An early reduction in GH peak amplitude in preproghrelin deficient male mice has a minor impact on linear growth

Hassouna, Rim, Zizzari, Philippe, Tomasetto, Catherine, Veldhuis, Johannes D., Fiquet, Oriane, Labarthe, Alexandra, Cognet, Julie, Steyn, Frederik, Chen, Chen, Epelbaum, Jacques and Tolle, Virginie (2014) An early reduction in GH peak amplitude in preproghrelin deficient male mice has a minor impact on linear growth. Endocrinology, 155 9: 3561-3571. doi:10.1210/en.2014-1126

Author Hassouna, Rim
Zizzari, Philippe
Tomasetto, Catherine
Veldhuis, Johannes D.
Fiquet, Oriane
Labarthe, Alexandra
Cognet, Julie
Steyn, Frederik
Chen, Chen
Epelbaum, Jacques
Tolle, Virginie
Title An early reduction in GH peak amplitude in preproghrelin deficient male mice has a minor impact on linear growth
Journal name Endocrinology   Check publisher's open access policy
ISSN 0013-7227
Publication date 2014
Year available 2014
Sub-type Article (original research)
DOI 10.1210/en.2014-1126
Open Access Status
Volume 155
Issue 9
Start page 3561
End page 3571
Total pages 11
Place of publication Chevy Chase, MD United States
Publisher The Endocrine Society
Collection year 2015
Language eng
Formatted abstract
Ghrelin is a gut hormone processed from the proghrelin peptide acting as the endogenous ligand of the GH secretagogue receptor 1a. The regulatory role of endogenous ghrelin on pulsatile GH secretion and linear growth had to be established. The aim of the present study was to delineate the endogenous actions of preproghrelin on peripheral and central components of the GH axis. Accordingly, the ultradian pattern of GH secretion was measured in young and old preproghrelindeficient males. Blood samples were collected by tail bleeding every 10 minutes over a period of 6 hours. Analysis of the GH pulsatile pattern by deconvolution showed that GH was secreted in an ultradian manner in all genotypes, with major secretory peaks occurring at about 3-hour intervals. In older mice, the peak number was reduced and secretion was less irregular compared with younger animals. Remarkably, in young Ghrl-/-mice, the amplitude of GH secretory bursts was significantly reduced. In older mice, however, genotype differences were less significant. Changes in GH pulsatility in young Ghrl-/-mice were associated with a tendency for reduced GH pituitary contentsandplasma IGF-I concentrations, but with only a minor impactonlinear growth. In Ghrl-/-mice, despite reduced Acyl ghrelin to des-acyl ghrelin ratio,GHsecretion was not impaired. Ghrelin deficiency was not associated with a reduction in hypothalamic GHRH content or altered response to GHRH stimulation. Therefore, reduction in GHRH production and/or sensitivity do not primarily account for the alteredGHpulsatile secretion of young Ghrl-/-mice. Instead,GHRHexpression was elevated in young but not old Ghrl-/-mice, suggesting that differential compensatory responses resulting from the absence of endogenous ghrelin is occurring according to age. These results show that endogenous ghrelin is a regulator of GH pulse amplitude in growing mice but does not significantly modulate linear growth.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Biomedical Sciences Publications
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Citation counts: TR Web of Science Citation Count  Cited 9 times in Thomson Reuters Web of Science Article | Citations
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Created: Mon, 08 Sep 2014, 17:18:37 EST by Mr Frederik Steyn on behalf of School of Biomedical Sciences