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Growth Hormone Secretion (growth + hormone_secretion)
Selected AbstractsThe Ghrelin/Obestatin Balance in the Physiological and Pathological Control of Growth Hormone Secretion, Body Composition and Food IntakeJOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2010R. Hassouna Ghrelin and obestatin are two gastrointestinal peptides obtained by post-translational processing of a common precursor, preproghrelin. Ghrelin is an orexigenic and adipogenic peptide and a potent growth hormone secretagogue (GHS) modified by the enzyme ghrelin- O -acyl-transferase to bind and activate its receptor, the GHS-R. The ghrelin/GHS-R pathway is complex and the effects of ghrelin on GH secretion, adiposity and food intake appear to be relayed by distinct mechanisms involving different transduction signals and constitutive activity for the GH-R, different cofactors as modulators of endogenous ghrelin signalling and/or alternative ghrelin receptors. The discovery of obestatin in 2005 brought an additional level of complexity to this fascinating system. Obestatin was initially identified as an anorexigenic peptide and as the cognate ligand for GPR39, but its effect on food intake and its ability to activate GPR39 are still controversial. Although several teams failed to reproduce the anorexigenic actions of obestatin, this peptide has been shown to antagonise GH secretion and food intake induced by ghrelin and could be an interesting pharmacological tool to counteract the actions of ghrelin. Ghrelin and obestatin immunoreactivities are recovered in the blood with an ultradian pulsatility and their concentrations in plasma vary with the nutritional status of the body. It is still a matter of debate whether both hormones are regulated by independent mechanisms and whether obestatin is a physiologically relevant peptide. Nevertheless, a significant number of studies show that the ghrelin/obestatin ratio is modified in anorexia nervosa and obesity. This suggests that the ghrelin/obestatin balance could be essential to adapt the body's response to nutritional challenges. Although measuring ghrelin and obestatin in plasma is challenging because many forms of the peptides circulate, more sensitive and selective assays to detect the different preproghrelin-derived peptides are being developed and may be the key to obtaining a better understanding of their roles in different physiological and pathological conditions. [source] Masculinizing Effect of Dihydrotestosterone on Growth Hormone Secretion is Inhibited in Ovariectomized Rats with Anterolateral Deafferentation of the Medial Basal Hypothalamus or in Intact Female RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2000Tamura There is a striking sex difference in the pattern of growth hormone (GH) secretion in rats. Our previous studies showed that short-term administration of pharmacological doses of testosterone or dihydrotestosterone (DHT) masculinized the GH secretory pattern in ovariectomized (OVX) rats. The locus where testosterone or DHT interacts with the somatotropic axis is believed to be the hypothalamus. To obtain insights into this phenomenon, we administered a single dose of DHT s.c. to adult OVX rats at 0.01, 0.1 or 1 mg/rat. Blood GH concentrations were measured in unanaesthetized rats. Six to12 h after the s.c. administration of all three doses of DHT, the GH secretory pattern revealed a male-like secretory pattern as shown by episodic bursts occurring at 2,3-h intervals with low or undetectable trough levels. When anterolateral deafferentation of the medial basal hypothalamus (ALC) was performed, the blood concentrations revealed irregularly occurring small fluctuations, instead of the usual high bursts, but the basal GH concentration was significantly higher than that of OVX-sham-operated rats. DHT treatment did not elicit pulsatile GH secretion or alter GH concentrations in OVX rats with ALC. When intact adult female rats received DHT at a dose of 1 mg/rat, the male-like GH secretory pattern was not induced. These results suggest that neural inputs from the anterolateral direction to the medial basal hypothalamus are necessary for the masculinizing effect of DHT on the GH secretory pattern in OVX rats, and that oestrogen in intact female rats prevents the masculinizing effect of DHT. [source] Ghrelin: a new peptide regulating the neurohormonal system, energy homeostasis and glucose metabolismDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2008Peter Pusztai Abstract Identification of ghrelin started with the discovery of growth hormone secretagogues, continued with the description of ghrelin receptors and ended with the elucidation of the chemical structure of ghrelin. However, several issues concerning the role of ghrelin in