NDLI: Testosterone supplementation in older men restrains insulin-like growth factor's dose-dependent feedback inhibition of pulsatile growth hormone secretion.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Paulo, Remberto Soares-Welch, Cacia Veldhuis, Johannes D. Bailey, Joy N. Adeniji, Adenborduin Miles, John M. Keenan, Daniel M. Cosma, Mihaela
Description	Country affiliation: United States Author Affiliation: Veldhuis JD ( Department of Medicine, Endocrine Research Unit, Mayo School of Graduate Medical Education, Clinical Translational Science Center, Mayo Clinic, Rochester, Minnesota 55905, USA. veldhuis.johannes@mayo.edu)
Abstract	BACKGROUND: Pulsatile GH secretion declines in older men. The causal mechanisms are unknown. Candidates include deficient feedforward (stimulation) by endogenous secretagogues and excessive feedback (inhibition) by GH or IGF-I due to age and/or relative hypoandrogenemia. HYPOTHESIS: Testosterone (T) supplementation in healthy older men will restrain negative feedback by systemic concentrations of IGF-I. SUBJECTS: Twenty-four healthy men (ages, 50 to 75 yr; body mass index, 24 to 30 kg/m(2)) participated in the study. METHODS: We performed a prospectively randomized, double-blind, placebo-controlled assessment of the impact of pharmacological T supplementation on GH responses to randomly ordered separate-day injections of recombinant human IGF-I doses of 0, 1.0, 1.5, and 2.0 mg/m(2). ANALYSIS: Deconvolution and approximate entropy analyses of pulsatile, basal, and entropic (pattern-sensitive) modes of GH secretion were conducted. RESULTS: Recombinant human IGF-I injections 1) elevated mean and peak serum IGF-I concentrations dose-dependently (both P < 0.001); 2) suppressed pulsatile GH secretion (P = 0.003), burst mass (P = 0.025), burst number (P = 0.005), interpulse variability (P = 0.032), and basal GH secretion (P = 0.009); and 3) increased secretory pattern regularity (P = 0.020). T administration did not alter experimentally controlled IGF-I concentrations, but it elevated mean GH concentrations (P = 0.015) and stimulated pulsatile GH secretion (frequency P = 0.037, mass per burst P = 0.038). Compared with placebo, T attenuated exogenous IGF-I's inhibition of GH secretory-burst mass (P < 0.038) without restoring pulse number, basal secretion, or pattern regularity. CONCLUSION: The capability of systemic T to mute IGF-I feedback on pulsatile GH secretion suggests a novel mechanism for augmenting GH production.
ISSN	0021972X
e-ISSN	19457197
DOI	10.1210/jc.2008-1516
Journal	The Journal of Clinical Endocrinology & Metabolism
Issue Number	1
Volume Number	94
Language	English
Publisher	Oxford University Press
Publisher Date	2009-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Human Growth Hormone Secretion Insulin-like Growth Factor I Pharmacology Testosterone Dose-response Relationship, Drug Double-blind Method Feedback, Physiological Antagonists & Inhibitors Prospective Studies Regression Analysis Randomized Controlled Trial Research Support, N.i.h., Extramural Discipline Endocrinology Discipline Metabolism
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Endocrinology, Diabetes and Metabolism Clinical Biochemistry Biochemistry Endocrinology

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