The Experts below are selected from a list of 183 Experts worldwide ranked by ideXlab platform
Allan L. Goldstein - One of the best experts on this subject based on the ideXlab platform.
-
Alpha-Tocopherol Succinate, But Not Alpha-Tocopherol Or Other Vitamin E Analogs Stimulates Prolactin And Growth Hormone Release From Rat Anterior Pituitary Cells in vitro
Neuropsychopharmacology, 1994Co-Authors: Mahnaz Badamchian, Bryan L. Spangelo, Hideaki Hagiwara, H Veyama, Y. Hagiwara, Allan L. GoldsteinAbstract:Alpha-Tocopherol Succinate, But Not Alpha-Tocopherol Or Other Vitamin E Analogs Stimulates Prolactin And Growth Hormone Release From Rat Anterior Pituitary Cells in vitro
Arthur Weltman - One of the best experts on this subject based on the ideXlab platform.
-
Growth Hormone Release During Acute and Chronic Aerobic and Resistance Exercise
Sports Medicine, 2002Co-Authors: Laurie Wideman, Judy Y. Weltman, Mark L. Hartman, Johannes D. Veldhuis, Arthur WeltmanAbstract:Exercise is a potent physiological stimulus for Growth Hormone (GH) secretion, and both aerobic and resistance exercise result in significant, acute increases in GH secretion. Contrary to previous suggestions that exercise-induced GH Release requires that a ’threshold’ intensity be attained, recent research from our laboratory has shown that regardless of age or gender, there is a linear relationship between the magnitude of the acute increase in GH Release and exercise intensity. The magnitude of GH Release is greater in young women than in young men and is reduced by 4-7-fold in older individuals compared with younger individuals. Following the increase in GH secretion associated with a bout of aerobic exercise, GH Release transiently decreases. As a result, 24-hour integrated GH concentrations are not usually elevated by a single bout of exercise. However, repeated bouts of aerobic exercise within a 24-hour period result in increased 24-hour integrated GH concentrations. Because the GH response to acute resistance exercise is dependent on the work-rest interval and the load and frequency of the resistance exercise used, the ability to equate intensity across different resistance exercise protocols is desirable. This has proved to be a difficult task. Problems with maintaining patent intravenous catheters have resulted in a lack of studies investigating alterations in acute and 24-hour GH pulsatile secretion in response to resistance exercise. However, research using varied resistance protocols and sampling techniques has reported acute increases in GH Release similar to those observed with aerobic exercise. In young women, chronic aerobic training at an intensity greater than the lactate threshold resulted in a 2-fold increase in 24-hour GH Release. The time line of adaptation and the mechanism(s) by which this training effect occurs are still elusive. Unfortunately, there are few studies investigating the effects of chronic resistance training on 24-hour GH Release. The decrease in GH secretion observed in individuals who are older or have obesity is associated with many deleterious health effects, although a cause and effect relationship has not been established. While exercise interventions may not restore GH secretion to levels observed in young, healthy individuals, exercise is a robust stimulus of GH secretion. The combination of exercise and administration of oral GH secret agogues may result in greater GH secretion than exercise alone in individuals who are older or have obesity. Whether such interventions would result in favourable clinical outcomes remains to be established.
-
Gender governs the relationship between exercise intensity and Growth Hormone Release in young adults.
Journal of Applied Physiology, 2002Co-Authors: Cathy J. Pritzlaff-roy, Laurie Widemen, Judy Y. Weltman, Rob Abbott, M. E. Gutgesell, Mark L. Hartman, Johannes D. Veldhuis, Arthur WeltmanAbstract:We previously reported that in young adult males Growth Hormone (GH) Release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498–504, 1999). To investigate the effects of gender and exercise intensity on GH Release, eight women (24.3 ± 1.3 yr, 171 ± 3.2 cm height, 63.6 ± 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900–0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700–1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men.
