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ABSTRACT
The effects of i.v. administration of thyrotrophin-releasing hormone (TRH) and of somatostatin on circulating plasma levels of porcine GH in the chronically catheterized pig fetus have been examined. Growth hormone levels increased markedly (P<0·01) following TRH administration, but there was no change in thyroxine levels by 1 h after treatment. Administration of somatostatin caused a significant (P<0·05) decrease in mean GH levels, but the response was variable between pigs. Saline administration had no significant effect on GH levels. These results suggest that the mechanisms regulating postnatal GH release are present in the fetal pig, but may not be fully developed 8–12 days before delivery.
J. Endocr. (1985) 106, 121–124
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ABSTRACT
Steers were actively immunized at 81 days of age against human serum albumin (hSA; controls) or hSA conjugated to either somatostatin (SRIF) or growth hormone-releasing factor (GRF). Binding titres were observed for the respective peptide antigens after all steers had been given booster immunizations. Although no effects of treatment were observed in SRIF-immunized steers, mean serum concentrations of GH and insulin-like growth factor (IGF-I) were suppressed (P<0·01) in GRF-immunized steers when compared with hSA-immunized controls. Mean concentrations of prolactin did not differ with treatment but showed seasonal fluctuations (P<0·001) associated with changes in the daylength. In contrast to its marked effect upon serum concentrations of IGF-I, immunization against GRF resulted in a relatively small (6%) but significant decrease in body weight gain (P<0·01) and an increase in carcass backfat thickness (P<0·05). In summary, our findings have shown the susceptibility of steers to growth modulation by GRF immunoneutralization. Secondly, the poor relationship observed between serum concentrations of IGF-I and growth rates in GRF-immunized steers suggested that circulating IGF-I may not be the principle factor determining the post-weaning growth rate in cattle.
Journal of Endocrinology (1990) 125, 123–129
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ABSTRACT
The temporal interactions of rat GH-releasing factor (GRF) and somatostatin (SRIF) on the secretion of GH from perifused rat anterior pituitary cells have been studied. SRIF and GRF were employed at concentrations in a range close to levels reported in the hypophysial circulation of the rat.
GH secretion was inhibited by pulses of 1 nmol SRIF/1 (6 min) or 0·3 nmol SRIF/1 (6 or 20 min). No rebound GH stimulation was observed. Exposure of cells to 6-min pulses of 0·3 nmol rat GRF/1 repeated three times resulted in rapid stimulatory responses which became attenuated. Concomitant exposure to 0·3 nmol SRIF/1 during a GRF pulse resulted in transient inhibition followed by a delayed and enhanced GH response, measured as the area under the curve but not peak height, whereas continuation of SRIF after a GRF pulse abolished the GH response. Exposure to 0·3 nmol SRIF/1 prior to but not during a GRF pulse did not delay or inhibit the GH response. The area under the curve was increased under these conditions because of the lowered baseline in cells perifused with SRIF.
SRIF alters somatotroph responsivity to equimolar concentrations of rat GRF and under different temporal conditions and can inhibit, enhance or delay GH secretion.
Journal of Endocrinology (1993) 138, 369–377
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Abstract
Factors contributing to sex differences in the somatotrophic axis were investigated in growing lambs. In the first experiment, circulating patterns of GH in venous blood, pituitary content of GH and GH mRNA, and median eminence (ME) contents of GH-releasing factor (GRF) and somatostatin (SRIF) were characterized in prepubertal ram and ewe lambs which were pair-fed to remove sex differences in feed intake. Mean and baseline plasma GH concentrations, GH pulse amplitude, and integrated plasma GH were greater in ram lambs than in ewe lambs, but GH interpulse interval did not differ between sexes. The pituitary GH content and ME contents of GRF and SRIF were greater in rams than in ewes, but steady-state levels of mRNA for GH in the pituitary gland did not differ between sexes. A second experiment investigated sex effects on the levels of SRIF in hypophysial portal blood, and found that these did not differ between sexes. We concluded that the presence of sexually dimorphic patterns of GH secretion in the growing lamb is independent of feed-intake differences between sexes. The lack of sex differences in circulating patterns of SRIF in portal plasma implies that there may be a difference in GRF secretion which may produce sexually dimorphic patterns of GH secretion in lambs.
