Manipulation of protein and fat accretion in growing cattle

1991 ◽  
Vol 1991 ◽  
pp. 18-18
Author(s):  
J.M. Dawson ◽  
D.E. Beever ◽  
P.J. Buttery ◽  
M. Gill
Keyword(s):  
Growth Hormone ◽  
Muscle Protein ◽  
Adrenergic Agonists ◽  
Plasma Growth Hormone ◽  
Direct Stimulation ◽  
Hormone Administration ◽  
Young Cattle ◽  
Plasma Gh

ß-adrenergic agonists are powerful repartitioning agents, increasing muscle protein accretion and reducing fat deposition in a variety of species. Their exact mode of action is not fully understood but some of their effects are similar to those elicited by exogenous growth hormone administration. Whilst there are few reports of plasma growth hormone (GH) concentrations being elevated in animals treated with ß-agonists, several in vitro studies have clearly demonstrated a direct stimulation of GH release from perifused or cultured pituitary or adenohypophyseal cells on administration of these agents. More recently, a brief, rapid rise in plasma GH has been demonstrated in rats infused intra-atrially with isoproterenol and this was sustained when the animals were pre-treated with somatotropin release inhibitory factor (somatostatin; SRIF) antiserum. This raises the possibility that ß-adrenergic agonists do stimulate GH release in vivo but that this response is rapidly counteracted by SRIF release.The aim of this work was to attempt to enhance the repartitioning effect of ß-adrenergic agonists by immunizing young cattle against SRIF whilst administering cimaterol.

Mechanism of action of Hexarelin. I. Growth hormone-releasing activity in the rat

1996 ◽  
Vol 135 (4) ◽  
pp. 481-488 ◽  
Author(s):  
Antonio Torsello ◽  
Roberta Grilli ◽  
Marina Luoni ◽  
Margherita Guidi ◽  
Maria Cristina Ghigo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Mechanism Of Action ◽  
Direct Action ◽  
Male Rats ◽  
Surgical Ablation ◽  
Adult Rats ◽  
Gh Secretion ◽  
Plasma Gh

Torsello A, Grilli R, Luoni M, Guidi M, Ghigo MC, Wehrenberg WB, Deghenghi R, Müller EE, Locatelli V. Mechanism of action of Hexarelin. I. Growth hormone-releasing activity in the rat. Eur J Endocrinol 1996;135:481–8. ISSN 0804–4643 We have reported Hexarelin (HEXA), an analog of growth hormone-releasing peptide 6 (GHRP-6), potently stimulates growth hormone (GH) secretion in infant and adult rats. This study was undertaken to further investigate Hexarelin's mechanisms of action. In 10-day-old pups, treatments with HEXA (80 μg/kg, b.i.d.) for 3–10 days significantly enhanced, in a time-related fashion, the GH response to an acute HEXA challenge. Qualitatively similar effects were elicited in pups passively immunized against growth hormone-releasing hormone (GHRH) from birth. In adult male rats, a 5-day pretreatment with HEXA (150 μg/kg, b.i.d.) did not enhance the effect of the acute challenge, and the same pattern was present after a 5-day pretreatment in male rats with surgical ablation of the mediobasal hypothalamus (MBH-ablated rats). In addition, in adult sham-operated rats, Hexarelin (300 μg/kg, iv) induced a GH response greater (p < 0.05) than that induced by GHRH (2 μg/kg, iv). However, in MBH-ablated rats 7 days after surgery, GHRH was significantly (p < 0.05) more effective than HEXA, and 30 days after surgery HEXA and GHRH evoked similar rises of plasma GH. Finally, the in vitro Hexarelin (10−6 mol/l) effect was transient while GHRH (10−8 mol/l) induced a longer lasting and greater GH release. Three different mechanisms, not mutually exclusive, are postulated for Hexarelin stimulation of GH secretion in vivo: a direct action on the pituitary, though of minor relevance; an indirect action that involves release of GHRH, of relevance only in adult rats; and an action through the release of a still unknown hypothalamic "factor", which in infant and adult rats elicits GH release acting sinergistically with GHRH. Antonio Torsello, Department of Pharmacology, via Vanvitelli 32, 20129 Milano, Italy

scholarly journals In vitro lipid metabolism, growth and metabolic hormone concentrations in hyperthyroid chickens

