability of PTH receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Affinity Labels↗
PubMed1983

The influence of aluminium on parathyroid hormone levels in haemodialysis patients.

In order to investigate the relationship between parathyroid hormone (PTH) and aluminium we studied 86 haemodialysis patients whom we separated into three groups according to their serum PTH values. Group I: PTH less than 600ng/L; Group II: PTH 600-900ng/L; Group III: PTH greater than 900ng/L. A significant difference was found between Groups I and III in the serum aluminium (Group I: 4.85 mumol/L; Group III: 2.84 mumol/L, p less than 0.003) and serum calcium (Group I: 2.43mmol/L; Group III: 2.32mmol/L, p less than 0.0125). The association of higher serum aluminium and calcium with lower PTH concentrations suggests that aluminium can suppress PTH release through an elevation of the serum calcium.

Adolescent↗
PubMed1985

The vasorelaxant action of parathyroid hormone fragments on isolated rat tail artery.

Previous studies have demonstrated that parathyroid hormone (PTH) and its 1-34 amino terminal fragment possess a hypotensive action in vivo which appeared to be direct and dose-dependent. However, attempts to demonstrate the phenomenon in isolated vascular tissue have been minimally successful at best. The present study reports that bovine PTH-(1-34) can relax isolated rat tail artery helical strips precontracted by either arginine vasopressin, depolarizing concentrations of potassium chloride, or norepinephrine. The phenomenon occurs in a dose-dependent manner and is not dependent upon the presence of the endothelial lining of the vessels. These studies support the hypothesis that bovine PTH-(1-34) produces a direct vasorelaxant action mainly in small arteries.

Animals↗
PubMed2000

Comparison of parathyroid hormone in angiographically-demonstrated coronary artery disease patients and healthy Thais.

Parathyroid hormone (PTH) influences the calcium metabolism. The idea of cardiovascular effects of PTH is not new. Target cells for PTH are cardiomyocytes and smooth muscle cells. Evidence from previous studies suggest that many patients with heart disease have elevated PTH concentrations. Our objective was to determine PTH status in patients with coronary artery disease (CAD). We compared intact PTH levels in 109 CAD patients with 103 healthy people by electrochemiluminescence immunoassay. Mean values of PTH in healthy Thais and CAD patients were 37.4 +/- 17.9 and 40.2 +/- 21.8 respectively. No statistical difference was shown. In addition, we compared PTH levels among various numbers of coronary occlusion and also found no differences. We propose that intact PTH concentrations in CAD patients are not higher than in the healthy population.

Aged↗
PubMed1987

Effects of calcium and parathyroid hormone on prostacyclin synthesis by vascular tissue.

Prostacyclin generation by rat aortic rings was studied at different calcium concentrations. Extracellular calcium influenced prostacyclin synthesis, as reflected by the release of 6-keto-PGF1 alpha into the medium, in a concentration-dependent fashion. Calcium levels beyond the physiological range (1.12-1.25 mM unbound calcium) markedly stimulated 6-keto-PGF1 alpha production when compared with calcium-free solutions. On the other hand, addition of purified parathyroid hormone did not change 6-keto-PGF1 alpha production at any calcium concentration tested. These data suggest that parathyroid hormone has no direct effect on prostacyclin synthesis by vascular tissue, although it might influence prostacyclin generation through changes in extracellular calcium levels.

Animals↗
PubMed2001

Effect of parathyroid hormone (hPTH[1-84]) treatment on bone mass and strength in ovariectomized rats.

Skeletal fragility in osteoporotic patients is a prominent underlying cause of low-trauma fractures of most bone sites in humans. Clinical research is now focused on developing treatment strategies, including anabolic agents such as parathyroid hormone (PTH), to recover osteoporosis-related bone loss. Female Sprague-Dawley rats (4.5 mo old) were allowed to become osteopenic for 10 wk postovariectomy. Eight rats were killed at the time of ovariectomy (-10 wk) as a baseline control; sham and ovariectomized (OVX) groups were killed at wk 0. Eight rats per group (sham, OVX + vehicle, OVX + hPTH [5 d/wk], and OVX + hPTH [3 d/wk]) were killed after 4, 8, 14, and 20 wk of treatment with 50 microg/kg of human parathyroid hormone (hPTH[1-84]). Bone mineral content and density were measured only in the vertebral body. Bone strength was evaluated in the vertebral body, femoral diaphysis, femoral neck, and distal femur. Significant, lasting osteopenia developed in the vertebral body of OVX rats by 10 wk postovariectomy. Bone mineral density of the vertebral body partially recovered by 8 wk and fully recovered to that seen in sham animals only by 20 wk posttreatment with either a 5 or 3 d/wk dosing schedule of PTH[1-84]. Therefore, hPTH[1-84] (50 microg/kg) given either 3 or 5 d/wk fully restores vertebral and femoral bone strength in osteopenic OVX rats.

Animals↗
PubMed1991

Direct and indirect assessment of the parathyroid hormone response to pamidronate therapy in Paget's disease of bone and hypercalcaemia of malignancy.

In patients with either Paget's disease or hypercalcaemia associated with malignancy (HCM) we have assessed the parathyroid response to pamidronate therapy, both by immunoassay of serum intact parathyroid hormone PTH (1-84) and by measurement of indirect parameters of PTH bioactivity, tubular maximum reabsorption of phosphate (TmPO4/GFR) and nephrogenous cyclic AMP (NcAMP). In 12 patients with Paget's disease, therapy with pamidronate produced a small but significant decrease in adjusted serum calcium within the reference interval which was accompanied by a progressive increase in PTH (1-84) secretion and a corresponding fall in TmPO4/GFR and increase in NcAMP. In 12 patients with HCM pretreatment, PTH (1-84) concentrations were suppressed, whilst mean TmPO4/GFR was reduced and NcAMP was increased, compatible in most patients, with parathyroid hormone-related peptide (PTHrP) driven hypercalcaemia. Therapy with pamidronate produced the expected fall in serum calcium but caused an increase in PTH (1-84) secretion in the presence of absolute hypercalcaemia. The initial subnormal TmPO4/GFR decreased further to a nadir on day 5, and there was a corresponding further increase in NcAMP. By day 7, however, when PTH (1-84) concentrations were maximal, there was a significant paradoxical rise in TmPO4/GFR and a corresponding decrease in NcAMP. These data are consistent with a variable trigger point for PTH (1-84) secretion, one consequence of which is a reduction in the risk of hypocalcaemia following pamidronate. The results have major clinical implications for the interpretation of PTH (1-84) measurements in patients who are being treated or about to be treated for bone disease or for hypercalcaemia of malignancy (HCM).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Refine your search to explore more results.