Journal of Endocrinology (1997) 152, 19–27
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ABSTRACT
We have studied the rebound secretion of GH following short-term somatostatin (SS) infusions in conscious rats, using an automatic sampling system for withdrawing frequent microsamples of blood. Intravenous infusions of SS (5–50 μg/h per rat) inhibited spontaneous GH secretion, but when SS was withdrawn there was a large burst of rebound GH secretion. A sub-anaesthetic dose of urethane reduced such rebound bursts of GH, suggesting a hypothalamic involvement in rebound GH secretion. Passive immunization with an antibody against rat GH-releasing factor (GRF) attenuated the rebound GH secretory response to the withdrawal of an SS infusion (GH concentration during rebound secretion was 26±21 μg/l vs 475 ± 127 μg/l (mean ± s.e.m.), after 0·5 ml anti-GRF serum or non-immune serum respectively). The inhibition of GH rebound secretion was related to the dose of anti-GRF serum administered. Intravenous infusions of human GH (20– 100 μg/h per rat) also reduced the size of the rebound GH secretion following SS withdrawal, in both male and female rats. We suggest that the rebound GH secretion that follows SS withdrawal in vivo is caused mainly by a hypothalamic release of GRF. Exogenous GH inhibits SS-induced rebound GH secretion in the conscious rat, possibly by inhibiting hypothalamic GRF release.
J. Endocr. (1988) 119, 397–404
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Changes in the secretion of GH induced by long-term alterations in nutritional status are thought to result from alterations in somatostatin (SRIF) and growth hormone-releasing hormone (GHRH) at the level of the hypothalamus. To date however, the effect of nutrition on the gene expression of SRIF and GHRH in a species where GH secretion is increased by food restriction, as is the case for the sheep and human, remains unknown. We determined the effect of under-nutrition on the expression of SRIF and GHRH in the hypothalamus of sheep. Ovariectomised ewes were randomly divided into two groups and either fed an ad lib diet (n=6) or a restricted diet of 500 g lucerne chaff per day (food-restricted; n=5) for 7 months. In situ hybridisation was used to study hypothalamic gene expression for GHRH, SRIF and galanin (GAL). The food-restricted animals had elevated plasma concentrations of GH; this was associated with an increase in GHRH mRNA levels in the arcuate nucleus (ARC) and reduced SRIF in the rostral periventricular nucleus and ventromedial hypothalamic nucleus. The level of gene expression of GAL in the ARC and SRIF in the caudal periventricular nucleus was similar in ad lib and food-restricted animals. In conclusion, the effect of chronic food-restriction on the secretion of GH reflects increased GHRH and reduced SRIF synthesis in the hypothalamus.
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ABSTRACT
The involvement of the cholinergic system in GH secretion has recently acquired increasing importance. Data have been presented suggesting that in rats the effect of cholinergic modulation on GH secretion takes place through inhibition or stimulation of hypothalamic somatostatin (SRIF) release. To investigate further the significance of cholinergic-SRIF link and its role in the regulation of GH secretion, the action of cholinergic agonist and antagonist drugs in the GH short-loop feedback mechanism mediated by SRIF was investigated. Intracerebroventricular (i.c.v.) infusion of 0·2 or 2·0 μg GH/rat into the lateral brain ventricle of adult male rats induced a significant reduction in the GH-releasing hormone (GHRH; 2 μg/kg, i.v.)-induced peak GH rise, but only the 2·0 μg dose reduced also the GH-integrated area after administration of GHRH. This effect was absent after central administration of 20·0μg GH/rat, due probably to leakage of some GH from the cerebral ventricle into the systemic circulation. Pretreatment with cysteamine (300 mg/kg, s.c.), a known depletor of hypothalamic SRIF, or with anti-SRIF serum (0·5 ml/rat) completely counteracted the lessening of the GH response to GHRH induced by 2·0μg GH injected i.c.v. Similarly, pretreatment with the cholinergic agonist pilocarpine (3 mg/kg, i.v.) completely antagonized the inhibitory effect of central infusion of GH on the GHRH-induced GH response. Atropine (1·0 mg/kg, i.v.), a muscarinic cholinergic antagonist, strikingly inhibited the GHRH-induced GH rise, but when given in combination with i.c.v. infusion of GH there was no additive inhibitory effect. These data reinforce the idea that the GH autofeedback triggered by i.c.v. infusion of GH is mediated by enhanced SRIF release, and suggest that the hypothalamic cholinergic system plays a major role in this mechanism.
