Central action of thyrotrophin-releasing hormone on growth hormone secretion in domestic fowl

Harvey, S.; Lea, Robert; Ahene, C. A.

doi:10.1677/joe.0.1260083

Cited by 8 publications

(3 citation statements)

References 19 publications

(41 reference statements)

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“…An extrapituitary action of ghrelin that suppresses the in vivo GH response of chicks to ghrelin is, however, suggested by the observation that the GH response to ghrelin in vitro (over four orders of magnitude) differed from the in vivo response (over two orders of magnitude). This contrasts with the in vivo GH-releasing activity of TRH in chickens, which is known to be partly due to stimulatory actions at CNS sites (Harvey et al 1990). Although this also contrasts with the central actions of GH secretagogue receptor agonists in chickens (Geris et al 2001), both stimulatory and inhibitory actions of GH secretagogues on SRIF release have been observed in rats (Bluet-Pajot et al 2001).…”

Section: Discussionmentioning

confidence: 96%

Ghrelin-induced GH secretion in domestic fowl in vivo and in vitro

Baudet¹,

Harvey²

2003

Journal of Endocrinology

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Although avian and mammalian species differ significantly in their regulation of GH secretion, preliminary studies have demonstrated in vivo GH responses to ghrelin in chickens, as in mammals. However, the relative potency of ghrelin as a GH-releasing hormone (GHRH) in birds is uncertain, as is its site of action.The intravenous administration of human ghrelin to immature chickens promptly increased the circulating GH concentration (within 10 min), although this was transitory and was only maintained for 20 min. This GH response was dose-related with an EC 50 of approximately 3·0 µg/kg, comparable with the reported potency of human GHRH in chickens. When incubated with dispersed pituitary cells, human ghrelin induced dosedependent GH release over a range of 10 6 to 10 9 M, with an EC 50 of 7·0 10 8 M, comparable with that induced by human GHRH (EC 50 6·0 10 8 M), although it was less effective at doses of 10 6 to 10 8 M. This was due to direct effects on pituitary somatotrophs, since human ghrelin increased GH release (determined by the reverse hemolytic plaque assay) from individual pituitary cells. The incubation of these cells with human ghrelin induced a dose-dependent increase in the numbers of somatotrophs secreting GH and in the amount of GH released by each cell.In summary, these results demonstrated that ghrelin is a dose-related GH-releasing factor in chickens with a potency comparable with that induced by human GHRH. The GH-releasing action of ghrelin is due, at least in part, to stimulatory actions on the numbers of somatotrophs induced to release GH and upon the amount of GH released from individual somatotrophs.

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Section: Discussionmentioning

confidence: 96%

Ghrelin-induced GH secretion in domestic fowl in vivo and in vitro

Baudet¹,

Harvey²

2003

Journal of Endocrinology

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“…These results are therefore likely to reflect actions of pGlu-Glu-ProNH2 at extra pituitary sites within the brain. Although TRH stimulated GH release at hypothalamic sites (Leung et al 1985;Harvey et al 1990) it may simultaneously increase inhibitory hypothalamic tone by receptor-mediated mechanisms sensitive to pGlu-Glu-ProNH2 antagonism. The inhibitory action of TRH on GH-releasing factor neurones (Ishikawa et al 1987;Shioda et al 1987) may, for instance, be antagonized by pGlu-Glu-ProNH2, as may the stimulatory action of TRH on SRIF release (Knudtzen & Hanssen, 1983;Katakami et al 1985).…”

Section: Discussionmentioning

confidence: 99%

pGlutamylglutamylprolineamide modulation of growth hormone secretion in domestic fowl: antagonism of thyrotrophin-releasing hormone action?

Harvey

Trudeau²,

Ashworth³

et al. 1993

Journal of Endocrinology

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Pyroglutamyglutamylprolineamide (pGlu-Glu-ProNH2) is a tripeptide with structural and immunological similarities to thyrotrophin-releasing hormone (TRH; pGlu-His-ProNH2). Since TRH stimulates GH secretion in domestic fowl, the possibility that pGlu-Glu-ProNH2 may also provoke GH release was investigated. Unlike TRH, pGlu-Glu-ProNH2 alone had no effect on GH release from incubated chicken pituitary glands and did not down-regulate pituitary TRH receptors. However, pGlu-Glu-ProNH2 suppressed TRH-induced GH release from pituitary glands incubated in vitro and competitively displaced [3H]methyl3-histidine2-TRH from pituitary membranes. Systemic injections of pGlu-Glu-ProNH2 had no significant effect on basal GH concentrations in conscious birds, but promptly lowered circulating GH levels in sodium-pentobarbitone anaesthetized fowl. Submaximal GH responses of conscious and anaesthetized birds to systemic TRH challenge were, however, potentiated by prior or concomitant administration of pGlu-Glu-ProNH2. These results demonstrate, for the first time, that pGlu-Glu-ProNH2 has biological activity, with inhibitory and stimulatory actions within the avian hypothalamo-pituitary axis. These results indicate that pGlu-Glu-ProNH2 may act as a TRH receptor antagonist within this axis.

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“…Accordingly, direct action of TRH on somatotrope function has been reported in amphibians 108 and reptiles 48 as well as in birds. TRH seems to be equipotent to GHRH 109 in the case of chickens 110 but not in fowl 110–113 . In mammals, TRH has been demonstrated to stimulate GH release in cattle 114 and in sheep 73,115,116 .…”

Section: Regulation Of Gh Secretionmentioning

confidence: 99%

Understanding the Multifactorial Control of Growth Hormone Release by Somatotropes

Gahete

Durán-Prado

Luque

et al. 2009

Annals of the New York Academy of Sciences

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Control of postnatal growth is the main, but not the only, role for growth hormone (GH) as this hormone also contributes to regulating metabolism, reproduction, immunity, development, and osmoregulation in different species. Likely owing to this variety of group-specific functions, GH production is differentially regulated across vertebrates, with an apparent evolutionary trend to simplification, especially in the number of stimulatory factors governing substantially GH release. Thus, teleosts exhibit a multifactorial regulation of GH secretion, with a number of factors, from the newly discovered fish GH-releasing hormone (GHRH) to pituitary adenylate cyclase-activating peptide (PACAP) but also gonadotropin-releasing hormone, dopamine, corticotropin-releasing hormone, and somatostatin(s) directly controlling somatotropes. In amphibians and reptiles, GH secretion is primarily stimulated by the major hypothalamic peptides GHRH and PACAP and inhibited by somatostatin(s), while other factors (ghrelin, thyrotropin-releasing hormone) also influence GH release. Finally, in birds and mammals, primary control of GH secretion is exerted by a dual interplay between GHRH and somatostatin. In addition, somatotrope function is modulated by additional hypothalamic and peripheral factors (e.g., ghrelin, leptin, insulin-like growth factor-I), which together enable a balanced integration of feedback signals related to processes in which GH plays a relevant regulatory role, such as metabolic and energy status, reproductive, and immune function. Interestingly, in contrast to the high number of stimulatory factors impinging upon somatotropes, somatostatin(s) stand(s) as the main primary inhibitory regulator(s) for this cell type.

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Central action of thyrotrophin-releasing hormone on growth hormone secretion in domestic fowl

Cited by 8 publications

References 19 publications

Ghrelin-induced GH secretion in domestic fowl in vivo and in vitro

Ghrelin-induced GH secretion in domestic fowl in vivo and in vitro

pGlutamylglutamylprolineamide modulation of growth hormone secretion in domestic fowl: antagonism of thyrotrophin-releasing hormone action?

Understanding the Multifactorial Control of Growth Hormone Release by Somatotropes

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