physiological and pathophysiological processes are still under investigation. Most of the ghrelin produced in the body is secreted in the stomach, but it is also expressed in the hypothalamus, pituitary, pancreas, intestine, kidney, heart and gonads. Ghrelin stimulates growth hormone secretion via growth hormone secretagogue receptors. Ghrelin secretion in the stomach depends on both acute and chronic changes in nutritional status and energy balance. Current data support the hypothesis that the stomach, in addition to its important role in digestion, not only influences pituitary hormone secretion but, via ghrelin production, it also sends orexigenic (appetite increasing) signals to hypothalamic nuclei involved in the regulation of energy homeostasis. In addition to these main effects, ghrelin influences insulin secretion and glucose metabolism and it may exert potentially important effects on cardiovascular and gastrointestinal functions. Because of its effects on a large number of physiological functions, ghrelin may be involved in the pathomechanism of several human disorders, including disturbances of appetite, energy homeostasis and glucose metabolism. Further research might lead to a better understanding of the pathophysiology of ghrelin and might provide more effective therapy for the above disorders. Copyright © 2008 John Wiley & Sons, Ltd. [source] Craniofacial morphology, dental occlusion, tooth eruption, and dental maturity in boys of short stature with or without growth hormone deficiencyEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 5 2000Heidrun Kjellberg The aim of this project was to study the craniofacial morphology, dental occlusion, dental maturation and tooth eruption in short-statured boys with growth hormone secretion ranging from low to high. The measurements from lateral and postero-anterior cephalograms, orthopantomograms and plaster models were used. Almost all linear measurements of the facial structures were significantly smaller. A disproportionate growth in the cranial base structures as well as in the jaws resulted in facial retrognathia, a proportionately smaller posterior than anterior facial height, and a steep vertical inclination of the mandible. Dental crowding was more common and the overbite was small. Dental maturity and tooth eruption were delayed 1.2 and 1.3 yr, respectively. No significant differences between the idiopathic short-statured and the growth hormone-deficient group in any of the above-mentioned variables were found. It can be concluded that although most of the cephalometric variables measured differed significantly from the average, the facial appearance of the boys is not conspicuous and is of minor clinical importance. However, the short-statured boys might be in greater need of orthodontic treatment due to the higher percentage of dental crowding. [source] Pharmacokinetic,pharmacodynamic study of apomorphine's effect on growth hormone secretion in healthy subjectsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2003Guy Aymard Abstract Apomorphine (APO) stimulates growth hormone (GH) release via dopamine D2 receptors (DRD2). There is no specific study assessing the relationship between APO pharmacokinetic (PK) and the pharmacodynamic (PD) response e.g. GH release. The objective of the study is the PK,PD modelling of APO in healthy subjects. This is a randomized crossover study with s.c. administration of 5, 10, and 20 ,g/kg of APO in 18 healthy subjects. APO concentrations were modelled according to both a bi-compartmental model with zero-order absorption and a bi-compartmental model with first-order absorption. PK,PD relationship was modelled in accordance with the Emax Hill equation using plasma concentrations of APO calculated according to the bi-compartmental model with zero-order absorption. Modelled parameters were very similar to the experimental parameters. PK of APO was linear and there was no significant difference between the tested doses for AUC0,, and Cmax (normalised to the dose 1 ,g/kg), t1/2, and t1/2,. These parameters expressed as mean (CV%: SD/mean) were: 17.2 (26.9) ng/mL·min, 0.26 (33.3) ng/mL, 17.1 (54.2) and 45.2 (20.6) min, respectively (n = 53). An anticlockwise hysteresis loop (effect function of APO plasma concentration) appeared for each dose and each subject. The predicted and measured GH concentrations for all subjects and times were similar whatever the dose (P > 0.27). Emax values were 246 (121), 180 (107), 205 (139) ng/mL, respectively, and EC50 were 0.98 (48.1), 1.70 (62.3), 3.67 (65.2) ng/mL, respectively at dose 5, 10, and 20 ,g/kg (P < 10,4). APO and GH concentrations were predicted with good accuracy using bi-compartmental with zero-order absorption PK model and sigmoid Emax PD model, respectively. [source] The effect of caloric