Pre- versus postmenopausal age, estradiol, and peptide-secretagogue type determine pulsatile growth hormone secretion in healthy women: Studies using submaximal agonist drive and an estrogen clamp

Susan B. Hudson, Darrell R. Schroeder, Joy N. Bailey, Kristi L. Mielke, Dana Erickson, John M. Miles, Cyril Y. Bowers, Johannes D Veldhuis

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Context: GH-releasing peptide (GHRP), GHRH, and somatostatin are physiological regulators of pulsatile GH secretion. Hypothesis: Age, independently of abdominal visceral fat (AVF) and basal (nonpulsatile) GH secretion, damps pulsatile GH secretion driven by physiological (rather than pharmacological) amounts of GHRP and GHRH in an experimentally controlled estradiol (E2) milieu. Design and Setting: A prospectively randomized, double-blind parallel-cohort study was conducted at an academic medical center. Participants: Community-dwelling healthy premenopausal (PRE, age 24 ± 0.8 yr, n = 20) and postmenopausal (POST, age 63 ± 1.8 yr, n = 22) women participated in the study. Interventions: Gonadal-axis down-regulation with leuprolide was followed by randomized add-back of placebo or transdermal E2 and separate-day iv bolus injections of a half-maximally stimulatory dose of GHRP-2 or GHRH (each 0.33 μg/kg). Analysis: Three-way analysis of covariance included main factors age, E 2 status, and secretagogue type and covariates AVF and basal GH secretion. Results: Submaximally stimulated pulsatile GH secretion was positively determined by PRE vs. POST age (P<0.001), E2 repletion vs. depletion (P = 0.001) and GHRP-2 vs. GHRH stimulation (P<0.001), after adjustment for AVF and basal secretion. E2 vs. placebo elevated fasting mean GH concentrations in both PRE and POST women (P = 0.006) but increased basal (nonpulsatile) GH secretion in PRE only (P = 0.002). PRE vs. POST age prolonged GHRH-driven GH secretory bursts by 36% (P = 0.006). Conclusion: PRE vs. POST age, E2 availability, and physiological peptide drive are triple determinants of pulsatile GH secretion independently of abdominal visceral fat and nonpulsatile GH secretion in healthy women.

Original languageEnglish (US)
Pages (from-to)353-360
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume95
Issue number1
DOIs
StatePublished - Jan 2010

Fingerprint

Clamping devices
Intra-Abdominal Fat
Growth Hormone
Estradiol
Estrogens
Peptides
Fats
Placebos
Leuprolide
Independent Living
Age Factors
Somatostatin
Fasting
Cohort Studies
Down-Regulation
Drive
Availability
Pharmacology
Injections

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Endocrinology
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Pre- versus postmenopausal age, estradiol, and peptide-secretagogue type determine pulsatile growth hormone secretion in healthy women : Studies using submaximal agonist drive and an estrogen clamp. / Hudson, Susan B.; Schroeder, Darrell R.; Bailey, Joy N.; Mielke, Kristi L.; Erickson, Dana; Miles, John M.; Bowers, Cyril Y.; Veldhuis, Johannes D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 95, No. 1, 01.2010, p. 353-360.

Research output: Contribution to journalArticle

Hudson, Susan B. ; Schroeder, Darrell R. ; Bailey, Joy N. ; Mielke, Kristi L. ; Erickson, Dana ; Miles, John M. ; Bowers, Cyril Y. ; Veldhuis, Johannes D. / Pre- versus postmenopausal age, estradiol, and peptide-secretagogue type determine pulsatile growth hormone secretion in healthy women : Studies using submaximal agonist drive and an estrogen clamp. In: Journal of Clinical Endocrinology and Metabolism. 2010 ; Vol. 95, No. 1. pp. 353-360.
@article{95942409b7ba47d9be235a73aae2f11f,
title = "Pre- versus postmenopausal age, estradiol, and peptide-secretagogue type determine pulsatile growth hormone secretion in healthy women: Studies using submaximal agonist drive and an estrogen clamp",
abstract = "Context: GH-releasing peptide (GHRP), GHRH, and somatostatin are physiological regulators of pulsatile GH secretion. Hypothesis: Age, independently of abdominal visceral fat (AVF) and basal (nonpulsatile) GH secretion, damps pulsatile GH secretion driven by physiological (rather than pharmacological) amounts of GHRP and GHRH in an experimentally controlled estradiol (E2) milieu. Design and Setting: A prospectively randomized, double-blind parallel-cohort study was conducted at an academic medical center. Participants: Community-dwelling healthy premenopausal (PRE, age 24 ± 0.8 yr, n = 20) and postmenopausal (POST, age 63 ± 1.8 yr, n = 22) women participated in the study. Interventions: Gonadal-axis down-regulation with leuprolide was followed by randomized add-back of placebo or transdermal E2 and separate-day iv bolus injections of a half-maximally stimulatory dose of GHRP-2 or GHRH (each 0.33 μg/kg). Analysis: Three-way analysis of covariance included main factors age, E 2 status, and secretagogue type and covariates AVF and basal GH secretion. Results: Submaximally stimulated pulsatile GH secretion was positively determined by PRE vs. POST age (P<0.001), E2 repletion vs. depletion (P = 0.001) and GHRP-2 vs. GHRH stimulation (P<0.001), after adjustment for AVF and basal secretion. E2 vs. placebo elevated fasting mean GH concentrations in both PRE and POST women (P = 0.006) but increased basal (nonpulsatile) GH secretion in PRE only (P = 0.002). PRE vs. POST age prolonged GHRH-driven GH secretory bursts by 36{\%} (P = 0.006). Conclusion: PRE vs. POST age, E2 availability, and physiological peptide drive are triple determinants of pulsatile GH secretion independently of abdominal visceral fat and nonpulsatile GH secretion in healthy women.",
author = "Hudson, {Susan B.} and Schroeder, {Darrell R.} and Bailey, {Joy N.} and Mielke, {Kristi L.} and Dana Erickson and Miles, {John M.} and Bowers, {Cyril Y.} and Veldhuis, {Johannes D}",
year = "2010",
month = "1",
doi = "10.1210/jc.2009-1769",
language = "English (US)",
volume = "95",
pages = "353--360",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "1",

