Introduction
In chickens, the anterior pituitary gland produces the same palette of hormones seen across the vertebrates:
Adrenocorticotropic hormone (ACTH) and β-endorphin
Follicle-stimulating hormone (FSH)
Growth hormone (GH)
Luteinizing hormone (LH)
Prolactin
Thyrotropin (TSH)
Neuropeptides, e.g.,
◦ Met-enkephalin
◦ Relaxin 3 ()
This discussion focuses on contributions of the author and his collaborators with comments on what is still not known.
Control of GH release and synthesis
Chicken somatotrophs respond to GH-releasing hormone (GHRH) and some neuropeptides. Intra-cellular concentrations of calcium ions in somatotrophs are increased by GHRH, thyrotropin-releasing hormone (TRH) (3/4 of somatotrophs), pituitary adenylate cyclase-activating peptide (85% of somatotrophs), leptin (51%), gonadotropin-releasing hormone (GnRH) (40%), and ghrelin (21%) (
).
Table 1summarizes the neuropeptides that influence the release of GH (reviewed:
). Some neuropeptides affect the release of more than one hormone. For instance, neuropeptide W decreases the secretion of GH, prolactin, and ACTH in chickens (
;
). What are still unknown are the following:
Why there are multiple stimulatory and inhibitory factors?
How pituitary cells influence the functioning of others?
What the role of folliculostellate cells is?
These produce growth factors/hormones including annexin 1, fibroblast growth factor 2 (FGF2), leptin, and vascular endothelial growth factor (VEGF), and these presumably exert paracrine effects ().
TABLE 1
| Releasing hormone/neuropeptide | GH |
|---|---|
| GHRH | + |
| GnRH | +? |
| Ghrelin | + |
| Leptin | + |
| NPW | − |
| PACAP | + |
| SRIF | − |
| TRH | + |
Summary of the hypothalamic releasing hormones/neuropeptides influencing the secretion of GH (based on discussions in Scanes, 2022).
+ indicates increase; − indicates decrease.
GH isoforms
There are multiple forms of GH in the chicken pituitary gland:
Monomer (40%)
Glycosylated (16%)
Dimer (14%)
15–16 kDa sub-monomeric isoform (16%) ()
The sub-monomeric isoform of GH predominates in immune tissues () and retinal ganglion cells in chickens ().
GH and growth
The hypothalamo-pituitary GH–insulin-like growth factor-1 (IGF-1) axis exists in chickens and other birds. GH increases growth in hypophysectomized young chickens (). Growth is reduced in sex-linked dwarf chickens with a mutation(s) in the GH receptor gene (). Plasma concentrations of IGF-1 are reduced in hypophysectomized young chickens and restored by GH treatment (). GH increases IGF-1 release from chick hepatocytes () and in adult chickens (). The mechanism for GH’s effect on growth is mediated via Janus kinase (JAK)-2 (). Studies addressing the question as to whether GH increases growth in intact broilers are at best equivocal (; ; ; ).
GH and thyroid hormones
GH decreases hepatic deiodination of triiodothyronine (T3) in young chickens () with optimal circulating concentrations of T3 essential for growth. GH-receptor-deficient dwarf chickens have reduced plasma concentrations of T3 ().
GH and lipolysis
Mammalian and avian GH stimulates
in vitrolipolysis (glycerol release from adipose tissue explants) (
) and inhibits glucagon-induced lipolysis (
). A GH antagonist prevents GH’s effect on lipolysis
per sebut unexpectedly retains full activity in suppressing glucagon-induced lipolysis (
). Moreover, reptilian, amphibian, and fish GH lacks lipolytic activity but inhibits glucagon-induced lipolysis (
). What are not known are the following:
Are the effects of GH physiologically relevant?
Are these direct effects on adipocytes, or are these effects mediated through other cell types present in adipose tissue, such as endothelial cells and macrophages, followed by paracrine effects of cytokines or other neuropeptides?
The lipolytic effect is probably mediated through JAK-2 based on studies in mice (). However, the mechanism for anti-lipolytic effects is yet to be determined.
GH and reproduction
Administration of GH to laying hens increases shell thickness (); this may be due to effects on the oviduct. This observation was followed by reports of oviductal and ovarian effects of GH. For instance, GH increases progesterone release from large yellow follicles (). GH decreases mucosal apoptosis in the oviduct but increases the expression of a specific gene (; ). Moreover, GH is present in the testes and ovary of chickens (). There are associations between GH polymorphisms and egg production ().
Stress and GH
Stress affects GH levels in post-hatch chickens. Plasma concentrations of GH were depressed following challenge with ACTH (). Plasma concentrations of GH are also decreased by epinephrine () and morphine (). Heat stress did not affect plasma concentrations of GH in young chickens but depressed hepatic expression of the GHR (). Corticosterone induces somatotrophs in chick embryos (e.g., ). Plasma concentrations of GH are increased by nutritional deprivation such as withholding feed or feeding a protein-deficient diet (); the latter being presumed to be due to dietary stress depressing negative feedback for T3 and IGF-1.
GH and the brain
Both GH- and prolactin-containing neurons are present within avian brains (). Chick embryo retinal ganglion cells express GH (reviewed: ; ). Moreover, GH exerts a neuroprotective role in reducing apoptosis of retinal ganglion cells (). In vitro, GH depresses apoptosis and expression of caspase-3 and apoptosis-inducing factor-1 in neural retina explants from chick embryos (). Apoptosis in retinal ganglion cells is increased by antisera to GH in ovo, supporting a role for locally produced GH in regulating retinal apoptosis (). In an avian model for ischemic stroke, GH exerts a neuroprotective effect on cultured chick embryo hippocampal cells exposed to oxygen–glucose deprivation (). Moreover, GH influences neurite development in the inner ear with increases in extension and branching of neurites in chick embryos (). Information on the underlying mechanism(s) for neuronal effects of GH is lacking.
GH and angiogenesis
Chick embryo chorioallantoic membranes (CAMs) are useful for examining the effects of hormones and growth factors on angiogenesis. reported that “the 16-kilodalton N-terminal fragment of human prolactin is a potent inhibitor of angiogenesis” using chick embryo CAMs. In contrast, the formation of blood vessels was stimulated by either an anterior pituitary tissue or GH (). The signal transduction mechanism for these effects remains unclear.
Statements
Author contributions
CS: Conceptualization, Formal Analysis, Project administration, Supervision, Writing – original draft, Writing – review and editing.
Funding
The author declares that no financial support was received for the research and/or publication of this article.
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Summary
Keywords
growth hormone, chicken, stress, lipolysis, growth
Citation
Scanes CG (2025) Growth hormone: lessons from chickens. Front. Physiol. 16:1705885. doi: 10.3389/fphys.2025.1705885
Received
15 September 2025
Revised
23 October 2025
Accepted
24 October 2025
Published
21 November 2025
Volume
16 - 2025
Edited by
Takeshi Ohkubo, Ibaraki University, Japan
Reviewed by
Mohammad Bahry, University of Guelph, Canada
Updates
Copyright
© 2025 Scanes.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Colin G. Scanes, cgscanes@icloud.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.