restriction interventions on growth hormone secretion in nonobese men and womenAGING CELL, Issue 1 2010Leanne M. Redman Summary Lifespan in rodents is prolonged by caloric restriction (CR) and by mutations affecting the somatotropic axis. It is not known if CR can alter the age-associated decline in growth hormone (GH), insulin-like growth factor (IGF)-1 and GH secretion. To evaluate the effect of CR on GH secretory dynamics; forty-three young (36.8 ± 1.0 years), overweight (BMI 27.8 ± 0.7) men (n = 20) and women (n = 23) were randomized into four groups; control = 100% of energy requirements; CR = 25% caloric restriction; CR + EX = 12.5% CR + 12.5% increase in energy expenditure by structured exercise; LCD = low calorie diet until 15% weight reduction followed by weight maintenance. At baseline and after 6 months, body composition (DXA), abdominal visceral fat (CT) 11 h GH secretion (blood sampling every 10 min for 11 h; 21:00,08:00 hours) and deconvolution analysis were measured. After 6 months, weight (control: ,1 ± 1%, CR: ,10 ± 1%, CR + EX: ,10 ± 1%, LCD: ,14 ± 1%), fat mass (control: ,2 ± 3%, CR: ,24 ± 3%, CR + EX: ,25 ± 3%, LCD: ,31 ± 2%) and visceral fat (control: ,2 ± 4%, CR: ,28 ± 4%, CR + EX: ,27 ± 3%, LCD: ,36 ± 2%) were significantly (P < 0.001) reduced in the three intervention groups compared to control. Mean 11 h GH concentrations were not changed in CR or control but increased in CR + EX (P < 0.0001) and LCD (P < 0.0001) because of increased secretory burst mass (CR + EX: 34 ± 13%, LCD: 27 ± 22%, P < 0.05) and amplitude (CR + EX: 34 ± 14%, LCD: 30 ± 20%, P < 0.05) but not to changes in secretory burst frequency or GH half-life. Fasting ghrelin was significantly increased from baseline in all three intervention groups; however, total IGF-1 concentrations were increased only in CR + EX (10 ± 7%, P < 0.05) and LCD (19 ± 4%, P < 0.001). A 25% CR diet for 6 months does not change GH, GH secretion or IGF-1 in nonobese men and women. [source] Nucleotide polymorphisms and the 5,-UTR transcriptional analysis of the bovine growth hormone secretagogue receptor 1a (GHSR1a) geneANIMAL SCIENCE JOURNAL, Issue 5 2010Masanori KOMATSU ABSTRACT Growth hormone secretagogue receptor 1a (GHSR1a) mediates the different actions of its endogenous ligand, ghrelin. Ghrelin-GHSR is involved in many important functions that include growth hormone secretion and food intake. We evaluated the haplotype variety and characterized the microsatellite ((TG)n, 5,-UTR) and nucleotide polymorphisms of the bovine GHSR1a gene. The nucleotide sequencing of this gene (,6 kb) revealed 47 single nucleotide polymorphisms (SNPs), four indels and the microsatellite ((GTTT)n, Intron 1). The 19 haplotypes were constructed from all nucleotide viability patterns and were divided into three major groups. Four SNPs (L24V, nt456(G>A), D191N and nt667(C>T)) and DelR242 in Exon 1 and a haplotype block of approximately 2.2 kb (nt667(C>T) , nt2884 (A>G)) were found in Bos taurus breeds. Breed differences in allele frequencies of the two microsatellites, nt-7(C>A), L24V, and DelR242 loci were found (P < 0.005). A DelR242 was found in the Japanese Shorthorn (frequency: , 0.44), Japanese Brown, five European cattle breeds, the Philippine native cattle, but none detected in the Japanese Black or the Mishima island cattle. Additionally, 5,-rapid amplification of cDNA ends and RT-PCR analyses revealed that there were two different kinds of transcripts: spliced, without a microsatellite within 5,-UTR (GHSR1a); and non-spliced, with the microsatellite (GHSR1b). [source] The somatotropic axis of the dairy cow revisitedANIMAL SCIENCE JOURNAL, Issue 1 2002Michael Terence ROSE ABSTRACT The greater understanding of the somatotropic axis in the lactating dairy cow that has been achieved in recent years is briefly reviewed in this article. Specifically discussed are: the significance of multiple forms of insulin-like growth factor messenger RNA (ribonucleic acid) caused by alternative splicing, and the possible functions of the various translated extension proteins; the possible roles of multiple sites of growth hormone secretion other than in the pituitary, and the implications for possible autocrine or paracrine growth hormone secretion; the consequences for increased circulating growth hormone half-life, and possibly biological effectiveness, caused by growth hormone binding proteins; and the increasing evidence for the presence of growth hormone receptors in the bovine mammary gland. The need for further research is highlighted in the present review; published information regarding the bovine, in many of these areas, is still largely insufficient. [source] Re-assessment of growth hormone secretion in young adult patients with childhood-onset growth hormone deficiencyCLINICAL