scholarly journals The role of neuropeptide Y and interaction with leptin in regulating feed intake and luteinizing hormone and growth hormone secretion in the pig

Reproduction ◽  
2006 ◽  
Vol 131 (6) ◽  
pp. 1127-1135 ◽  
Author(s):  
C Richard Barb ◽  
Robert R Kraeling ◽  
George B Rampacek ◽  
Gary J Hausman

Two experiments (EXP) were conducted in ovariectomized prepubertal gilts to test the hypothesis that neuropeptide Y (NPY) stimulates appetite and modulates LH and GH secretion, and that leptin modifies such acute effects of NPY on feeding behavior and LH and GH secretion. In EXP I, gilts received intracerebroventricular (ICV) injections of 0.9% saline (saline; n=6), or 10 μg (n=7), 50 μg (n=5) or 100 μg (n=7) NPY in saline and blood samples were collected. In EXP II, gilts received ICV injections of S (n=4), or 50 μg leptin (n=4), or 100 μg NPY (n=4) or 100 μg NPY +50 μg leptin (n=4) in saline, and feed intake was measured at 4, 20 and 44 h after feed presentation and blood samples collected. In EXP I, NPY suppressed LH secretion and the 100 μg dose stimulated GH secretion. In EXP II, NPY reversed the inhibitory effect of leptin on feed intake and suppressed LH secretion, but serum GH concentrations were unaffected. These results support the hypothesis that NPY modulates feed intake, and LH and GH secretion and may serve as a neural link between metabolic state and the reproductive and growth axis in the pig.

1987 ◽  
Vol 115 (1) ◽  
pp. 149-154 ◽  
Author(s):  
Eric F. Adams ◽  
Maria S. Venetikou ◽  
Christine A. Woods ◽  
S. Lacoumenta ◽  
J. M. Burrin

Abstract. Neuropeptide Y (NPY) is a 36 amino acid peptide, widely distributed throughout the brain and is found in hypothalamic neurones. This latter finding suggests that NPY may possess a hypophysiotropic function. A number of studies have demonstrated effects of NPY on LH and GH secretion by rat pituitary cells. We report here the results of experiments investigating the effects of NPY on GH secretion by tumorous human somatotropic pituitary cells in culture. NPY (0.25–25 nmol/l) inhibited GH secretion by 20–53%, the maximal effect depending upon the tumour studied. The potency of NPY was less than that of somatostatin (SRIH). The stimulatory effects of growth hormone releasing factor (GHRH) and theophylline were reduced by NPY, but NPY did not modify the inhibitory effect of SRIH on GH secretion. It is concluded that NPY may be involved in the control of GH secretion, at least by tumorous human pituitary somatotropes.


1996 ◽  
Vol 134 (1) ◽  
pp. 73-76 ◽  
Author(s):  
Giuseppe Fanciulli ◽  
Osvaldo Oliva ◽  
Paolo A Tomasi ◽  
Alessandra Pala ◽  
Alba Bertoncelli ◽  
...  

Fanciulli G, Oliva O, Tomasi PA. Pala A. Bertoncelli A, Dettori A, Delitala G. Effect of exogenous growth hormone administration on endogenous growth hormone secretion induced by a met-enkephalin analog. Eur J Endocrinol 1996:134:73–6. ISSN 0804–4643 Exogenous growth hormone (hGH) administration in humans attenuates the endogenous growth hormone (GH) response to some pharmacological stimuli: in particular, pretreatment with hGH completely blocks the serum GH response to growth hormone-releasing hormone. In order to evaluate the mechanism(s) whereby opioids induce GH secretion in man, we gave the following treatments to six healthy male volunteers: (a) IV saline: (b) a met-enkephalin analog G-DAMME 250 μg IV as a bolus at time ′: (c) hGH 2 IU as an IV bolus at time −180′; (d) G-DAMME as above, preceded by hGH as above. In our study. G-DAMME stimulated GH secretion both basally (peak 17.9 ± 6.0 ng/ml) and, to a lesser extent, after hGH pretreatment (6.0 ± 2.7 ng/ml). Since in our study G-DAMME was able to partially overcome the inhibitory effect of hGH administration, it is suggested that opioids act through an inhibition of somatostatin release and not through a GHRH-dependent pathway. However, an additional direct effect of hGH on pituitary somatotrophes cannot be excluded. Giuseppe Delitala, Chair of Endocrinology, Viale S. Pietro 12, University of Sassari, 07100 Sassari. Italy


