PTH(1–84)/PTH(7–84): a balance of power

2006 ◽  
Vol 290 (5) ◽  
pp. F975-F984 ◽  
Author(s):  
Peter A. Friedman ◽  
William G. Goodman
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Bone Histomorphometry ◽  
Bone Biopsy ◽  
Balance Of Power ◽  
Receptor Activation ◽  
Experimental Models ◽  
Failure Diagnosis ◽  
Clinical Aspects ◽  
The Relationship

This review considers many new basic and clinical aspects of parathyroid hormone (PTH). We focus especially on the identification of PTH fragments and how they may relate to renal failure, diagnosis, and treatment of secondary hyperparathyroidism and renal osteodystrophy. The biosynthesis and metabolism of PTH, measurement of circulating forms of PTH, the effects of PTH on receptor activation and turnover, the relationship between PTH levels and bone turnover in renal failure in humans, and the involvement of PTH in experimental models of renal failure are discussed. Despite these developments in understanding the etiology of renal failure and the availability of new assays for bioactive PTH, no adequate surrogate for bone biopsy and quantitative bone histomorphometry has been developed.

Abnormal calcitonin basal levels and pentagastrin response in patients with chronic renal failure on maintenance hemodialysis

1995 ◽  
Vol 132 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Patricia Niccoli ◽  
Philippe Brunet ◽  
Christa Roubicek ◽  
François Roux ◽  
Eric Baudin ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Thyroid Carcinoma ◽  
Maintenance Hemodialysis ◽  
Intact Parathyroid Hormone ◽  
Regulatory Pathway ◽  
Alkaline Phosphatases ◽  
Medullary Thyroid ◽  
The Relationship

Niccoli P, Brunet P, Roubicek C, Roux F, Baudin E, Lejeune P-J, Berland Y, Conte-Devolx B. Abnormal calcitonin basal levels and pentagastrin response in patients with chronic renal failure on maintenance hemodialysis. Eur J Endocrinol 1995;132:75–81. ISSN 0804–4643 Hypercalcitoninemia has been reported in renal failure. Using a specific monomeric calcitonin (CT) immunoassay, we measured CT levels in 154 hemodialyzed patients. The relationship between CT and serum intact parathyroid hormone (PTH), gastrin, alkaline phosphatases, phosphate and calcium was studied. The pentagastrin test was performed in 26 patients exhibiting basal hypercalcitoninemia. Basal CT levels over 5.7 pmol/l (20 ng/l) were found in 25.3% of the patients and values higher than 26 pmol/l (90 ng/l) in 7.8%. Although CT is cleared by hemodialysis, post-dialysis CT levels either were unchanged or increased as compared with pre-dialysis values. This suggests that hypercalcitoninemia is not related to a decreased renal clearance, and that hemodialysis induces a specific regulatory pathway. None of the parameters studied were found to explain high CT levels. Of the patients with hypercalcitoninemia, 11.5% exhibited abnormal CT response to pentagastrin but no relationship between CT and phosphate, calcium and PTH levels was evidenced. Our findings confirm high CT monomer levels in renal failure. As there was no correlation with parameters classically involved in CT regulation, its physiological significance remains unclear. Abnormal CT response to pentagastrin raises the problem of its specificity as a tumoral marker with regard to medullary thyroid carcinoma. B Conte-Devolx, Service d'Endocrinologie et Maladies Métaboliques, Hôpital de la Conception, 147 Bd Baille, Marseille 13385 cedex 05, France

scholarly journals Role of parathyroid hormone in the glucose intolerance of chronic renal failure.

1985 ◽  
Vol 75 (3) ◽  
pp. 1037-1044 ◽  
Author(s):  
M Akmal ◽  
S G Massry ◽  
D A Goldstein ◽  
P Fanti ◽  
A Weisz ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Glucose Intolerance

scholarly journals Parathyroid hormone secretion in chronic renal failure

1996 ◽  
Vol 50 (5) ◽  
pp. 1700-1705 ◽  
Author(s):  
Jesper C. Madsen ◽  
Anne Q. Rasmussen ◽  
Søren D. Ladefoged ◽  
Peter Schwarz
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Hormone Secretion

Experimental Models of Acute Renal Failure and Erythropoietin: What Evidence of a Direct Effect?

Renal Failure ◽  
2007 ◽  
Vol 29 (3) ◽  
pp. 379-386 ◽  
Author(s):  
Alessio Sturiale ◽  
Susanna Campo ◽  
Eleonora Crascì ◽  
Carmela Aloisi ◽  
Michele Buemi
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Direct Effect ◽  
Experimental Models

Bone histomorphometry in diabetic patients with and without renal failure

Bone ◽  
1992 ◽  
Vol 13 (5) ◽  
pp. A17-A17
Author(s):  
V. Jorqetti ◽  
M.E. Duarte ◽  
L.M. dos Reis ◽  
C.S. Teixeira ◽  
R.C.L.G. Silva ◽  
...  
Keyword(s):  
Renal Failure ◽  
Bone Histomorphometry ◽  
Diabetic Patients

scholarly journals Actions of the Small Molecule Ligands SW106 and AH-3960 on the Type-1 Parathyroid Hormone Receptor

2015 ◽  
Vol 29 (2) ◽  
pp. 307-321 ◽  
Author(s):  
Percy H. Carter ◽  
Thomas Dean ◽  
Brijesh Bhayana ◽  
Ashok Khatri ◽  
Raj Rajur ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Small Molecule ◽  
Hormone Receptor ◽  
Transmembrane Domain ◽  
Receptor Activation ◽  
Blood Calcium ◽  
Parathyroid Hormone Receptor ◽  
Peptide Analog ◽  
Amino Terminal ◽  
Small Molecule Ligands

Abstract The parathyroid hormone receptor-1 (PTHR1) plays critical roles in regulating blood calcium levels and bone metabolism and is thus of interest for small-molecule ligand development. Of the few small-molecule ligands reported for the PTHR1, most are of low affinity, and none has a well-defined mechanism of action. Here, we show that SW106 and AH-3960, compounds previously identified to act as an antagonist and agonist, respectively, on the PTHR1, each bind to PTHR1-delNT, a PTHR1 construct that lacks the large amino-terminal extracellular domain used for binding endogenous PTH peptide ligands, with the same micromolar affinity with which it binds to the intact PTHR1. SW106 antagonized PTHR1-mediated cAMP signaling induced by the peptide analog, M-PTH(1–11), as well as by the native PTH(1–9) sequence, as tethered to the extracellular end of transmembrane domain (TMD) helix-1 of the receptor. SW106, however, did not function as an inverse agonist on either PTHR1-H223R or PTHR1-T410P, which have activating mutations at the cytoplasmic ends of TMD helices 2 and 6, respectively. The overall data indicate that SW106 and AH-3960 each bind to the PTHR1 TMD region and likely to within an extracellularly exposed area that is occupied by the N-terminal residues of PTH peptides. Additionally, they suggest that the inhibitory effects of SW106 are limited to the extracellular portions of the TMD region that mediate interactions with agonist ligands but do not extend to receptor-activation determinants situated more deeply in the helical bundle. The study helps to elucidate potential mechanisms of small-molecule binding at the PTHR1.

Sign in / Sign up

Export Citation Format

Share Document