scholarly journals The role of melanocortin-3 and -4 receptor in regulating appetite, energy homeostasis and neuroendocrine function in the pig

2004 ◽  
Vol 181 (1) ◽  
pp. 39-52 ◽  
Author(s):  
CR Barb ◽  
AS Robertson ◽  
JB Barrett ◽  
RR Kraeling ◽  
KL Houseknecht
Keyword(s):  
Missense Mutation ◽  
Feed Intake ◽  
Energy Homeostasis ◽  
Dose Range ◽  
Critical Role ◽  
Hormone Secretion ◽  
Growing Pigs ◽  
Hek293 Cells ◽  
Pituitary Hormone ◽  
Gh Secretion

A recently discovered class of receptors, melanocortin-3 and -4 receptor (MC3/4-R), are located within the brain and modulate feed intake in rodents. Stimulation of the receptor (agonist) inhibits feed intake whereas blockade (antagonist) of the receptor increases intake. Our knowledge of factors regulating voluntary feed intake in humans and domestic animals is very limited. i.c.v. administration of an MC3/4-R agonist, NDP-MSH, suppressed (P<0.05) feed intake compared with controls at 12, 24, 48 and 72 h after treatment in growing pigs. Fed pigs were more responsive to the MC3/4-R agonist then fasted animals. However, i.c.v. treatment with MC3/4-R antagonist, SHU9119, failed to stimulate intake. The failure of MC3/4-R antagonist to stimulate feed intake suggests involvement of other brain hormone(s) which antagonize the action of SHU9119 at the MC3/4-R, blocking its stimulatory effect on intake. Treatment with NDP-MSH or SHU9119, across a wide dose range, failed to affect LH and GH secretion, except for the 10 micro g dose of NDP-MSH, which exhibited both a stimulatory and an inhibitory effect on GH secretion in fasted animals. Treatment with agouti-related peptide, a natural brain hormone that blocks the MC3/4R, failed to stimulate feed intake. These results do not support the idea that endogenous melanocortin pays a critical role in regulating feed intake and pituitary hormone secretion in the pig. SHU9119 blocked the NDP-MSH-induced increase in cAMP in HEK293 cells expressing the porcine MC4-R sequence without the missense mutation. The EC(50) and IC(50) values were similar to the human MC4-R, confirming that SHU9119 is a pig MC4-R antagonist. However, pigs were heterozygous for an MC4-R gene missense mutation. It is possible that the MC4-R mutation alters function and this may explain the failure to demonstrate MC3/4-R involvement in modulating feeding behavior and LH and GH secretion in the pig.

scholarly journals MOLECULAR EVOLUTION OF GPCRS: 26Rfa/GPR103

2014 ◽  
Vol 52 (3) ◽  
pp. T119-T131 ◽  
Author(s):  
Kazuyoshi Ukena ◽  
Tomohiro Osugi ◽  
Jérôme Leprince ◽  
Hubert Vaudry ◽  
Kazuyoshi Tsutsui
Keyword(s):  
Energy Homeostasis ◽  
Hormone Secretion ◽  
Pituitary Hormone ◽  
Nociceptive Transmission ◽  
Functional Studies ◽  
Cognate Receptor ◽  
Current State ◽  
Representative Species ◽  
Peptide Family ◽  
G Protein Coupled

Neuropeptides possessing the Arg-Phe-NH2 (RFamide) motif at their C-termini (designated as RFamide peptides) have been characterized in a variety of animals. Among these, neuropeptide 26RFa (also termed QRFP) is the latest member of the RFamide peptide family to be discovered in the hypothalamus of vertebrates. The neuropeptide 26RFa/QRFP is a 26-amino acid residue peptide that was originally identified in the frog brain. It has been shown to exert orexigenic activity in mammals and to be a ligand for the previously identified orphan G protein-coupled receptor, GPR103 (QRFPR). The cDNAs encoding 26RFa/QRFP and QRFPR have now been characterized in representative species of mammals, birds, and fish. Functional studies have shown that, in mammals, the 26RFa/QRFP–QRFPR system may regulate various functions, including food intake, energy homeostasis, bone formation, pituitary hormone secretion, steroidogenesis, nociceptive transmission, and blood pressure. Several biological actions have also been reported in birds and fish. This review summarizes the current state of identification, localization, and understanding of the functions of 26RFaQRFP and its cognate receptor, QRFPR, in vertebrates.

