Physiological control of growth hormone secretion by thyrotrophin-releasing hormone in the domestic fowl

Journal of Endocrinology

Klandorf²,

Scanes³

1990

Self Cite

Surgical thyroidectomy increases basal and TRH-induced GH concentrations in the peripheral plasma of immature domestic fowl. Replacement therapy with thyroxine (T4; 100 micrograms/kg per day for 7 days, i.m.) suppressed the GH responses to thyroidectomy. Bolus administration of T4 (10 micrograms/kg, i.m.) to thyroidectomized birds promptly lowered the circulating GH concentrations, which remained suppressed for at least 4 h. Chronic (daily injections for 7 days) or acute (one injection) pretreatment of thyroidectomized birds with iopanoic acid (IOP; 40 mg/bird, i.m.) before the bolus administration of T4 attenuated, but did not prevent, inhibition of circulating GH levels by T4. Administration of IOP (40 mg/bird i.m.) 24 h and immediately before the administration of tri-iodothyronine (T3; 3 micrograms/kg, i.m.) or T4 (10 micrograms/kg, i.m.) also failed to suppress thyroidal inhibition of circulating GH concentrations in thyroidectomized birds. Administration of IOP alone had no effect on GH concentrations. Circulating T3 concentrations were not enhanced following the administration of T4 to IOP-treated birds, indicating its inhibition of hepatic monodeiodinase activity. The metabolic clearance rate (MCR) of 125I-labelled chicken GH in the plasma of thyroidectomized fowl was less than that in sham-thyroidectomized birds. Following pretreatment with T4 (100 micrograms/kg per day for 7 days) sham-thyroidectomized and thyroidectomized birds did not differ significantly in their MCR. The GH secretion rate in thyroidectomized birds was similar to that in sham-thyroidectomized birds and in both groups was markedly reduced following pretreatment with T4. These results demonstrate thyroidal inhibition of circulating GH concentrations in fowl.(ABSTRACT TRUNCATED AT 250 WORDS)

Section: Discussionmentioning

confidence: 99%

Participation of tri-iodothyronine and metabolic clearance rate in the inhibition of growth hormone secretion in thyroxine-treated domestic fowl

Journal of Endocrinology

Klandorf²,

Scanes³

1990

Self Cite

“…TRH is an extremely po¬ tent GH-releasing factor in birds, and the finding of increased GH secretion in hypothyroid birds (Scanes, Lance, Harvey et al 1976;Chiasson, Sharp, Klandorf et al 1979;Harvey et al 1983; Har¬ vey, Scanes & Klandorf, 1988) in which endogenous TRH secretion would be high (Almeida & Thomas 1981), and suppressed GH secretion in hyperthyroid birds (Harvey, 19836;Scanes, Denver & Bowen, 1986) in which endogenous TRH would also be sup¬ pressed (Almeida & Thomas 1981), suggests a phys¬ iological role for TRH in avian GH regulation. This possibility is supported by the prompt and sustained decline in the circulating GH level in chickens fol¬ lowing passive immunoneutralization of their endo¬ genous TRH (Klandorf, Harvey & Fraser, 1985).…”

Section: Introductionmentioning

confidence: 97%

Thyrotrophin-releasing hormone (TRH)-induced growth hormone secretion in fowl: binding of TRH to pituitary membranes