-
Growth Hormone Release during acute and chronic aerobic and resistance exercise recent findings
Sports Medicine, 2002Co-Authors: Laurie Wideman, Judy Y. Weltman, Mark L. Hartman, Johannes D. Veldhuis, Arthur WeltmanAbstract:Exercise is a potent physiological stimulus for Growth Hormone (GH) secretion, and both aerobic and resistance exercise result in significant, acute increases in GH secretion. Contrary to previous suggestions that exercise-induced GH Release requires that a "threshold" intensity be attained, recent research from our laboratory has shown that regardless of age or gender, there is a linear relationship between the magnitude of the acute increase in GH Release and exercise intensity. The magnitude of GH Release is greater in young women than in young men and is reduced by 4-7-fold in older individuals compared with younger individuals. Following the increase in GH secretion associated with a bout of aerobic exercise, GH Release transiently decreases. As a result, 24-hour integrated GH concentrations are not usually elevated by a single bout of exercise. However, repeated bouts of aerobic exercise within a 24-hour period result in increased 24-hour integrated GH concentrations. Because the GH response to acute resistance exercise is dependent on the work-rest interval and the load and frequency of the resistance exercise used, the ability to equate intensity across different resistance exercise protocols is desirable. This has proved to be a difficult task. Problems with maintaining patent intravenous catheters have resulted in a lack of studies investigating alterations in acute and 24-hour GH pulsatile secretion in response to resistance exercise. However, research using varied resistance protocols and sampling techniques has reported acute increases in GH Release similar to those observed with aerobic exercise. In young women, chronic aerobic training at an intensity greater than the lactate threshold resulted in a 2-fold increase in 24-hour GH Release. The time line of adaptation and the mechanism(s) by which this training effect occurs are still elusive. Unfortunately, there are few studies investigating the effects of chronic resistance training on 24-hour GH Release. The decrease in GH secretion observed in individuals who are older or have obesity is associated with many deleterious health effects, although a cause and effect relationship has not been established. While exercise interventions may not restore GH secretion to levels observed in young, healthy individuals, exercise is a robust stimulus of GH secretion. The combination of exercise and administration of oral GH secretagogues may result in greater GH secretion than exercise alone in individuals who are older or have obesity. Whether such interventions would result in favourable clinical outcomes remains to be established.
-
effects of gender on exercise induced Growth Hormone Release
Journal of Applied Physiology, 1999Co-Authors: Laurie Wideman, Judy Y. Weltman, Johannes D. Veldhuis, Niki Shah, Shannon Story, Arthur WeltmanAbstract:We examined gender differences in Growth Hormone (GH) secretion during rest and exercise. Eighteen subjects (9 women and 9 men) were tested on two occasions each [resting condition (R) and exercise...
-
impact of acute exercise intensity on pulsatile Growth Hormone Release in men
Journal of Applied Physiology, 1999Co-Authors: C J Pritzlaff, Judy Y. Weltman, M. E. Gutgesell, Mark L. Hartman, Johannes D. Veldhuis, Laurie Wideman, Robert D Abbott, Arthur WeltmanAbstract:To investigate the effects of exercise intensity on Growth Hormone (GH) Release, 10 male subjects were tested on 6 randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. ...
Willis K Samson - One of the best experts on this subject based on the ideXlab platform.
-
intermedin adrenomedullin 2 inhibits Growth Hormone Release from cultured primary anterior pituitary cells
Endocrinology, 2006Co-Authors: Meghan M Taylor, Sara L Bagley, Willis K SamsonAbstract:Intermedin (IMD), a novel member of the adrenomedullin (AM), calcitonin gene-related peptide (CGRP), amylin (AMY) peptide family, has been reported to act promiscuously at all the known receptors for these peptides. Like AM and CGRP, IMD acts in the circulation to decrease blood pressure and in the brain to inhibit food intake, effects that could be explained by activation of the known CGRP, AM, or AMY receptors. Because AM, CGRP, and AMY have been reported to affect Hormone secretion from the anterior pituitary gland, we examined the effects of IMD on GH, ACTH, and prolactin secretion from dispersed anterior pituitary cells harvested from adult male rats. IMD, in log molar concentrations ranging from 1.0 pm to 100 nm, failed to significantly alter basal Release of the three Hormones. Similarly, IMD failed to significantly alter CRH-stimulated ACTH or TRH-stimulated prolactin secretion in vitro. However, IMD concentration-dependently inhibited GHRH-stimulated GH Release from these cell cultures. The effec...