1992 ◽  
Vol 68 (3) ◽  
pp. 667-676 ◽  
Author(s):  
R. W. Rosebrough ◽  
J. P. McMurtry ◽  
R. Vasilatos-Younken
Keyword(s):  
Growth Hormone ◽  
Broiler Chickens ◽  
Lipid Synthesis ◽  
High Rate ◽  
Feed Consumption ◽  
Plasma Growth Hormone ◽  
Indian River ◽  
Plasma Gh ◽  
Metabolic Hormone

Indian River male broiler chickens growing from 7 to 28 d of age were fed on diets containing energy: protein values varying from 43 to 106 MJ/kg protein and containing 0 or 1 mg triiodothyronine (T3)/kg diet to study effects on growth, metabolic hormone concentrations and in vitro lipogenesis. In vitro lipid synthesis was determined in liver explants in the presence and absence of ouabain (Na+, K+-transporting ATPase (EC 3.6.1.37) inhibitor) to estimate the role of enzyme activity in explants synthesizing lipid. Growth and feed consumption increased (P < 0.01) when the energy: protein value decreased from 106 to 71 MJ/kg protein; however, both variables decreased as the value was further decreased from 53 to 43 MJ/kg protein. Triiodothyronine depressed (P < 0.01) growth, but not food intake. Large energy:protein diets (> 53 MJ/kg protein) and dietary T3 lowered (P < 0.01) plasma growth hormone. Large energy:protein diets (> 53 MJ/kg protein) increased (P < 0.01) lipogenesis, plasma growth hormone (GH) and decreased plasma insulin-like growth factor 1 (IGF-1). Also, T3 decreased plasma GH, IGF-1 in vitro lipogenesis. Ouabain inhibited a greater proportion of in vitro lipogenesis in those explants synthesizing fat at a high rate. Both dietary T3 and in vitro ouabain decrease lipogenesis, but, when combined, the effects are not cumulative

Relationship between plasma growth hormone concentration and cellular sodium transport in acromegaly

1992 ◽  
Vol 127 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Hans Herlitz ◽  
Olof Jonsson ◽  
Bengt-Åke Bengtsson
Keyword(s):  
Growth Hormone ◽  
Sodium Transport ◽  
Negative Relationship ◽  
Sodium Content ◽  
Plasma Growth Hormone ◽  
Sodium Influx ◽  
Active Acromegaly ◽  
One Year ◽  
Plasma Gh

We investigated the relationship between mean plasma growth hormone (GH) concentration and cellular sodium transport in untreated and treated acromegaly. Seventeen patients (age 55±3 years) with active acromegaly were studied with respect to plasma GH (mean of 24 h GH profile) and erythrocyte electrolyte content as well as transmembrane sodium transport. The patients were reinvestigated two weeks after successful surgery (N=14) and again after one year (N=13). Erythrocyte electrolytes were analyzed by flame photometry and sodium influx and efflux rate constant determined by in vitro incubation using a modified Keyne's formula. In patients with active acromegaly there was a significant positive correlation between IGF-1 and cellular sodium transport, while GH tended to show a negative relationship to the same parameter. After successful treatment, both IGF-1 and GH disclosed a positive relationship to cellular sodium transport. After one year, a significant increase in erythrocyte sodium content was seen in the patients compared to the preoperative situation. In conclusion, if this is a generalized phenomenon the results are compatible with a sodium-retaining effect of GH via stimulation of transmembrane sodium transport. In active acromegaly this may be counteracted by a sodium transport inhibitor giving the reverse relationship between GH and cellular sodium transport.

TRH and GRF stimulate release of growth hormone through different mechanisms

1986 ◽  
Vol 250 (5) ◽  
pp. E512-E517
Author(s):  
M. Szabo
Keyword(s):  
Growth Hormone ◽  
Response Curves ◽  
Calcium Dependent ◽  
System A ◽  
Effective Doses ◽  
Primary Monolayer ◽  
Plasma Gh ◽  
Primary Monolayer Cultures