Journal of Molecular Endocrinology

Baidwan²

1989

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Heat-labile specific binding sites for [3H]3-methylhistidine2-TRH [( 3H]Me-TRH) were demonstrated on chicken adenohypophysial membranes. These binding sites were of both high affinity (dissociation constant, Kd = 15.53 nM) and low capacity (maximum binding capacity, Bmax = 8.73 pmol/g tissue) and of low affinity (Kd = 104.5 nM) and high capacity (Bmax = 32.41 pmol/g). Binding of [3H]Me-TRH to the pituitary membranes was greater at 4 degrees C than at 39 degrees C and occurred with rate constants (k1) of 1.6 x 10(6) and 3.39 x 10(6) M-1 min-1 respectively. Dissociation of [3H]Me-TRH binding at 4 degrees C occurred with a rate constant (k-1) of 0.125 min-1. Binding sites for [3H]Me-TRH were found in the cephalic lobe of the pituitary gland (the location of most lactotrophs and thyrotrophs) and in the caudal lobe (the location of most somatotrophs). The number of binding sites was greater in the caudal lobe than in the cephalic lobe, although the affinity of [3H]Me-TRH binding did not differ. The binding of [3H]Me-TRH to caudal lobe membranes was displaced by Me-TRH, TRH, pGlu-His-Pro-Gly-NH2 and [Glu1]-TRH, with half-maximal effective doses of 33 nM, 70.7 nM, 1.23 microM and 22 microM respectively, but not by [Phe2]-TRH, TRH free acid or His-Pro-diketopiperazine. The number of caudal lobe binding sites for [3H]Me-TRH in old birds was less than that in young ones, and the number of binding sites was increased in birds deprived of food for 48 h. TRH-induced GH secretion in birds would thus appear to be mediated by specific receptors on caudal lobe somatotrophs, and these results suggest that physiological changes in GH secretion (during growth and periods of fasting) are causally related to the abundance of TRH-binding sites.

“…The down-regulation of these binding sites by T3 may, therefore, indicate a feedback mechanism in the regulation of GH secretion in avian species. TRH is a physiological GH-releasing factor in birds (Harvey, 1983a;Klandorf et al 1985), and basal and TRH-induced GH release are markedly suppressed by exogenous T3 (Harvey, 19836;; Scanes & Harvey, 1989a), the concentration of which is increased by GH (Kühn et al 1987;1988;Berghman et al 1989). The up-regulation of TRH-binding sites and increased GH secretion in birds made hypothyroid by methimazole treatment is consistent with this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…TRH is a physiological GH-releasing factor in birds (Harvey, 1983a;Klandorf, Harvey & Fraser, 1985) and is likely to stimulate GH release by binding to specific, high-affinity receptors on pituit¬ ary somatotrophs (Harvey & Baidwan, 1989). Since the TRH-binding sites on mammalian thyrotrophs or adenomatous somatotrophs are down-regulated by thyroid hormones (Hinkle, 1984;Sharif, 1987Sharif, , 1988, the possibility that thyroidal inhibition of GH secretion in birds might be mediated by alterations in TRH binding has been examined in the present study.…”

Section: Introductionmentioning

confidence: 99%

Thyroidal inhibition of growth hormone secretion in fowl: tri-iodothyronine-induced down-regulation of thyrotrophin-releasing hormone-binding sites on pituitary membranes

Journal of Molecular Endocrinology

Baidwan²

1990

Self Cite

The number, but not affinity, of binding sites for [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) on chicken adenohypophysial plasma membranes was increased in chickens made hypothyroid by goitrogen (methimazole) treatment (50 mg/kg per day for 7 days), which also increased circulating GH concentrations. Daily i.p. injection of thyroxine (T4; 100 micrograms/kg for 7 days) had no effect on [3H]Me-TRH binding to pituitary membranes, although it suppressed endogenous GH secretion. Binding of [3H]Me-TRH to pituitary caudal lobe membranes was, however, suppressed by tri-iodothyronine (T3) injected chronically (100 micrograms/kg per day, i.p., for 7 days) or acutely (100 micrograms/kg, 2 h before being killed). The suppression of [3H]Me-TRH binding and inhibition of GH secretion following T3 administration was dose related. Binding of [3H]Me-TRH to caudal lobe membranes was also suppressed following the incubation of pituitary glands with T3 in vitro, and the response was both dose and time related. These results suggest that T3 inhibits GH secretion in fowl by a down-regulation of pituitary TRH receptors. However, other mechanisms are involved in thyroidal inhibition of GH release in birds, since T4 had no effects on [3H]Me-TRH binding yet suppressed GH secretion in vivo.