-
neuropeptide w acts in brain to control prolactin corticosterone and Growth Hormone Release
Endocrinology, 2003Co-Authors: Jennifer R Baker, Meghan M Taylor, Kara Cardinal, Cynthia Bober, Willis K SamsonAbstract:The endogenous, peptide ligand for the orphan receptors GPR7 and GPR8 was identified to be neuropeptide W (NPW). Because these receptors are expressed in brain and in particular in hypothalamus, we hypothesized that NPW might interact with neuroendocrine systems that control Hormone Release from the anterior pituitary gland. No significant effects of NPW were observed on the in vitro Releases of prolactin (PRL), ACTH, or GH when log molar concentrations ranging from 1 pM to 100 nM NPW were incubated with dispersed anterior pituitary cells. However, NPW, when injected into the lateral cerebroventricle of conscious, unrestrained male rats, in a dose-related fashion elevated PRL and corticosterone and lowered GH levels in circulation. The threshold dose for all three effects was 1.0 nmol. We conclude that endogenous NPW may play a regulatory role in the organization of neuroendocrine signals accessing the anterior pituitary gland but does not itself act as a true releasing or inhibiting factor in the gland. Central administration of NPW23 also stimulated water drinking and food intake. The ability of exogenous peptide to decrease GH but stimulate PRL secretion and activate the hypothalamo-pituitary adrenal axis, together with the observed behavioral effects, suggests that endogenous NPW may play a role in the hypothalamic response to stress.
Kenji Kangawa - One of the best experts on this subject based on the ideXlab platform.
-
Purification and Characterization of Caprine Ghrelin and Its Effect on Growth Hormone Release
Journal of Molecular Neuroscience, 2010Co-Authors: Takanori Ida, Mikiya Miyazato, Xing-zi Lin, Hiroyuki Kaiya, Takahiro Sato, Keiko Nakahara, Noboru Murakami, Kenji Kangawa, Masayasu KojimaAbstract:Ghrelin, a novel peptide modified by n -octanoic acid at the third serine residue (Ser^3), serves as an endogenous ligand for the Growth Hormone secretagogue receptor (GHS-R) 1a. The octanoyl modification at Ser^3 is essential for receptor binding or Growth Hormone Release. Here, we report the purification of caprine ghrelin and its physiological role in goats. The major form of caprine ghrelin is a 27 amino acid peptide that is octanoylated (C8:0) at Ser^3 and lacks Gln^14, which is present in rat and human ghrelin. Additionally, we identified various acyl modifications in caprine ghrelin: nonanoic (C9:0), decanoic (10:0), unsaturated octanoic acids (C8:1), and an unidentified fatty acid modification. We observed that differences in acyl modifications affected GHS-R1a activation. In addition, administration of synthetic bovine ghrelin increased plasma Growth Hormone (GH) levels in goats. Thus, the present study indicates a structural divergence in caprine ghrelin and suggests that ghrelin is involved in GH Release in ruminants.
-
Ghrelin: a novel peptide for Growth Hormone Release and feeding regulation.