Thyrotropin-releasing hormone (TRH) is an effective stimulator of growth hormone (GH) release from cultured adenohypophysial cells of chronically hypothyroid rats in vitro. The present study explored the question of cAMP and calcium mediation of the GH-stimulatory effect of TRH in this system. A maximally stimulatory concentration of TRH was added together with various concentrations of human GH-releasing factor 40 (hGRF-40) whose action is cAMP mediated, or of dibutyryl cAMP (DBcAMP), to primary monolayer cultures of adenohypophysial cells from thyroidectomized rats. The GH responses to the combined addition of TRH with all doses of GRF or DBcAMP were fully additive, causing parallel elevations of the dose-response curves. Whereas the GH response to maximally effective concentrations of hGRF-40 and DBcAMP, added together, was not greater than that to either secretagogue alone, the inclusion of TRH increased the response to a new Emax. The calcium inhibitors, verapamil, EGTA, and CoCl2, markedly suppressed basal GH release and virtually completely blocked the GH response to TRH, suggesting calcium mediation. In chronically hypothyroid, urethan-anesthetized rats, the in vivo effect of the combined administration of maximally effective doses of TRH and GRF on plasma GH levels was also additive. These findings indicate that TRH stimulates GH release in adenohypophysial cells of hypothyroid rats by a cAMP-independent, calcium-dependent mechanism.

Effect of corticotrophin-releasing hormone administration on growth hormone levels in acromegaly: in vivo and in vitro studies

1994 ◽  
Vol 131 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Annamaria Colao ◽  
Bartolomeo Merola ◽  
Diego Ferone ◽  
Maria Rosaria Calabrese ◽  
Salvatore Longobardi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Vitro Study ◽  
In Vitro Studies ◽  
Vitro Study ◽  
Releasing Hormone ◽  
Paradoxical Response ◽  
Hormone Administration ◽  
Active Acromegaly

Colao A, Merola B, Ferone D, Calabrese MR, Longobardi S, Spaziante R, Di Renzo G, Annunziato L, Lombardi G. Effect of corticotrophin-releasing hormone administration on growth hormone levels in acromegaly: in vivo and in vitro studies. Eur J Endocrinol 1994;131:14–19. ISSN 0804–4643 The ability of CRH to cause a paradoxical response of GH in acromegaly is still under debate. In this study, the effect of CRH administration on GH release was evaluated in a large series of patients with active acromegaly, both in vivo, compared to that of TRH and GnRH, and in vitro. The study was organized as follows. In vivo study: 30 acromegalic patients were submitted to TRH, GnRH, and CRH tests on non-consecutive days: blood samples were collected before and 10, 20, 30, 45, 60, 90, and 120 min after bolus. In nine patients the CRH test was repeated after a 3-month therapy with octreotide and at the dose of 300–600 μg sc thrice daily. In vitro study: CRH (10 nmol/l, 100 nmol/l, and 1 μmol/l) was tested on pituitary tumor tissue obtained in eight patients during transsphenoidal adenomectomy and immediately placed in sterile Ca2+ and Mg2+ free buffer phosphate. A paradoxical GH response to TRH (evaluated as a GH increase over 50% of basal values) was recorded in 19 patients (63.3%), whereas 7 patients (23.3%) responded to GnRH and 4 others to CRH (13.3%). TRH administration induced a maximal percent GH increase significantly greater than that induced by GnRH and CRH (p < 0.05). Octreotide caused the normalization of GH and insulin-like growth factorI levels in all the patients, as well as the disappearance of the GH paradoxical response to CRH in 3/4 patients. All four CRH responders and four CRH non-responders, used as controls, were surgically treated and adenomatous tissue was used for the in vitro study. No significant GH increase was found in the CRH non-responders and in the three CRH responders in whom the GH paradoxical response to CRH disappeared during octreotide treatment. Conversely, a significant GH increase (over 250% of pre-incubation values) after CRH administration was found in the remaining case. In conclusion, the results of the present study show that CRH is rarely able to stimulate paradoxical GH response in patients with active acromegaly and that the in vivo recorded GH release after CRH is in vitro reproducible only in extremely rare cases. Annamaria Colao, Corso Europa 63, 80127 Napoli, Italy

On the role of the peptide galanin in regulation of growth hormone secretion

1991 ◽  
Vol 125 (5) ◽  
pp. 518-525 ◽  
Author(s):  
Anna-Lena Hulting ◽  
Björn Meister ◽  
Lena Carlsson ◽  
Agneta Hilding ◽  
Olle Isaksson
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Human Anterior Pituitary ◽  
Plasma Gh