J. Endocr. (1988) 117, 273–281
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Somatostatin (SRIH) functions as an endocrine mediator in processes such as growth, immune resistance and reproduction. Five SRIH receptors (sstr1-5) have been identified in mammals, where they are expressed in both the brain and peripheral tIssues. To study the specific function of each receptor subtype, specific agonists (ag1-5) have been synthesized. The high degree of homology between mammalian and avian SRIH receptors suggests that these agonists might also be used in chickens. In this paper we describe two in vitro protocols (static incubation and perifusion system) to identify the SRIH receptors controlling the secretion of GH and TSH from the chicken pituitary. We found that basal GH or TSH secretion were never affected when SRIH or an agonist (1 microM) were added. SRIH diminished the GH as well as the TSH response to TSH-releasing hormone (TRH; 100 nM) in both systems. Our results have indicated that the SRIH actions at the level of the pituitary are regulated through specific receptor subtypes. In both the static and flow incubations, ag2 lowered the GH response to TRH, whereas stimulated TSH release was diminished by both ag2 and ag5. Ag3 and ag4 tended to increase rather than decrease the responsiveness of both pituitary cell types to TRH in perifusion studies. Our data have indicated that SRIH inhibits chicken pituitary function through sstr2 and sstr5. Only sstr2 seems to be involved in the control of chicken GH release, whereas both sstr2 and sstr5 inhibit induced GH secretion in mammals. The possible stimulatory action of ag3 and ag4 may point towards a species-specific function of sstr3 and sstr4.
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ABSTRACT
The effect of acute or chronic immunoneutralization of somatostatin (SRIF) on plasma GH, thyrotrophin (TSH) and thyroid hormones was examined. Acute responses to SRIF immunoneutralization were examined using 30 intact male lambs (19·8 ±0·6 kg) assigned to one of five treatment groups such that control (C) lambs received no anti-SRIF immunoglobulin and SRIF-immunized (SI) lambs received 2 mg (SI2), 10 mg (SI10), 20 mg (SI20) or 100 mg (SI100) anti-SRIF immunoglobulin/kg body weight (BW). Control immunoglobulin was administered such that all lambs received 100 mg total immunoglobulin protein/kg BW. Effects of chronic SRIF immunoneutralization were examined using C and SI100 lambs which received additional (40 mg/kg BW) control and anti-SRIF immunoglobulin respectively, 4 and 8 days following the initial dose. Blood samples were collected from all lambs, at 10-min intervals, for 5 h immediately following initial immunoglobulin infusion and, from C and SI100 lambs, at 10-min intervals, for 5 h at 11 days following initial immunoglobulin infusion. At the end of each 5-h sampling period, pituitary and thyroid function was examined by i.v. challenge with thyrotrophin-releasing hormone (TRH; 0·33 μg/kg BW). Basal plasma GH and thyroxine (T4) and the GH, TSH, T4 and tri-iodothyronine (T3) responses to TRH were not influenced by acute or chronic immunoneutralization of SRIF. Acute, but not chronic, immunoneutralization of SRIF elevated basal plasma T3 in SI100 lambs only. The results suggest that SRIF, under physiological conditions, does not influence GH or thyroid hormone secretion in sheep but may influence thyroid hormone metabolism acutely.
Journal of Endocrinology (1993) 136, 261–269
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ABSTRACT
Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE-and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species.
J. Endocr. (1984) 102, 175–180