Current opinion in clinical nutrition and metabolic care, 2002Co-Authors: Fumiki Yoshihara, Masayasu Kojima, Hiroshi Hosoda, Masamitsu Nakazato, Kenji KangawaAbstract:Purpose of review A novel peptide Hormone, ghrelin, has been identified from the stomach and recognized as an important regulator of Growth Hormone Release and energy homeostasis. It is interesting to note that the stomach may play an important role in not only digestion but also pituitary Growth Hormone Release and central feeding regulation. Thus, we summarize the recent findings on the mechanism of these effects induced by ghrelin. Recent findings The coadministration of ghrelin and Growth Hormone releasing Hormone was found to have a synergistical effect on pituitary Growth Hormone secretion. The infusion of Growth Hormone releasing Hormone in rats resulted in a significant increase in pituitary gene expression of ghrelin and its receptor system, suggesting that this system in the pituitary gland could modulate the regulation of Growth Hormone secretion by Growth Hormone releasing Hormone. Ghrelin promoted the production of orexigenic neuropeptides (neuropeptide Y and agouti-related protein) in the hypothalamic arcuate nuclei and activated the neurons which produce these orexigenic neuropeptides, resulting in an increase in feeding and body weight. Gastric acid Release and pancreatic protein secretions were also regulated by ghrelin through vagal and intrapancreatic neuronal activation, respectively. It is possible that ghrelin may participate in the regulation of cell proliferation, glucose homeostasis, and the immune system. Summary Ghrelin, secreted from the stomach, modulates Growth Hormone Release and feeding promotion. Further elucidation of the mechanisms of ghrelin effects will help to improve the diagnosis and treatment of eating disorders and disturbed conditions of nutritional homeostasis.
-
central effects of a novel acylated peptide ghrelin on Growth Hormone Release in rats
Biochemical and Biophysical Research Communications, 2000Co-Authors: Yukari Date, Masayasu Kojima, Noboru Murakami, Kenji Kangawa, Shigeru Matsukura, Takatoshi Kuroiwa, Masamitsu NakazatoAbstract:Abstract Ghrelin, a novel Growth-Hormone-releasing acylated peptide, was recently isolated from rat stomach by the search of an endogenous ligand to an “orphan” G-protein-coupled-receptor. Ghrelin neuron is present in the arcuate nucleus of rat hypothalamus, but its central effect on Growth Hormone (GH) Release has yet to be clarified. We determined the plasma GH concentration and GH mRNA level in the pituitary in response to central administration of ghrelin. A single intracerebroventricular (ICV) administration of ghrelin to rats increased the plasma GH concentration dose-dependently. A continuous ICV administration of ghrelin via osmotic pump for 12 days increased the plasma GH concentration on day 6, but did not keep the high GH concentration on day 12. The GH mRNA levels in both groups of single and continuous administration of ghrelin were not significantly different from those of controls. A single administration of Growth-Hormone secretagogue also did not stimulate GH synthesis. Central ghrelin stimulated GH Release but did not augment GH synthesis. In addition to gastric ghrelin, hypothalamic ghrelin functions to regulate GH Release.
-
purification and characterization of rat des gln14 ghrelin a second endogenous ligand for the Growth Hormone secretagogue receptor
Journal of Biological Chemistry, 2000Co-Authors: Hiroshi Hosoda, Masayasu Kojima, Hisayuki Matsuo, Kenji KangawaAbstract:Ghrelin, a peptide purified from the stomach, is an endogenous ligand for the Growth Hormone secretagogue receptor (GHS-R) and potently stimulates Growth Hormone Release from the pituitary. Ghrelin is modified with an n-octanoyl group at Ser3. This modification is essential for the activity of ghrelin. Previously, it was not known whether other ligands for GHS-R existed. Here, we report the purification of the second endogenous ligand for GHS-R from rat stomach. This ligand, named des-Gln14-ghrelin, is a 27-amino acid peptide, whose sequence is identical to ghrelin except for one glutamine. Southern blotting analysis under low hybridization conditions indicates that no homologue for ghrelin exists in rat genomic DNA. Furthermore, genomic sequencing and cDNA analysis indicate that des-Gln14-ghrelin is not encoded by a gene distinct from ghrelin but is encoded by an mRNA created by alternative splicing of the ghrelin gene. This is the first example of a novel mechanism that produces peptide multiplicity. Des-Gln14-ghrelin has an n-octanoyl modification at Ser3 like ghrelin, which is also essential for its activity. Des-Gln14-ghrelin-stimulated Growth Hormone Releases when injected into rats. Thus, Growth Hormone Release is regulated by two gastric peptides, ghrelin and des-Gln14-ghrelin.