scholarly journals Signal Transduction Mechanisms for Glucagon-Induced Somatolactin Secretion and Gene Expression in Nile Tilapia (Oreochromis niloticus) Pituitary Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Chaoyi Zhang ◽  
Anji Lian ◽  
Yue Xu ◽  
Quan Jiang
Keyword(s):  
Gene Expression ◽  
Oreochromis Niloticus ◽  
Nile Tilapia ◽  
Primary Cultures ◽  
Hormone Secretion ◽  
Hek293 Cells ◽  
Luciferase Reporter ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Mrna Levels

Glucagon (GCG) plays a stimulatory role in pituitary hormone regulation, although previous studies have not defined the molecular mechanism whereby GCG affects pituitary hormone secretion. To this end, we identified two distinct proglucagons, Gcga and Gcgb, as well as GCG receptors, Gcgra and Gcgrb, in Nile tilapia (Oreochromis niloticus). Using the cAMP response element (CRE)-luciferase reporter system, tilapia GCGa and GCGb could reciprocally activate the two GCG receptors expressed in human embryonic kidney 293 (HEK293) cells. Quantitative real-time PCR analysis revealed that differential expression of the Gcga and Gcgb and their cognate receptors Gcgra and Gcgrb was found in the various tissues of tilapia. In particular, the Gcgrb is abundantly expressed in the neurointermediate lobe (NIL) of the pituitary gland. In primary cultures of tilapia NIL cells, GCGb effectively stimulated SL release, with parallel rises in the mRNA levels, and co-incubation with the GCG antagonist prevented GCGb-stimulated SL release. In parallel experiments, GCGb treatment dose-dependently enhanced intracellular cyclic adenosine monophosphate (cAMP) accumulation with increasing inositol 1,4,5-trisphosphate (IP3) concentration and the resulting in transient increases of Ca2+ signals in the primary NIL cell culture. Using selective pharmacological approaches, the adenylyl cyclase (AC)/cAMP/protein kinase A (PKA) and phospholipase C (PLC)/IP3/Ca2+/calmodulin (CaM)/CaMK-II pathways were shown to be involved in GCGb-induced SL release and mRNA expression. Together, these results provide evidence for the first time that GCGb can act at the pituitary level to stimulate SL release and gene expression via GCGRb through the activation of the AC/cAMP/PKA and PLC/IP3/Ca2+/CaM/CaMK-II cascades.

Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis

2006 ◽  
Vol 290 (5) ◽  
pp. E982-E988 ◽  
Author(s):  
Gabriella Segal-Lieberman ◽  
Hadara Rubinfeld ◽  
Moran Glick ◽  
Noga Kronfeld-Schor ◽  
Ilan Shimon
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Pituitary Hormones ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Cells ◽  
Human Pituitary ◽  
Gh Secretion ◽  
Melanin Concentrating Hormone

Melanin-concentrating hormone (MCH), a 19-amino acid orexigenic (appetite-stimulating) hypothalamic peptide, is an important regulator of energy homeostasis. It is cleaved from its precursor prepro-MCH (ppMCH) along with several other neuropeptides whose roles are not fully defined. Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21–22 wk gestation) and cultured GH-secreting adenomas. We found that MCH receptor-1 (MCH-R1), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas. MCH (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation ( P < 0.05). Interestingly, neuropeptide EI (10 nM), which is also cleaved from ppMCH, increased human GH secretion by up to 124% in fetal pituitaries. A milder, albeit significant, induction of GH secretion by MCH (20%) was seen in cultured GH-secreting pituitary adenomas. A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH. Treatment of cultured GH adenoma cells with MCH (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1. In aggregate, these data suggest that MCH may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.

scholarly journals The Complex World of Regulation of Pituitary Growth Hormone Secretion: The Role of Ghrelin, Klotho, and Nesfatins in It