2021 ◽  
Vol 12 ◽  
Author(s):  
Jesús Devesa

The classic concept of how pituitary GH is regulated by somatostatin and GHRH has changed in recent years, following the discovery of peripheral hormones involved in the regulation of energy homeostasis and mineral homeostasis. These hormones are ghrelin, nesfatins, and klotho. Ghrelin is an orexigenic hormone, released primarily by the gastric mucosa, although it is widely expressed in many different tissues, including the central nervous system and the pituitary. To be active, ghrelin must bind to an n-octanoyl group (n = 8, generally) on serine 3, forming acyl ghrelin which can then bind and activate a G-protein-coupled receptor leading to phospholipase C activation that induces the formation of inositol 1,4,5-triphosphate and diacylglycerol that produce an increase in cytosolic calcium that allows the release of GH. In addition to its direct action on somatotrophs, ghrelin co-localizes with GHRH in several neurons, facilitating its release by inhibiting somatostatin, and acts synergistically with GHRH stimulating the synthesis and secretion of pituitary GH. Gastric ghrelin production declines with age, as does GH. Klotho is an anti-aging agent, produced mainly in the kidneys, whose soluble circulating form directly induces GH secretion through the activation of ERK1/2 and inhibits the inhibitory effect that IGF-I exerts on GH. Children and adults with untreated GH-deficiency show reduced plasma levels of klotho, but treatment with GH restores them to normal values. Deletions or mutations of the Klotho gene affect GH production. Nesfatins 1 and 2 are satiety hormones, they inhibit food intake. They have been found in GH3 cell cultures where they significantly reduce the expression of gh mRNA and that of pituitary-specific positive transcription factor 1, consequently acting as inhibitors of GH production. This is a consequence of the down-regulation of the cAMP/PKA/CREB signaling pathway. Interestingly, nesfatins eliminate the strong positive effect that ghrelin has on GH synthesis and secretion. Throughout this review, we will attempt to broadly analyze the role of these hormones in the complex world of GH regulation, a world in which these hormones already play a very important role.


1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


1987 ◽  
Vol 116 (2) ◽  
pp. 165-171 ◽  
Author(s):  
Koji Nakagawa ◽  
Tatsuya Ishizuka ◽  
Takao Obara ◽  
Miyao Matsubara ◽  
Kazumasa Akikawa

Abstract. The mechanism of apparently discrepant actions of glucocorticoids (GC) on GH secretion, in vivo suppression and in vitro potentiation, was studied in rats. Dexamethasone (Dex), at the concentration of 50 nmol/l, Potentiated basal and GHRH-stimulated GH release from monolayer culture of normal rat pituitary cells in 48 h. On the other hand, in vivo administration of Dex, 165 μg daily for 3 days, consistently suppressed serum GH levels in female rats. In these rats, the hypothalamic content of immunoreactive (IR) SRIH was significantly increased, whereas that of IR-GHRH was significantly decreased in comparison with the untreated rats. Bioassayable GH-releasing activity was also lower in Dex-treated rats. These findings indicate that the suppressing effect of GC on GH release in vivo is, at least partially, due to the increase in hypothalamic SRIH release and probably also to the decrease in GHRH release, and these effects surpass the potentiating effect of GC on GH release at the pituitary level, resulting in a net inhibitory effect in vivo.


1987 ◽  
Vol 114 (4) ◽  
pp. 465-469 ◽  
Author(s):  
Gian Paolo Ceda ◽  
Robert G. Davis ◽  
Andrew R. Hoffman

Abstract. Glucocorticoids have been shown to have both stimulatory and suppressive effects on GH secretion in vitro and in vivo. In order to study the kinetics of glucocorticoid action on the somatotrope, cultured rat pituitary cells were exposed to dexamethasone for varying periods of time. During short-term incubations (≤ 4 h), dexamethasone inhibited GHRH and forskolin-elicited GH secretion, but during longer incubation periods, the glucocorticoid enhanced both basal and GHRH-stimulated GH release. The inhibitory effect of brief dexamethasone exposure was also seen in cells which previously had been exposed to dexamethasone. In addition, growth hormone secretion from cultured rat and human somatotropinoma cells was inhibited by a brief exposure to dexamethasone. Thus, the nature of glucocorticoid action on the isolated cultured somatotrope is biphasic, with brief exposure inhibiting, and more prolonged exposure stimulating GH secretion.


1986 ◽  
Vol 111 (1) ◽  
pp. 91-97 ◽  
Author(s):  
S. Harvey ◽  
S.-K. Lam ◽  
T. R. Hall

ABSTRACT Passive immunization of immature chickens with sheep somatostatin (SRIF) antiserum promptly increased the basal plasma GH concentration and augmented TRH-induced GH secretion. Although exogenous SRIF had no inhibitory effect on the basal GH concentration in untreated birds or birds pretreated with non-immune sheep serum, it suppressed the stimulatory effect of SRIF immunoneutralization on GH secretion. These results suggest that SRIF is physiologically involved in the control of GH secretion in birds, in which it appears to inhibit GH release tonically. J. Endocr. (1986) 111, 91–97


1984 ◽  
Vol 106 (4) ◽  
pp. 443-447 ◽  
Author(s):  
M. Ishibashi ◽  
T. Hara ◽  
Y. Tagusagawa ◽  
T. Fukushima ◽  
H. Numata ◽  
...  