Roy G. Smith - One of the best experts on this subject based on the ideXlab platform.
-
From GH to Billy Ghrelin
Cell metabolism, 2009Co-Authors: Roy G. SmithAbstract:The octanoylated peptide Hormone ghrelin regulates episodic Growth Hormone Release and energy balance. Work in genetically modified mice (Kirchner et al., 2009) now shows that in vivo activity of ghrelin O -acyltransferase (GOAT), responsible for ghrelin octanoylation, decreases during fasting but increases after ingesting medium-chain fatty acid triglycerides (MCT).
-
a new orphan receptor involved in pulsatile Growth Hormone Release
Trends in Endocrinology and Metabolism, 1999Co-Authors: Roy G. Smith, Xiaoming Guan, Scott D Feighner, Kris Prendergast, Andrew D HowardAbstract:In all species studied to date, Growth Hormone (GH) is Released episodically. Traditionally, the regulation of this process was considered to be mediated by two hypothalamic Hormones, Growth Hormone-releasing Hormone (GHRH) and somatostatin (sst). More recently, we identified a new orphan G-protein-coupled receptor that causes episodic GH Release upon activation by synthetic ligands. These ligands include the GH-releasing peptides (GHRPs) first described by Bowers and their small molecule mimetics such as L-692,429 and MK-0677. Site-directed mutagenesis of this GH secretagogue receptor (GHS-R) has defined key amino acid residues essential for binding and activation by the synthetic ligands. The GHS-R is not activated by GHRH or sst. It is expressed exclusively in the anterior pituitary lobe and central nervous system and although this new receptor does not belong to any of the known families of G-protein-coupled receptors, the GHS-R is highly conserved across species. The Puffer fish homolog, in common with the human GHS-R, is activated by the structurally distinct ligands GHRP-6, MK-0677 and L-163,540. Thus, the GHS-R ligand-binding pocket has apparently been conserved for at least 400 million years. Studies in humans suggest that production of an endogenous ligand declines during aging. For example, chronic treatment with the synthetic ligand MK-0677 reverses the age-related physiological changes in the GH/IGF-I (insulin-like Growth factor I) axis of 70-94 year old subjects. Based on the localization of expression of GHS-R in the brain, reduced production of the natural ligand might also be involved in age-associated changes in cognition, memory, mood and behavior.
-
distribution of mrna encoding the Growth Hormone secretagogue receptor in brain and peripheral tissues
Molecular Brain Research, 1997Co-Authors: Xiaoming Guan, Roy G. Smith, Oksana C Palyha, Karen K Mckee, Scott D Feighner, D J S Sirinathsinghji, Lex H T Van Der Ploeg, Andrew D HowardAbstract:Growth Hormone Release is under tight control by two hypothalamic Hormones: Growth Hormone-releasing Hormone and somatostatin. In addition, synthetic Growth Hormone secretagogues have also been shown to regulate Growth Hormone Release through the Growth Hormone secretagogue receptor (GHS-R), suggesting the existence of an additional physiological regulator for Growth Hormone Release. To understand the physiological role of the GHS-R in more detail, we mapped the expression of mRNA for the receptor by in situ hybridization and RNase protection assays using rat and human tissues. In the rat brain, the major signals were detected in multiple hypothalamic nuclei as well as in the pituitary gland. Intense signals were also observed in the dentate gyrus of the hippocampal formation. Other brain areas that displayed localized and discrete signals for the receptor include the CA2 and CA3 regions of the hippocampus, the substantia nigra, ventral tegmental area, and dorsal and median raphe nuclei. In resemblance to the results from rat brain, RNase protection assays using human tissues revealed specific signals in pituitary, hypothalamus and hippocampus. Moreover, a weak signal was noted in the pancreas. The demonstration of hypothalamic and pituitary localization of the GHS-R is consistent with its role in regulating Growth Hormone Release. The expression of the receptor in other central and peripheral regions may implicate its involvement in additional as yet undefined physiological functions.