2021 ◽  
Vol 12 ◽  
Author(s):  
Jesús Devesa
Keyword(s):  
Energy Homeostasis ◽  
Direct Action ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Cytosolic Calcium ◽  
Inhibitory Effect ◽  
Complex World ◽  
Gh Secretion ◽  
Acyl Ghrelin

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.

scholarly journals Growth Hormone Secretion Does Not Increase After Interleukin-2 Administration in Healthy Men

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A520-A520
Author(s):  
Ferdinand Roelfsema ◽  
Rebecca Yang ◽  
Johannes D Veldhuis
Keyword(s):  
Low Dose ◽  
Hormone Secretion ◽  
Interleukin 2 ◽  
Growth Hormone Secretion ◽  
Pituitary Hormone ◽  
Deconvolution Analysis ◽  
Healthy Men ◽  
Gh Secretion ◽  
Older Subjects ◽  
Young Subjects

Abstract Context: Interleukin-2 (IL2), a proinflammatory cytokine, is used for treatment of malignancies. Increased cortisol and ACTH were noted, but GH secretion was not investigated in detail. This is the first study in healthy men which uses moderate high IL2 doses as used in cancer treatment. Objective: The goal of this study was to quantify GH secretion after a single sc injection of IL2 in young and older healthy men in relation to dose, age and body composition. Design: This was a placebo-controlled, blinded, prospectively randomized cross-over study in 17 young subjects (mean age 24.1 yr) and 18 older subjects (mean age 63.9 yr). The subjects underwent 24 h of blood sampling at 10-min intervals, starting at 1800 h. At 2000 h IL2 (3 or 6 million units per m2 body surface) or saline was injected sc. Lights were off between 2300 and 0700 h. Outcome Measures: Deconvolution analysis of GH. Abdominal visceral fat (AVF) was calculated from single slice CT. Results: GH secretion (pulsatile and total) was negatively related to AVF (R=0.67, P&lt;0.0001) and to age (R=0.56, P=0.001). These relations were maintained after IL2 administration. GH profiles were pulsatile under both experimental conditions. Since the effect of IL2 might be limited in time, GH deconvolution analyses were performed on the complete 24 h data series, the period with lights off and 6 h after IL2 administration. Total 24 h GH secretion decreased non-significantly from 74.6 ±10.2 to 67.5±7.4 µg/L (P=0.25) and pulsatile secretion from 69.4±9.8 to 62.2±7.4 µg/L (P=0.23). In the GLM procedure the effect of IL2 treatment was borderline significant (P=0.08), no interaction with age (P=0.28), but borderline with IL2 dose (P=0.07), and caused by decreased GH secretion (88 to 67 µg/L) at a low dose IL2. In a sub-analysis of the two age groups no effect on GH secretion in the older group was noted, in contrast to young subjects, especially on low dose IL2 (P=0.07). The analysis was refined further by calculating cumulative pulse masses in 2-h bins. By this approach it could be demonstrated that the cumulative GH pulse mass in older subjects across the 24 h was unchanged, while that in young subjects was temporarily inhibited in the bins between midnight and 0400 h (P=0.019 and 0.038). Conclusion: This study demonstrated that IL2 temporarily diminished GH secretion in young but not elderly volunteers. Pituitary hormone secretion by IL2 has not been studied as extensively as other cytokines, including IL1, IL6 and TNF. IL2 stimulates ACTH and TSH, inhibits LH and has no effect on GH secretion by rat pituitary (PNAS 58:185,1993). In patients with renal cancer IL2 infusion has no effect on GH levels (Anti-Cancer Res 10:753,1990. The present findings extend these observations to a large group of healthy volunteers, in whom we demonstrated previously suppression of the gonadal axis and activation of the HPA-axis (JCEM 101:539,2016, Endocr Connect 9:637,2010).

