Short-loop inhibition of thyrotrophin-releasing hormone-induced growth hormone secretion in fowl

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

doi:10.1677/joe.0.1260237

Cited by 10 publications

(5 citation statements)

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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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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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“…This enhanced sensitivity of central and immune GHRs to autoregulatory influences would suggest that GH has an important role in the these tissues, as high concentrations of GH would reduce GHR abundance and thus protect the tissue from excess GH stimulation. Inhibitory autoregulation of central GHRs may, for instance, protect the hypothalamus from excess GH-induced negative feedback (Lea et al 1990), as somatostatinergic tone is increased ) and catecholamine synthesis is decreased (Harvey 1993, Lea & Harvey 1993 in response to peripheral GH. Although factors regulating immune GH secretion have not been elucidated, similar mechanisms could occur in these tissues.…”

Section: Figurementioning

confidence: 99%

“…Indeed, in the chicken, GHRs have recently been demonstrated in the central nervous system (Hull et al 1993) and immune system (Hull et al 1996c), suggesting novel roles for GH in neural and neuroendocrine function (Buntin & Figge 1989, Lea et al 1990) and in cellular and humeral immunity (Marsh 1992, Hull et al 1996a. These nonhepatic GHRs may also be dependent upon GH status, but may be regulated differently than the hepatic GHR.…”

Section: Introductionmentioning

confidence: 99%

Autoregulation of central and peripheral growth hormone receptor mRNA in domestic fowl

Hull

Harvey²

1998

Journal of Endocrinology

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Growth hormone (GH) regulates numerous cellular functions in many different tissues. A common receptor is believed to mediate these tissue-specific effects, suggesting that post-receptor signalling molecules or tissue sensitivity to GH may differ between tissues. Tissue sensitivity depends upon the abundance of GH receptors (GHRs), thus tissue-specific GHR regulation could enable tissuespecific GH actions. The comparative autoregulation of GHR gene transcription in central (whole brain or hypothalami) and peripheral (liver, bursa, spleen and thymus) tissues was therefore examined in domestic fowl. In all tissues, a 4·4 kb GHR gene transcript that encodes the full-length GHR was identified. The abundance of this transcript was inversely related to endogenous GH status; it was lower in males with high circulating concentrations of GH and higher in females with lower basal concentrations of plasma GH. The abundance of this transcript was also rapidly downregulated in response to a bolus systemic injection of recombinant chicken GH, designed to mimic an episodic burst of endogenous GH release. This autoregulatory response was observed within 2 h of GH administration and was of greater magnitude in the brain than in peripheral tissues. Intracerebroventricular injections of GH also downregulated GHR gene expression in the brain, although hepatic GHR transcripts were unaffected 24 h after central administration of GH. In contrast, the induction of hyposomatotropism by passive GH immunoneutralization increased the abundance of the GHR transcript in the thymus, but not in other central (brain) or peripheral (bursa, liver) tissues. GH is not the sole regulator of GHR abundance, however; hypersomatropism induced by hypothyroidism was associated with an increase in GHR mRNA. The expression of the GHR gene in the domestic fowl would thus appear to be autoregulated by GH in a tissue-specific way.

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“…In one experiment, the medial basal hypothalamus (MBH) was also dissected out (Macnamee & Sharp, 1989) and homogenized in 0-1 mol HCl/1. The hypothalamic extract was then heated above 65°C for 15 min, centrifuged and assayed for SRIF content using a specific radio¬ immunoassay (Lea, Ahene, Marsh & Harvey, 1990) and an antiserum raised in sheep against an SRIFbovine serum globulin conjugate ). The protein content of the hypothalamic extract was quantified by the Bradford (1976) method.…”

Section: In Vivo Studiesmentioning

confidence: 99%

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

Harvey

Baidwan²,

Attardo³

1990

Journal of Endocrinology

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Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1-100 micrograms/kg. In-vitro preincubation of chicken pituitary glands for 0.5-4.0 h with 0.1 mumol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0.1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulating concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

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Short-loop inhibition of thyrotrophin-releasing hormone-induced growth hormone secretion in fowl

Cited by 10 publications

References 0 publications

Understanding the Multifactorial Control of Growth Hormone Release by Somatotropes

Understanding the Multifactorial Control of Growth Hormone Release by Somatotropes

Autoregulation of central and peripheral growth hormone receptor mRNA in domestic fowl

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

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