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ABSTRACT
To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake.
J. Endocr. (1984) 102, 381–386
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ABSTRACT
Variations in the concentrations of plasma and pituitary GH were determined in ducks for 66 and 87 days after hatch, and compared with somatostatin-like immunoreactivity (SLI) in the plasma, hypothalamus and neural lobe. Plasma GH levels gradually decreased during growth, while pituitary GH content increased. The concentration of pituitary GH increased during the first 3 weeks of age and remained relatively constant thereafter. The decline in plasma GH concentration was paralleled by a similar fall in the level of plasma SLI. While the content of hypothalamic SLI increased during development, the SLI concentration was maximal at 14 days of age and lowest in adults. The content and concentration of SLI in the neural lobe, in contrast, increased progressively during development. Gel filtration of hypothalamic and neural lobe extracts demonstrated that both young and older birds had two main peaks of SLI, corresponding to somatostatin-14 and somatostatin-28, and a third, larger form. The elution pattern of plasma SLI was similar in young and older birds and was principally composed of a large molecular species ('big' somatostatin), although an additional small peak eluting between somatostatin-28 and somatostatin-14 was eluted from a large pool of plasma from 90-day-old ducks. These results suggest that increased plasma GH levels in young birds do not result from a hypothalamic somatostatin deficiency nor from variations in molecular forms of SLI, and that the age-related decline in plasma GH concentration is not due to a deficiency in pituitary GH content. The decline in the circulating GH level during growth is probably due to an increase in hypothalamic somatostatin release.
J. Endocr. (1987) 113, 57–63
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ABSTRACT
Pancreatic somatostatin-like immunoreactivity (SLI), immunoreactive insulin (IRI) and glucagon-like immunoreactivity (GLI) were measured during growth in ducks. The content of each hormone increased progressively but at different rates in the dorsal, ventral and splenic lobes of the pancreas. In the almost fully grown duck, the splenic lobe contained 80 and 63% of the total content of GLI and SLI respectively but low levels of IRI (23%), which were highest in the dorsal lobe (53%). In contrast to the hormonal content, only total GLI concentrations increased during development, the SLI concentrations remaining stable and IRI concentrations declining during growth. Gel filtration of pancreatic extracts indicated that most of the SLI in the pancreas of young and adult birds was somatostatin-14, although somatostatin-28 was present in the ventral lobe of young birds and larger molecular forms were present in the ventral and dorsal lobes. These changes in pancreatic hormonal content and concentration are dissimilar to age-related changes in SLI, GLI and IRI previously observed in the plasma of ducks. Plasma levels of pancreatic hormones may thus be controlled by hormonal and/or neural factors during post-hatch growth.
J. Endocr. (1987) 113, 65–70
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ABSTRACT
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 μg/ml; 2·7 μmol/l) and GRF (0·5 μg/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 μg/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.
These results demonstrate direct effects and interactions of TRH, GRF and SRIF on the release of GH from duck pituitary glands. GRF is the most potent releasing factor for GH in both young and adult ducks although in adult ducks it is less effective. These results also provide evidence that the age-related decline in the in-vivo GH response to TRH is due to a desensitization of pituitary somatotrophs.
J. Endocr. (1988) 119, 421–429
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ABSTRACT
Human pancreatic GH-releasing factor (hpGRF) increased the concentrations of plasma GH when infused i.v. into immature ducks. A dose-dependent increase in plasma GH was observed within 10 min of the start of infusion and was maintained during the 30-min infusion period. Simultaneous infusion of somatostatin S-14 prevented the increase in plasma GH induced by hpGRF, but when the infusion had finished there was a rebound increase in plasma GH. Infusion of the highest dose of hpGRF (800 ng/kg per min) in adult ducks had no significant effect on plasma GH.
Plasma somatostatin concentrations were reduced during the infusion of hpGRF in young but not in adult ducks. This observation suggests that the stimulatory effect of hpGRF on GH secretion may be partly due to its inhibitory effect on somatostatin secretion. Infusion of hpGRF in ducklings also increased the concentrations of glucagon and decreased levels of insulin in the plasma. Peripheral plasma glucagon and insulin levels in adult ducks were unaffected by hpGRF infusion. These results indicate that in ducklings, hpGRF increases plasma GH and glucagon concentrations and lowers plasma somatostatin and insulin levels. In the adult, these hormonal responses to hpGRF are not maintained. The highly stimulatory effect of hpGRF on GH secretion in ducklings may explain why plasma GH concentrations are high in these birds.
