Interactions of growth hormone and parathyroid hormone in renal phosphate, calcium, and calcitriol metabolism and bone remodeling in postmenopausal women

Steven Lieberman, Leah Holloway, Robert Marcus, Andrew R. Hoffman

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 ± 22.3 versus - 144.1 ± 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 ± 17 to 163 ± 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 ± 0.005 to 0.073 ± 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 ± 0.05 mM), basal TmP/GFR (4.29 ± 0.24 mg/dl), and basal CEI (0.067 ± 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 ± 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 ± 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment. Neither short-term nor sustained rhGH affected plasma ionized Ca, serum PTH levels, or the magnitude of the acute hydroxyproline, calcitriol, or cAMP responses to hPTH. We conclude that GH has PTH-independent effects on renal phosphate handling and 1α-hydroxylase activity, exerting its effects at a postreceptor step beyond adenylate cyclase activation.

Original languageEnglish (US)
Pages (from-to)1723-1728
Number of pages6
JournalJournal of Bone and Mineral Research
Volume9
Issue number11
StatePublished - Nov 1994

Fingerprint

Human Growth Hormone
Calcitriol
Bone Remodeling
Parathyroid Hormone
Growth Hormone
Kidney
Calcium
Phosphorus
Serum
Teriparatide
Hydroxyproline
Mixed Function Oxygenases
calcium phosphate
Adenylyl Cyclases
Vitamin D
Minerals
Therapeutics
Biomarkers
Phosphates
Bone and Bones

ASJC Scopus subject areas

  • Surgery

Cite this

Interactions of growth hormone and parathyroid hormone in renal phosphate, calcium, and calcitriol metabolism and bone remodeling in postmenopausal women. / Lieberman, Steven; Holloway, Leah; Marcus, Robert; Hoffman, Andrew R.

In: Journal of Bone and Mineral Research, Vol. 9, No. 11, 11.1994, p. 1723-1728.

Research output: Contribution to journalArticle

@article{aaca5b4c15274ccf9f277f5e64a35cae,
title = "Interactions of growth hormone and parathyroid hormone in renal phosphate, calcium, and calcitriol metabolism and bone remodeling in postmenopausal women",
abstract = "The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 ± 22.3 versus - 144.1 ± 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 ± 17 to 163 ± 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 ± 0.005 to 0.073 ± 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 ± 0.05 mM), basal TmP/GFR (4.29 ± 0.24 mg/dl), and basal CEI (0.067 ± 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 ± 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 ± 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment. Neither short-term nor sustained rhGH affected plasma ionized Ca, serum PTH levels, or the magnitude of the acute hydroxyproline, calcitriol, or cAMP responses to hPTH. We conclude that GH has PTH-independent effects on renal phosphate handling and 1α-hydroxylase activity, exerting its effects at a postreceptor step beyond adenylate cyclase activation.",
author = "Steven Lieberman and Leah Holloway and Robert Marcus and Hoffman, {Andrew R.}",
year = "1994",
month = "11",
language = "English (US)",
volume = "9",
pages = "1723--1728",
journal = "Journal of Bone and Mineral Research",
issn = "0884-0431",
publisher = "Wiley-Blackwell",
number = "11",

}

TY - JOUR

T1 - Interactions of growth hormone and parathyroid hormone in renal phosphate, calcium, and calcitriol metabolism and bone remodeling in postmenopausal women

AU - Lieberman, Steven

AU - Holloway, Leah

AU - Marcus, Robert

AU - Hoffman, Andrew R.

PY - 1994/11

Y1 - 1994/11

N2 - The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 ± 22.3 versus - 144.1 ± 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 ± 17 to 163 ± 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 ± 0.005 to 0.073 ± 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 ± 0.05 mM), basal TmP/GFR (4.29 ± 0.24 mg/dl), and basal CEI (0.067 ± 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 ± 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 ± 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment. Neither short-term nor sustained rhGH affected plasma ionized Ca, serum PTH levels, or the magnitude of the acute hydroxyproline, calcitriol, or cAMP responses to hPTH. We conclude that GH has PTH-independent effects on renal phosphate handling and 1α-hydroxylase activity, exerting its effects at a postreceptor step beyond adenylate cyclase activation.

AB - The mechanisms underlying the effects of recombinant human growth hormone (rhGH) on vitamin D, mineral, and bone metabolism are not known. We examined whether these effects are mediated by parathyroid hormone (PTH) by measuring renal phosphorus (P) and calcium (Ca) handling, serum calcitriol, and markers of bone turnover for 24 h before and 72 h after an infusion of hPTH(1-34) in eight healthy postmenopausal women at baseline and following short-term (1 week) and sustained (5 weeks) rhGH treatment. On short-term rhGH, serum phosphorus and basal TmP/GFR were unaffected, but the fall in TmP/GFR after hPTH infusion was exaggerated (integrated response: -99.2 ± 22.3 versus - 144.1 ± 15.0 minute-mg/dl, P = 0.0021). Basal calcitriol levels rose from 115 ± 17 to 163 ± 16 pM (P = 0.0002), but the increase in calcitriol following hPTH infusion was unaffected by short-term rhGH. The basal Ca excretion index (CEI) rose from 0.054 ± 0.005 to 0.073 ± 0.007 mM (P = 0.0095), but markers of bone turnover were unaffected. With sustained rhGH treatment, serum P (1.47 ± 0.05 mM), basal TmP/GFR (4.29 ± 0.24 mg/dl), and basal CEI (0.067 ± 0.005 mM) were elevated compared with control values, and the PTH-induced lowering of TmP/GFR was again enhanced (-158.7 ± 22.8 minute-mg/dl, P = 0.0021). Basal calcitriol concentrations returned to control levels (108 ± 10 pM), but the calcitriol response to hPTH remained unchanged. Markers of bone remodeling were elevated with sustained rhGH treatment. Neither short-term nor sustained rhGH affected plasma ionized Ca, serum PTH levels, or the magnitude of the acute hydroxyproline, calcitriol, or cAMP responses to hPTH. We conclude that GH has PTH-independent effects on renal phosphate handling and 1α-hydroxylase activity, exerting its effects at a postreceptor step beyond adenylate cyclase activation.

UR - http://www.scopus.com/inward/record.url?scp=0028144055&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028144055&partnerID=8YFLogxK

M3 - Article

C2 - 7863823

AN - SCOPUS:0028144055

VL - 9

SP - 1723

EP - 1728

JO - Journal of Bone and Mineral Research

JF - Journal of Bone and Mineral Research

SN - 0884-0431

IS - 11

ER -