ENDOCRINOLOGY, Issue 4 2003Juliane Donaubauer Summary objective Patients with childhood-onset GH deficiency (coGHD) need retesting in late adolescence or young adulthood to verify whether they need to continue GH treatment. For this purpose the Growth Hormone Research Society (GRS) recommends the insulin tolerance test (ITT), or as an alternative the arginine + growth hormone releasing hormone test (ARG + GHRH test) as a diagnostic tool in adolescents and adults. However, there are no standardized cut-off levels based on normal GH secretion for determining GHD vs. GH sufficiency in young adults for the ITT, the ARG + GHRH test or the pyridostigmine + GHRH (PD + GHRH) test, a further new GH stimulation test. patients and measurements We studied 43 patients (28 with organic coGHD, 15 with idiopathic coGHD; 30 males, 13 females; aged 20·4 years, range 16·2,25·4; body mass index 23·5, range 16·3,35·8) using the ARG [0·5 g/kg intravenously (i.v.)] + GHRH (1 µg/kg i.v.) test, the PD (120 mg orally) + GHRH (1 µg/kg i.v.) test and the ITT (0·1 IU/kg i.v.) and compared these data with the results of 40 healthy age- and weight-matched volunteers. results The GH response in patients was significantly lower than in healthy controls: ARG + GHRH test, 0·8 µg/l (interquartile range 0·3,2·6) vs. 51·8 µg/l (32·6,71·2) in controls (P < 0·0001); PD + GHRH test, 0·9 µg/l (0·3,1·9) vs. 40·4 µg/l (27·1,54·4) in controls (P < 0·0001); ITT, 0.1 µg/l (0·0,0·8) vs. 20·3 µg/l (14·7,31·7) in controls (P < 0·0001). In the ARG + GHRH test we found a diagnostic sensitivity of 100% and a specificity of 97·5% for a cut-off range from 15·1 to 20·3 µg/l, in the PD + GHRH test a sensitivity of 100% and a specificity of 97% (cut-off range 9·1,13·1 µg/l) and in the ITT a sensitivity and specificity of 100% each within a cut-off range from 2·7 to 8·8 µg/l. conclusion There were no marked differences in sensitivity and specificity in young adults among ARG + GHRH test, PD + GHRH test and the ITT in assessing GH secretion. Because of the lack of side-effects, the ARG + GHRH test is the recommended method for re-evaluation of coGHD in young adults when pituitary GHD is suspected. Furthermore, in adult patient groups where organic pituitary coGHD is common, the ITT may be completely replaced by the ARG + GHRH test. Because of the predominance of hypothalamic GHD in childhood, the ITT is commonly performed for the re-evaluation of patients with childhood-onset GHD because of its mechanism of GH stimulation. The present results confirm the high discriminatory capability of the ITT in young adults. [source] Do stress reactions cause abdominal obesity and comorbidities?OBESITY REVIEWS, Issue 2 2001P. Björntorp Summary ,Stress' embraces the reaction to a multitude of poorly defined factors that disturb homeostasis or allostasis. In this overview, the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system have been utilized as objective measurements of stress reactions. Although long-term activation of the sympathetic nervous system is followed by primary hypertension, consequences of similar activation of the HPA axis have not been clearly defined. The focus of this overview is to examine whether or not repeated activation of these two stress centres may be involved in the pathogenesis of abdominal obesity and its comorbidities. In population studies adrenal hormones show strong statistical associations to centralization of body fat as well as to obesity. There is considerable evidence from clinical to cellular and molecular studies that elevated cortisol, particularly when combined with secondary inhibition of sex steroids and growth hormone secretions, is causing accumulation of fat in visceral adipose tissues as well as metabolic abnormalities (The Metabolic Syndrome). Hypertension is probably due to a parallel activation of the central sympathetic nervous system. Depression and ,the small baby syndrome' as well as stress exposure in men and non-human primates are followed with time by similar central and peripheral abnormalities. Glucocorticoid exposure is also followed by increased food intake and ,leptin resistant' obesity, perhaps disrupting the balance between leptin and neuropeptide Y to the advantage of the latter. The consequence might be ,stress-eating', which, however, is a poorly defined entity. Factors activating the stress centres in humans include psychosocial and socioeconomic handicaps, depressive and anxiety traits, alcohol and smoking, with some differences in profile between personalities and genders. Polymorphisms have been defined in several genes associated with the cascade of events along the stress axes. Based on this evidence it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abdominal obesity with its associated comorbidities. [source] | |||||||||||||