Somatostatin tonically inhibits growth hormone secretion in domestic fowl

Temporal plasma GH secretory patterns were measured in cannulated male and female meat-type chickens of two commercial strains at 17, 38 and 60 days of age. Pulse height, amplitude and baseline values were similar in both male and female chickens at 17 days of age, with high amplitude and low baseline values. However, by 38 days of age pulsatile GH secretion was not detectable in females, whereas males exhibited a continued pulsatile secretory pattern similar to that at 17 days of age. Pulsatile GH secretion was not evident in either males or females at 60 days of age. These results clearly demonstrate a sexually dimorphic ontogeny of GH secretion in meat-type chickens.

Section: Resultsmentioning

confidence: 98%

Diminution of pulsatile growth hormone secretion in the domestic fowl (Gallus domesticus): evidence of sexual dimorphism

Johnson

1988

“…The GH response of domestic fowl to pas¬ sive somatostatin immunoneutralization is similarly rapid and only transitory and presumably reflects the acquisition of homeostatic control measures to restore GH secretion around the pretreatment set-point (Harvey, Lam & Hall, 1986). Moreover, since thyroid hormones are required for the induction of GH messenger RNA in mammalian species (Seo, Vassart, Brocas & Refetoff, 1977;Seo, Refetoff, Martino et al 1979;Coulombe, Ruel & Dussault, 1980), in which exogenous thyroid hormones also inhibit GH release in euthyroid or hyperthyroid animals (Root, Shulman, Root & Diamond, 1986), the temporal GH re¬ sponse of birds to exogenous T3 or T4 may reflect an initial inhibitory effect on GH release and a later sti¬ mulatory effect on GH gene expression.…”

Section: Discussionmentioning

confidence: 99%

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

Harvey

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)

“…Like¬ wise, SRIF has no effect on basal GH release in vitro and in vivo in young chickens (Harvey et al 1978;Leung & Taylor, 1983). However, immunization of immature chickens with somatostatin antiserum increases the basal plasma GH concentration (Harvey et al 1986). These results therefore support the hypothesis that SRIF inhibits basal GH secretion indirectly, by inhibiting the secretion of GRF and/or TRH by the hypothalamus and/or the stimulatory effect of GRF and TRH on GH secretion.…”

Section: Srif Perifusionmentioning

confidence: 99%

“…Thyrotrophin-releasing hor¬ mone (TRH) also appears to be physiologically important as a GH-releasing factor in birds, increas¬ ing the circulating GH level in young chickens Klandorf, Harvey & Fraser, 1985), ducklings (Pethes, Scanes & Rudas, 1979;Harvey, Foltzer-Jourdainne, Karmann & Mialhe, 1988) and turkey poults (Proudman, 1984). Somato¬ statin (SRIF), in contrast, has been demonstrated in the avian hypothalamus (Calas, Dubois & Assenmacher, 1975;Blahser, 1984;Foltzer, Harvey & Mialhe, 1987) and has inhibitory effects on in-vivo GH secretion in immature birds (Strosser, Harvey, Foltzer & Mialhe, 1984Harvey, Lam & Hall, 1986).…”

Section: Introductionmentioning

confidence: 99%

In-vitro control of growth hormone secretion by synthetic releasing factors in young and adult ducks (Anas platyrhynchos)

Foltzer-Jourdainne¹,

Harvey²,

Mialhe³

1988

Self Cite

Release of GH from perifused duckling hemipituitaries was stimulated, in a biphasic manner, by synthetic TRH and human pancreatic GH-releasing factor (GRF). At all effective concentrations, the level of GH release was increased within 5 min of TRH or GRF perifusion and was maximal after 10 min of TRH perifusion and after 20 min of GRF perifusion. Although TRH was perifused for 20 min the level of GH release declined during the last 10 min. The most effective dose of TRH (1.0 micrograms/ml; 2.7 mumol/l) and GRF (0.5 micrograms/ml; 110 nmol/l) provoked similar (250-300%) increases in the level of GH release. However, since the effect of TRH was only of short duration, the total release of GH induced by GRF was higher than that elicited by TRH, especially with the low dose. The increase in release of GH induced by TRH or GRF was blunted when pituitaries from adult ducks were used. As in young ducks, the GH response to GRF was higher, whereas the response to TRH was very low. The GH response of perifused adult pituitaries to GRF was, however, potentiated when TRH was perifused simultaneously. The basal release of GH from both young and adult pituitary glands was unaffected by perifusion with somatostatin-14 (SRIF-14) at doses of 1 and 2 micrograms/ml. The perifusion of hemipituitary glands with similar doses of SRIF-14 was also unable to suppress the stimulation of GH release induced by prior perifusion with GRF, although when SRIF-14 and TRH were simultaneously perifused TRH-induced GH release was markedly suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)