Long-term in-vitro maintenance of growth hormone secretion from human somatotrophinomas with cortisol, and its effects on growth hormone-releasing factor

1987 ◽  
Vol 114 (3) ◽  
pp. 503-509 ◽  
Author(s):  
M. Daniels ◽  
M. C. White ◽  
P. Kendall-Taylor
Keyword(s):  
Growth Hormone ◽  
Dose Range ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Test Dose ◽  
Gh Secretion ◽  
Term Maintenance ◽  
Secretion Rates

ABSTRACT The effect of cortisol (206 nmol/l) on GH secretion from enzymatically dispersed human somatotrophinoma cells in long-term culture was studied using adenomas from 13 patients with acromegaly. Basal GH secretion from cultures of three out of five tumours measured during periods of 4 hours declined to < 10 μu. GH/culture within 21 days. Secretion from two other tumours measured during 24 h also declined but GH concentrations were still readily detectable (> 100 μu./culture) by 28 or 58 days after cell dispersal. The decline in GH secretion was reversed in all seven tumours when cultures were maintained in cortisol-supplemented medium (CM), 4-h secretion rates being increased or retained at ≥ 100 μu./culture for as long as the studies were continued (range 18–291 days), and 24-h secretion rates at > 1000 μu./culture (range 28–58 days). GH secretion and content from cultures of two additional somatotrophinomas were increased by treatment with cortisol for 5 or 9 days but there was no concomitant effect on cell number. During long-term maintenance of cultures in CM (range 5–40 days), cortisol partially or completely blocked the 4-h GH response to a test dose of GH-releasing factor (GRF) (20 nmol/l) in five out of six tumours, and to a dose range of GRF (0·01–20 nmol/l) in two of them. However, when cultures maintained in this way (range 7–89 days) were rinsed and acute studies performed in medium without added cortisol, a significant (P < 0·05) stimulatory effect of GRF either at a test dose of 20 nmol/l or with a dose range (0·02–20 nmol/l) was observed in all six tumours tested. In conclusion, long-term maintenance of human somatotrophinoma cells in medium supplemented with cortisol (206 nmol/l) prevents the early decline in GH secretion and extends their functional lifespan for several weeks or months. However, the stimulatory effects of GRF during such treatment are usually partially or completely blocked in the presence of medium containing cortisol but restored when cortisol is excluded from the medium. J. Endocr. (1987) 114, 503–509

Effects of trifluoperazine on rat prolactin, growth hormone, thyroid stimulating hormone and adrenocorticotrophin secretion in vitro

1983 ◽  
Vol 103 (4) ◽  
pp. 492-496 ◽  
Author(s):  
Ruth C. Powell ◽  
Mark Daniels ◽  
Graham K. Innes ◽  
Michael J. Ashby ◽  
Keith Mashiter
Keyword(s):  
Growth Hormone ◽  
Primary Cultures ◽  
Hormone Secretion ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Hormone ◽  
Gh Secretion ◽  
Tsh Secretion ◽  
Stimulation Of ◽  
Stimulating Hormone

Abstract. We have studied the effects of trifluoperazine, a proposed inhibitor of calmodulin directed cellular function, on adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH), prolactin (Prl) and growth hormone (GH) secretion from primary cultures of rat adenohypophyseal cells. 5 × 10−6 m and 10−5 m trifluoperazine caused a significant (P < 0.005) reversible dose-related decrease in basal Prl secretion but was less effective on basal GH secretion, significant reversible inhibition (P< 0.005) occurring only with 10−5 m. Trifluoperazine did not consistently alter basal ACTH or TSH secretion but did inhibit 10−2 m theophylline stimulation of ACTH, Prl and GH secretion and 1.5 × 10−7 m TRH stimulation of TSH and Prl secretion. Paradoxically 10−5 m trifluoperazine enhanced theophylline stimulation of TSH secretion. Our results show trifluoperazine to have differential effects on Prl, GH, ACTH and TSH secretion, which are consistent with the known calcium dependence of pituitary hormone secretion and may suggest a role for calmodulin in this process.

METTL3-mediated RNA m6A hypermethylation promotes tumorigenesis and GH secretion of pituitary somatotroph adenomas

2021 ◽  
Author(s):  
Mengqi Chang ◽  
Zihao Wang ◽  
Jun Gao ◽  
Chengxian Yang ◽  
Ming Feng ◽  
...  
Keyword(s):  
Protein Expression ◽  
Pituitary Adenomas ◽  
Critical Role ◽  
Hormone Secretion ◽  
Dependent Manner ◽  
Initiation Point ◽  
Gh Secretion ◽  
Mutation Burden ◽  
Tissue Specimens