Abstract. In an attempt to test the hypothesis that pituitary adenomas of acromegaly may possess altered cellular membrane receptors, the response of growth hormone (GH) secretion to ovine corticotrophin-releasing factor (CRF) in cultured adenoma cells of acromegaly was studied. In three out of seven experiments using different pituitary adenoma cells in culture, nanomolar concentrations of CRF caused a significant increase in GH release. The CRF-induced GH release was reproducible and a dose-response relationship was observed between the CRF concentrations and the amounts of GH released into the incubation media. Hydrocortisone, at a concentration of 1 μm, on the other hand, resulted in a significant decrease in GH secretion in four out of five experiments. When adenoma cells were co-incubated with CRF and 1 μm hydrocortisone, CRF-induced GH release was partially overcome. In one experiment, the inhibitory effect of hydrocortisone was reversed by coincubation with CRF, although CRF alone was ineffective in the stimulation of GH. These results suggest that CRF may stimulate GH release in some, though not all, patients with acromegaly, and that glucocorticoids may block this effect of CRF acting directly on the pituitary adenoma cells of acromegaly.


1992 ◽  
Vol 126 (2) ◽  
pp. 113-116 ◽  
Author(s):  
SM Corsello ◽  
A Tofani ◽  
S Della Casa ◽  
R Sciuto ◽  
CA Rota ◽  
...  

Previous studies have shown that corticotropin-releasing hormone (CRH) is capable of inhibiting growth hormone (GH) secretion in response to GH-releasing hormone (GHRH). In an attempt to clarify the mechanism of the CRH action, we have studied the effect of enhanced cholinergic tone induced by pyridostigmine on the CRH inhibition of the GH response to GHRH in a group of six normal men and six normal women. All subjects presented a normal GH response to 50 μg iv GHRH administration (mean peak±sem plasma GH levels 20±2.9 μg/l in men and 28.9±2.9 μg/l in women) with a further significant increase after pyridostigmine pretreatment (60mg orally given 60 min before GHRH) in men (GH peaks 43.1±6.9 μg/l, p<0.005) but not in women (GH peaks 39.2±3.0 μg/l). In the same subjects, peripherally injected CRH (100 μg) significantly inhibited the GH response to GHRH (GH peaks 8.1±0.6 μg/l in men, p<0.005 and 9.9±0.7 μg/l in women, p<0.005). Pyridostigmine (60 mg) given orally at the same time of CRH administration (60 min before GHRH) reversed the CRH inhibition of GHRH-induced GH secretion (GH peaks 35.3±8.2 μg/l in men and 35±3.3 μg/l in women) with a response not significantly different to that seen in the pyridostigmine plus GHRH test. Our data confirm that pyridostigmine is capable of potentiating the GHRH-induced GH release in normal male but not female subjects. In addition, our studies show that the potentiating action of pyridostigmine on the GHRH-induced GH secretion prevails on the inhibiting effect of CRH when the two drugs are given together 1 h before GHRH injection. Both CRH and pyridostigmine could exert their action by modifying, in opposite ways, somatostatin release from the hypothalamus.


1974 ◽  
Vol 76 (3) ◽  
pp. 488-494 ◽  
Author(s):  
M. Peracchi ◽  
F. Cavagnini ◽  
A. E. Pontiroli ◽  
U. Raggi ◽  
A. Malinverni ◽  
...  

ABSTRACT The effects of intravenously administered aminophylline on growth hormone (GH) secretion have been studied in sixteen normal subjects and four acromegalic patients. Intravenous infusion of theophylline ethylenediamine 480 mg over a 30 min period did not alter the blood glucose and serum GH levels in six normal subjects but raised the plasma FFA by 88 %. By contrast, in four acromegalic patients theophylline administration resulted in a fall of the serum GH levels by 17.6–51.7 %, mean 36.5%. In ten normal subjects the infusion of the drug clearly blunted the GH response to insulin hypoglycaemia without modifying the decrease in blood glucose and plasma FFA induced by insulin: mean peak GH values decreased from 32.7 ± 3.39 to 21.4 ± 4.10 ng/ml (P < 0.025). These data seem to indicate that theophylline has an overall inhibiting effect on the hypothalamic-hypophyseal axis for GH secretion.


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