The Stimulation of Vertebral and Tibial Bone Growth by the Parathyroid Hormone Fragments, hPTH-(1-31)NH2, [Leu27]cyclo(Glu22-Lys26)hPTH-(1-31)NH2, and hPTH-(1-30)NH2

2000 ◽  
Vol 66 (4) ◽  
pp. 307-312 ◽  
Author(s):  
J. F. Whitfield ◽  
P. Morley ◽  
L. Fraher ◽  
A. B. Hodsman ◽  
D. W. Holdsworth ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Growth ◽  
Tibial Bone ◽  
Parathyroid Hormone Fragments ◽  
Stimulation Of

Stimulation of Femoral Trabecular Bone Growth in Ovariectomized Rats by Human Parathyroid Hormone (hPTH)-(1-30)NH 2

1999 ◽  
Vol 65 (2) ◽  
pp. 143-147 ◽  
Author(s):  
J. F. Whitfield ◽  
P. Morley ◽  
G. E. Willick ◽  
S. MacLean ◽  
V. Ross ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Trabecular Bone ◽  
Bone Growth ◽  
Ovariectomized Rats ◽  
Human Parathyroid Hormone ◽  
Stimulation Of

Parathyroid hormone fragments may stimulate bone growth in ovariectomized rats by activating adenylyl cyclase

2009 ◽  
Vol 9 (8) ◽  
pp. 1179-1189 ◽  
Author(s):  
Ray H. Rixon ◽  
James F. Whitfield ◽  
Lyne Gagnon ◽  
Richard J. Isaacs ◽  
Susanne Maclean ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Adenylyl Cyclase ◽  
Bone Growth ◽  
Ovariectomized Rats ◽  
Parathyroid Hormone Fragments

The Control of Bone Growth by Parathyroid Hormone, Leptin, & Statins

2002 ◽  
Vol 12 (1) ◽  
pp. 30 ◽  
Author(s):  
James F. Whitfield ◽  
Paul Morley ◽  
Gordon E. Willick
Keyword(s):  
Parathyroid Hormone ◽  
Bone Growth

Interaction between amrinone and parathyroid hormone on bone in culture

1982 ◽  
Vol 243 (6) ◽  
pp. E499-E504
Author(s):  
N. S. Krieger ◽  
P. H. Stern
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Direct Interaction ◽  
Inhibitory Effects ◽  
Dihydroxyvitamin D3 ◽  
Basal Bone ◽  
Cardiotonic Agent ◽  
Neonatal Mouse Calvaria ◽  
Dose Dependent ◽  
Stimulation Of

The cardiotonic agent amrinone has been postulated to directly affect Na-Ca exchange. Because stimulated bone resorption has been proposed to require Na-Ca exchange, we examined the effects of amrinone on bone. Amrinone inhibited release of Ca from neonatal mouse calvaria in organ culture stimulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin d3, or prostaglandin E2. Inhibition was dose dependent and maximal at 2 X 10(-4) M. The effect of amrinone differed from the inhibitory effects of calcitonin, ouabain, or nigericin in that 1) 6-h exposure to amrinone alone prevented the effect of subsequently added PTH; 2) amrinone was only partially effective if added after resorption was initiated by 24-h treatment with PTH; 3) coincubation with amrinone and PTH during the first 48 h of culture allowed for a response to PTH after amrinone was removed; no such protection by a stimulator occurred with ouabain or nigericin. Also submaximal concentrations of amrinone plus calcitonin, ouabain, or nigericin gave greater than additive inhibition of Ca release. Amrinone had no effect on basal bone cAMP or on the acute stimulation of cAMP by PTH. The results suggest that amrinone could have a more direct interaction with the pathway involved in stimulated bone resorption than the other inhibitors.

Parathyroid hormone-stimulation of Runx2 during osteoblast differentiation via the regulation of lnc-SUPT3H-1:16 (RUNX2-AS1:32) and miR-6797-5p

Biochimie ◽  
2019 ◽  
Vol 158 ◽  
pp. 43-52 ◽  
Author(s):  
B. Arumugam ◽  
M. Vishal ◽  
S. Shreya ◽  
D. Malavika ◽  
V. Rajpriya ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Osteoblast Differentiation ◽  
Hormone Stimulation ◽  
Stimulation Of

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

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