}

TY - JOUR

T1 - Pre- versus postmenopausal age, estradiol, and peptide-secretagogue type determine pulsatile growth hormone secretion in healthy women

T2 - Studies using submaximal agonist drive and an estrogen clamp

AU - Hudson, Susan B.

AU - Schroeder, Darrell R.

AU - Bailey, Joy N.

AU - Mielke, Kristi L.

AU - Erickson, Dana

AU - Miles, John M.

AU - Bowers, Cyril Y.

AU - Veldhuis, Johannes D

PY - 2010/1

Y1 - 2010/1

N2 - Context: GH-releasing peptide (GHRP), GHRH, and somatostatin are physiological regulators of pulsatile GH secretion. Hypothesis: Age, independently of abdominal visceral fat (AVF) and basal (nonpulsatile) GH secretion, damps pulsatile GH secretion driven by physiological (rather than pharmacological) amounts of GHRP and GHRH in an experimentally controlled estradiol (E2) milieu. Design and Setting: A prospectively randomized, double-blind parallel-cohort study was conducted at an academic medical center. Participants: Community-dwelling healthy premenopausal (PRE, age 24 ± 0.8 yr, n = 20) and postmenopausal (POST, age 63 ± 1.8 yr, n = 22) women participated in the study. Interventions: Gonadal-axis down-regulation with leuprolide was followed by randomized add-back of placebo or transdermal E2 and separate-day iv bolus injections of a half-maximally stimulatory dose of GHRP-2 or GHRH (each 0.33 μg/kg). Analysis: Three-way analysis of covariance included main factors age, E 2 status, and secretagogue type and covariates AVF and basal GH secretion. Results: Submaximally stimulated pulsatile GH secretion was positively determined by PRE vs. POST age (P<0.001), E2 repletion vs. depletion (P = 0.001) and GHRP-2 vs. GHRH stimulation (P<0.001), after adjustment for AVF and basal secretion. E2 vs. placebo elevated fasting mean GH concentrations in both PRE and POST women (P = 0.006) but increased basal (nonpulsatile) GH secretion in PRE only (P = 0.002). PRE vs. POST age prolonged GHRH-driven GH secretory bursts by 36% (P = 0.006). Conclusion: PRE vs. POST age, E2 availability, and physiological peptide drive are triple determinants of pulsatile GH secretion independently of abdominal visceral fat and nonpulsatile GH secretion in healthy women.

AB - Context: GH-releasing peptide (GHRP), GHRH, and somatostatin are physiological regulators of pulsatile GH secretion. Hypothesis: Age, independently of abdominal visceral fat (AVF) and basal (nonpulsatile) GH secretion, damps pulsatile GH secretion driven by physiological (rather than pharmacological) amounts of GHRP and GHRH in an experimentally controlled estradiol (E2) milieu. Design and Setting: A prospectively randomized, double-blind parallel-cohort study was conducted at an academic medical center. Participants: Community-dwelling healthy premenopausal (PRE, age 24 ± 0.8 yr, n = 20) and postmenopausal (POST, age 63 ± 1.8 yr, n = 22) women participated in the study. Interventions: Gonadal-axis down-regulation with leuprolide was followed by randomized add-back of placebo or transdermal E2 and separate-day iv bolus injections of a half-maximally stimulatory dose of GHRP-2 or GHRH (each 0.33 μg/kg). Analysis: Three-way analysis of covariance included main factors age, E 2 status, and secretagogue type and covariates AVF and basal GH secretion. Results: Submaximally stimulated pulsatile GH secretion was positively determined by PRE vs. POST age (P<0.001), E2 repletion vs. depletion (P = 0.001) and GHRP-2 vs. GHRH stimulation (P<0.001), after adjustment for AVF and basal secretion. E2 vs. placebo elevated fasting mean GH concentrations in both PRE and POST women (P = 0.006) but increased basal (nonpulsatile) GH secretion in PRE only (P = 0.002). PRE vs. POST age prolonged GHRH-driven GH secretory bursts by 36% (P = 0.006). Conclusion: PRE vs. POST age, E2 availability, and physiological peptide drive are triple determinants of pulsatile GH secretion independently of abdominal visceral fat and nonpulsatile GH secretion in healthy women.

UR - http://www.scopus.com/inward/record.url?scp=75149186448&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=75149186448&partnerID=8YFLogxK

U2 - 10.1210/jc.2009-1769

DO - 10.1210/jc.2009-1769

M3 - Article

C2 - 19858315

AN - SCOPUS:75149186448

VL - 95

SP - 353

EP - 360

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 1

ER -