Abstract. The effects of the peptide galanin on growth hormone secretion were studied in vitro using cultured rat and human anterior pituitary cells, and in vivo by iv administration of galanin in both rats and humans. Galanin in concentrations from 10 nmol/l to 1 μmol/l did not alter basal GH release, but slightly inhibited GHRH-stimulated GH release from cultured rat anterior pituitary cells. Galanin (1 μmol/l) did not significantly change basal or GHRH-stimulated GH secretion from cultured human anterior pituitary cells. In contrast, iv injection of 1 μg (300 pmol) galanin to rats induced an increase in plasma GH that was reproducible at repetitive injections. The galanin-induced GH release in rats was of a lower magnitude than the increase in plasma GH after iv injections of GHRH, and was seen with a 5-15 min delay in comparison to iv administered GHRH. In man, iv infusions of galanin (40 pmol ·kg−1 · min−1 · (40 min)) also caused a significant increase in plasma GH, but it occurred 25-30 min after the beginning of the infusion. These results suggest an indirect action of galanin on GH release in both rats and humans, i.e. galanin does not directly affect the somatotropes. In agreement with a central action, no binding sites for galanin could be demonstrated in the rat anterior pituitary by autoradiography. Since galanin did not affect somatostatin release from fragments of rat mediobasal hypothalamus, the stimulatory effects of galanin on GH release are most likely mediated via a stimulatory effect on GHRH neurons.

In vitro and in vivo evidence that dopamine exerts growth hormone-releasing activity in goldfish

1993 ◽  
Vol 264 (6) ◽  
pp. E925-E932 ◽  
Author(s):  
A. O. Wong ◽  
J. P. Chang ◽  
R. E. Peter
Keyword(s):  
Growth Hormone ◽  
Body Growth ◽  
The Body ◽  
D1 Receptors ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
D1 Agonist ◽  
Plasma Gh

We have previously demonstrated that dopamine (DA) and the DA D1 agonist SKF 38393 stimulate growth hormone (GH) release from perifused pituitary fragments of the goldfish, suggesting an involvement of DA D1 receptors in GH regulation. In the present study, the role of DA on GH release and body growth of the goldfish was further investigated both in vivo and in vitro. DA consistently stimulated GH release in a dose-dependent manner from perifused goldfish pituitary fragments. The GH-releasing action of DA was seasonal, being the highest in sexually regressed fish, intermediate in recrudescent fish, and the lowest in sexually mature (prespawning) fish. Somatostatin, a known GH-release inhibitor in the goldfish, suppressed basal GH release and abolished the GH response to DA in perifused pituitary fragments as well as pituitary cells under static incubation. Intraperitoneal administration of the nonselective DA agonist apomorphine and the D1 agonist SKF 82958 increased the plasma GH levels in the goldfish. These GH responses were blocked by simultaneous treatment with the D1 antagonist Sch 23390 but not the D2 antagonist pimozide. Apomorphine administered orally also induced a similar elevation in plasma GH levels. Long-term feeding with apomorphine was found to be stimulatory to the body growth of goldfish. These results provide evidence that the neurotransmitter DA, by acting through DA D1 receptors in the pituitary, also functions as a GH-releasing factor in the goldfish.

Reduced and S-carboxymethylated human growth hormone: a probe for diabetogenic action

1984 ◽  
Vol 247 (5) ◽  
pp. E639-E644
Author(s):  
C. M. Cameron ◽  
J. L. Kostyo ◽  
J. A. Rillema ◽  
S. E. Gennick
Keyword(s):  
Growth Hormone ◽  
Amino Acid ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Mouse Mammary Gland ◽  
Amino Acid Incorporation ◽  
Acid Incorporation ◽  
Hypophysectomized Rats

The biological activity profile of reduced and S-carboxymethylated human growth hormone (RCM-hGH) was determined to establish its suitability for study of the diabetogenic property of hGH. RCM-hGH was found to have greatly attenuated in vivo growth-promoting activity in the 9-day weight-gain test in hypophysectomized rats (approximately 1%) and to have a similar low order of in vitro activity in stimulating amino acid incorporation into the protein of the isolated rat diaphragm. RCM-hGH also only had approximately 1% of the in vitro insulin-like activity of the native hormone on isolated adipose tissue from hypophysectomized rats. In contrast, RCM-hGH retained substantial in vivo diabetogenic activity in the ob/ob mouse, appearing to have approximately 50% of the activity of the native hormone. RCM-hGH was also found to retain significant, although attenuated (25%), in vitro lactogenic activity when tested for the ability to stimulate amino acid incorporation into a casein-rich protein fraction in mouse mammary gland explants. Because RCM-hGH exhibits a high degree of diabetogenic activity, although lacking significant anabolic or insulin-like activities, it will be useful as a "monovalent" probe for the study of the molecular mechanism of the diabetogenic action of GH.

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