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Ghrelin Secretion (ghrelin + secretion)
Selected AbstractsGhrelin: 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] Ghrelin: more than a natural GH secretagogue and/or an orexigenic factorCLINICAL ENDOCRINOLOGY, Issue 1 2005E. Ghigo Summary Ghrelin, an acylated peptide produced predominantly by the stomach, has been discovered to be a natural ligand of the growth hormone secretagogue receptor type 1a (GHS-R1a). Ghrelin has recently attracted considerable interest as a new orexigenic factor. However, ghrelin exerts several other neuroendocrine, metabolic and also nonendocrine actions that are explained by the widespread distribution of ghrelin and GHS-R expression. The likely existence of GHS-R subtypes and evidence that the neuroendocrine actions, but not all the other actions, of ghrelin depend on its acylation in serine-3 revealed a system whose complexity had not been completely explored by studying synthetic GHS. Ghrelin secretion is mainly regulated by metabolic signals and, in turn, the modulatory action of ghrelin on the control of food intake and energy metabolism seems to be among its most important biological actions. However, according to a recent study, ghrelin-null mice are neither anorectics nor dwarfs and this evidence clearly depicts a remarkable difference from leptin null mice. Nevertheless, the original and fascinating story of ghrelin, as well as its potential pathophysiological implications in endocrinology and internal medicine, is not definitively cancelled by these data as GHS-R1a null aged mice show significant alterations in body composition and growth, in glucose metabolism, cardiac function and contextual memory. Besides potential clinical implications for natural or synthetic ghrelin analogues acting as agonists or antagonists, there are several open questions awaiting an answer. How many ghrelin receptor subtypes exist? Is ghrelin ,the' or just ,a' GHS-R ligand? That is, are there other natural GHS-R ligands? Is there a functional balance between acylated and unacylated ghrelin forms, potentially with different actions? Within the next few years suitable answers to these questions will probably be found, making it possible to gain a better knowledge of ghrelin's potential clinical perspectives. [source] Ghrelin levels are reduced in prepubertal epileptic children under treatment with carbamazepine or valproic acidEPILEPSIA, Issue 2 2010Flavia Prodam Summary A relationship between ghrelin and epilepsy has been already shown in humans, although the results are controversial. Ghrelin levels are reduced in obesity. Epileptic patients progressively develop a therapy-linked weight gain; however, the mechanisms for this have not been fully explained. The aim of our study is to evaluate if ghrelin secretion is modulated by treatment with carbamazepine or valproic acid in young prepubertal epileptic children. Ghrelin levels were reduced in normal-weight young epileptic prepubertal children under treatment with carbamazepine (p < 0.0001) or valproic acid (p < 0.006) compared to healthy age- and weight-matched subjects. Ghrelin was also lower in children under carbamazepine when compared to those under valproic acid (p < 0.01). A derangement in ghrelin secretion in epilepsy during specific pharmacologic therapies and independent of weight gain could be hypothesized. [source] Effects of glucose and amino acids on ghrelin secretion in sheepANIMAL SCIENCE JOURNAL, Issue 2 2010Toshihisa SUGINO ABSTRACT Two experiments were conducted to elucidate the effects of post-ruminal administration of starch and casein (Exp. 1), plasma amino acids concentrations (Exp. 2), and plasma glucose and insulin concentrations (Exp. 2) on plasma ghrelin concentrations in sheep. In Exp. 1, plasma ghrelin concentrations were determined by four infusion treatments (water, cornstarch, casein and cornstarch plus casein) in four wethers. Abomasal infusion of casein increased plasma ,-amino N (AAN) concentrations. Infusion of starch or casein alone did not affect plasma ghrelin concentrations, but starch plus casein infusion increased plasma levels of ghrelin, glucose and AAN. In Exp 2, we investigated the effects of saline or amino acids on ghrelin secretion in four wethers. Two hours after the initiation of saline or amino acid infusion into the jugular vein, glucose was also continuously infused to investigate the effects of blood glucose and insulin by hyper-glycemic clump on plasma ghrelin concentrations. Infusion of amino acids alone raised plasma levels of ghrelin, but the higher plasma glucose and insulin concentrations had no effect on plasma ghrelin concentrations. These results suggest that high plasma levels of amino acids can stimulate ghrelin secretion, but glucose and insulin do not affect ghrelin secretion in sheep. [source] Perioperative plasma active and total ghrelin levels are reduced in acromegaly when compared with in nonfunctioning pituitary tumours even after normalization of serum GHCLINICAL ENDOCRINOLOGY, Issue 1 2007Takakazu Kawamata Summary Objective, Ghrelin is a novel gastric peptide known to stimulate GH secretion, but the relationship between ghrelin and the GH-insulin-like growth factor (IGF)-1 axis in GH excess or deficiency is poorly understood. This study investigated dysregulation of ghrelin secretion in acromegaly and its short-term postoperative recovery. Methods, A prospective study was conducted on eight patients who underwent complete