J. Endocr. (1987) 114, 25–32
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ABSTRACT
The effects of plasma free fatty acids (FFA) and somatostatin-14 (S-14) on concentrations of plasma GH, glucagon and insulin were investigated in juvenile ducks. Oleic acid, S-14 or both were infused into 4- to 7-week-old birds and plasma GH, glucagon-like immunoreactivity (GLI), immunoreactive insulin (IRI) and FFA were measured.
An increase in plasma GH and a decrease in GLI but no change in IRI was observed after infusion of 9 mg oleic acid/kg per min. A decrease in plasma GH, FFA and IRI and an increase in plasma GLI was seen after infusion of 800 ng S–14/kg per min. These effects of S-14 on IRI and GLI were abolished when S-14 was infused simultaneously with oleic acid.
It is concluded that FFA have a direct stimulatory effect on GH secretion and an inhibitory effect on glucagon secretion. Somatostatin-14 directly inhibits the secretion of GH and its stimulatory effect on the secretion of glucagon is mediated by a depression in concentrations of plasma FFA. Finally, S-14 has no effect on plasma insulin when basal levels of plasma FFA are maintained.
J. Endocr. (1985) 106, 21–25
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ABSTRACT
A sensitive and specific radioimmunoassay without an extraction step was developed for somatostatin in duck plasma. Degradation of Tyr1-125I-labelled somatostatin-14 (S-14) averaged 2% for blood collected with EDTA and zymofren. Recovery of somatostatin-like immunoreactivity (SLI), added to the plasma, averaged 91% for S-14 and 86% for S-28. Chromatographic analysis of portal plasma on Sephadex G-25 showed three peaks: one peak coeluted with cytochrome c (mol. wt 12 500) in the void volume and was called 'big' somatostatin; of the two smaller forms, one coeluted with synthetic S-28 and the other with synthetic S-14; these were immunologically and physicochemically indistinguishable from synthetic S-28 and S-14. In peripheral plasma only the large form of somatostatin, 'big' somatostatin, was found. The mean portal plasma concentration of SLI was 4·1 ±0·41 μg/l (n = 11, range 2·8–5·1 μg/l). In peripheral plasma the SLI concentration was 1·05 ±0·45 μg/l (n = 11, range 0·84–1·2 μg/l). The metabolic clearance rate, distribution volume and calculated half-life values were 63·1 ± 14 ml/kg per min, 40·9±8·9 ml/kg and 1·06±0·19 min for S-14 compared with 45·7 ±7 ml/kg per min, 14·8 ±2·5 ml/kg and 2·14± 0·54 min for S-28. These results indicated that S-28 was cleared from plasma at a slower rate than S-14 in the duck. It was concluded that: (1) portal plasma SLI was four times higher than peripheral SLI; (2) SLI in portal plasma existed as 'big' somatostatin, S-28 and S-14, whereas in peripheral plasma it existed mainly as 'big' somatostatin; (3) invivo studies indicated that S-28 was metabolized less rapidly than S-14.
J. Endocr. (1984) 100, 329–335
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An inverse age-related pattern of GH secretion has been identified in immature ducks between 2 and 9 weeks of age, the plasma level of GH falling progressively from 30–40 ng/ml at 2 weeks of age to the adult level (< 10 ng/ml) by 9 weeks of age. This decrease in GH secretion was not accompanied by any age-related changes in the concentrations of plasma immunoreactive insulin or glucagon-like immunoreactivity or in plasma glucose or free fatty acid level.
In 4- to 6-week-old ducklings the intravenous infusion of insulin (2·5 or 10 mu./kg per min for 30 min) and glucagon (0·1 or 0·5 μg/kg per min for 30 min) induced some inhibition of GH secretion, independently of changes in blood glucose level. These results suggest that although insulin and especially glucagon have direct effects on GH secretion in the duck, maturational differences in pancreatic function are unlikely to be causally related to the decrease in GH secretion during growth.