Abstract Introduction Pituitary growth hormone (GH)-secreting adenomas (GH-PAs) cause mass effects and dysregulated hypersecretion of GH. However, somatic mutation burden is low in PAs. While progress has been made in identifying the epigenetic changes involved in GH-PA initiation, the precise details of its tumorigenesis in GH-PA patients remains to be elucidated. As N 6-methyladenosine (m 6A) has been shown to often play a critical role in various tumors, it represents a possible initiation point for the tumorigenesis of pituitary adenomas. However, the role of RNA methylation in GH adenomas remains unclear. Methods Protein expression of m 6A regulators was measured by immunohistochemistry. Global levels and distribution of m 6A methylation were separately analyzed by m 6A ELISA and m 6A-seq. RNA interference and lentivirus knockdown system were used to investigate the role of methyltransferase METTL3 and its m 6A dependent regulatory mechanism in tumor progression and GH secretion. Results We show that both METTL3 mRNA and protein expression are elevated in GH-PA samples when compared with both normal pituitary tissue specimens and nonsecreting pituitary adenomas. Levels of m 6A modification increased in GH-PAs, and hypermethylated RNAs are involved in hormone secretion and cell development. Knockdown of METTL3 in GH3 cell line resulted in decreased cell growth and GH secretion. Importantly, we found that GNAS and GADD45γ act as the downstream targets in this process. Conclusion Our findings strongly suggest that m 6A methyltransferase METTL3 promotes tumor growth and hormone secretion by increasing expression of GNAS and GADD45γ in a m 6A-dependent manner. Thus, METTL3 and the methylated RNAs constitute suitable targets for clinical treatment of GH-PAs.

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
Keyword(s):  
Neuropeptide Y ◽  
Feed Intake ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Inhibitory Effect ◽  
Blood Samples ◽  
Gh Secretion ◽  
Lh Secretion ◽  
Serum Gh

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.

scholarly journals The Effects of Dose, Nutrition, and Age on Hexarelin-Induced Anterior Pituitary Hormone Secretion in Adult Patients on Maintenance Hemodialysis1

1999 ◽  
Vol 84 (4) ◽  
pp. 1220-1225
Author(s):  
Richard C. Jenkins ◽  
A. Meguid El Nahas ◽  
Martin E. Wilkie ◽  
Colin B. Brown ◽  
Jenny Jones ◽  
...  
Keyword(s):  
Effective Dose ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Area Under The Curve ◽  
Pituitary Hormone ◽  
Gh Secretion ◽  
Anterior Pituitary Hormone ◽  
Anabolic Action ◽  
Dose Response Study

Malnutrition is common in chronic renal failure (CRF) and adversely affects prognosis. In view of the anabolic action of GH in CRF, we have studied the effects of hexarelin, a GH secretagogue, on CRF. An iv dose-response study in six 20- to 40-yr-old well nourished hemodialysis (HD) patients was followed by administration of the maximally effective dose to six 20- to 40-yr-old healthy controls, six 20- to 40-yr-old poorly nourished HD patients, and six 50- to 70-yr-old poorly nourished HD patients. GH secretion (area under the curve over 180 min, mean ± se) after 2 and 1 μg/kg doses (10.7 ± 4.2 and 8.2 ± 5.2 min/U·L, respectively) was greater than after placebo (0.60 ± 0.11 min/U·L; P &lt; 0.001 and P &lt; 0.05, respectively). The most effective dose (2 μg/kg) produced similar GH secretion (11.4 ± 3.3 min/U·L) in controls. GH secretion in the younger poorly nourished HD group (19.0 ± 4.4 min/U·L) was not significantly different from that in the well nourished 20- to 40-yr-old HD patients (P = 0.06). GH secretion in the older, poorly nourished HD patients (9.4 ± 2.2 min/U·L) was similar to that in the young, poorly nourished group (P = 0.18). ACTH and cortisol concentrations increased in all groups, whereas PRL concentrations were not affected in CRF. The profound action of hexarelin on GH secretion has been shown to extend to CRF. Trends were evident toward increasing efficacy in malnourished subjects and decreasing efficacy with age. Further studies are required to determine whether the acute actions of hexarelin can be translated into long term anabolic changes.

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