transsphenoidal resection of GH-producing pituitary adenomas (acromegaly group) and 22 for endocrinologically nonfunctioning pituitary tumours (control group). Active and total plasma ghrelin levels were measured serially before and after surgery. Results, Preoperative active and total plasma ghrelin concentrations (mean ± SD; fmol/ml) were significantly reduced in acromegalic patients when compared with those in the controls (9·6 ± 4·3 and 157·4 ± 65·6 vs. 21·8 ± 13·0 and 267·1 ± 111·4; P = 0·023 and P = 0·021, respectively). Both levels were still significantly suppressed on postoperative Day 7 in the acromegaly group when compared with those in the control group (11·7 ± 4·3 and 197·8 ± 68·9 vs. 22·5 ± 12·6 and 302·7 ± 100·0; P = 0·038 and P = 0·018, respectively). The ratios of active to total ghrelin were not significantly different between the two groups before and after operation. In acromegalic patients, active and total ghrelin levels remained significantly suppressed even after normalization of serum GH levels. Conclusions, The putative negative feedback mechanism of GH on ghrelin secretion may in part account for the low ghrelin levels observed in acromegalic patients, and the mechanism may persist even after normalization of serum GH. [source] Ghrelin does not regulate the GH response to insulin-induced hypoglycaemia in children but could be involved in the regulation of cortisol secretionCLINICAL ENDOCRINOLOGY, Issue 1 2007J. Huber Summary Objective, Ghrelin activates the growth hormone secretagogue receptor GHS-R. It strongly stimulates GH secretion and has a role in energy homeostasis. The relationship between plasma ghrelin and cortisol levels during insulin-induced hypoglycaemia in prepubertal and pubertal children has not yet been investigated. The aim of the present study was to establish whether insulin-induced hypoglycaemia stimulates ghrelin secretion and whether changes in ghrelin concentrations are related to changes in GH and cortisol in children. Design and patients, We studied a group of 20 children and adolescents (five girls, 15 boys, mean age 10·8 ± 3·7 years) undergoing insulin tolerance tests (ITTs) for clinical investigation of GH deficiency. Measurements, Stimulation tests were performed to investigate the relationship between ghrelin, GH, cortisol and glucose levels according to age and pubertal stage by determining the ghrelin profiles during insulin-induced hypoglycaemia (at 0, 60 and 120 min). Results, Ghrelin was significantly and inversely related to body weight, height, body mass index (BMI) and age of children (P < 0·05). Significant changes in ghrelin levels (P = 0·00013) were found after the insulin bolus, with a decline at 60 min and an increase to baseline values at 120 min. Changes in cortisol levels were negatively correlated with changes in ghrelin at 60 min (r = ,0·59, P = 0·004) and at 120 min (r = ,0·605, P = 0·003). Conclusions, This study shows that ghrelin might not regulate the GH response to insulin-induced hypoglycaemia in prepubertal and pubertal children. A role for ghrelin in the regulation of cortisol secretion can be hypothesized concerning the negative correlation between changes in ghrelin and cortisol. Furthermore, the results imply that ghrelin secretion is age dependent and is a function of growth. [source] Serum ghrelin concentrations in patients with chronic renal failure undergoing dialysisCLINICAL ENDOCRINOLOGY, Issue 1 2006Pedro Iglesias Summary Background, ,Ghrelin is a recently discovered protein hormone mainly synthesized in the gastric endocrine cells. This hormone not only is a potent growth hormone secretagogue but also is involved in the regulation of food ingestion and energy metabolism. Derangements in ghrelin secretion in patients with chronic renal failure (CRF) have not been fully evaluated. Objective, ,Our aim has been to quantify serum concentrations of total ghrelin in a group of patients with CRF on chronic therapy with both haemodialysis (HD) and peritoneal dialysis (PD) in comparison with a group of patients on conservative management (predialysis). Patients and measurements, ,We studied 68 CRF patients treated by HD (n = 30, 16 men, age 61·2 ± 1·8 years) and PD groups (n = 38, 21 men, age 54·4 ± 1·7 years). A group of 19 uraemic patients on conservative management served as the control. Serum concentrations of ghrelin, leptin, insulin, IGF I and GH were measured in all subjects. Results, ,Patients undergoing HD showed similar concentrations of ghrelin in comparison with the control group (9491 ± 787 vs 9280 ± 918 pg/ml, NS). However, PD patients exhibited baseline ghrelin concentrations significantly lower than those found in patients on conservative management (3230 ± 216 pg/ml, P < 0·0001). Men and women showed similar serum ghrelin levels in both HD (9845·9 ± 1071 vs 9085 ± 1194 pg/ml) and PD patients (3214 ± 297 vs 3250 ± 324 pg/ml). Hypertension and diabetes mellitus did not influence ghrelin levels. Serum GH levels were positively correlated with serum ghrelin concentrations in both HD (r = 0·46, P < 0·05) and PD (r = 0·53, P < 0·001) patients; however, no relationships between ghrelin, leptin, insulin and IGF I were found. Conclusions, ,These results suggest that PD is accompanied by a striking decrement in baseline ghrelin concentrations in comparison with values found both in HD and control patients. Further studies are necessary to determine mechanisms involved in ghrelin regulation in uraemic patients. [source] | ||||||||||