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[PMID]:28974369
[Au] Autor:Ávila-Mendoza J; Pérez-Rueda E; Urban-Sosa V; Carranza M; Martínez-Moreno CG; Luna M; Arámburo C
[Ad] Endereço:Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Campus Juriquilla, Universidad Nacional Autónoma de México, Querétaro, Qro. 76230, Mexico.
[Ti] Título:Characterization and distribution of GHRH, PACAP, TRH, SST and IGF1 mRNAs in the green iguana.
[So] Source:Gen Comp Endocrinol;255:90-101, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The somatotropic axis (SA) regulates numerous aspects of vertebrate physiology such as development, growth, and metabolism and has influence on several tissues including neural, immune, reproductive and gastric tract. Growth hormone (GH) is a key component of SA, it is synthesized and released mainly by pituitary somatotrophs, although now it is known that virtually all tissues can express GH, which, in addition to its well-described endocrine roles, also has autocrine/paracrine/intracrine actions. In the pituitary, GH expression is regulated by several hypothalamic neuropeptides including GHRH, PACAP, TRH and SST. GH, in turn, regulates IGF1 synthesis in several target tissues, adding complexity to the system since GH effects can be exerted either directly or mediated by IGF1. In reptiles, little is known about the SA components and their functional interactions. The aim of this work was to characterize the mRNAs of the principal SA components in the green iguana and to develop the tools that allow the study of the structural and functional evolution of this system in reptiles. By employing RT-PCR and RACE, the cDNAs encoding for GHRH, PACAP, TRH, SST and IGF1 were amplified and sequenced. Results showed that these cDNAs coded for the corresponding protein precursors of 154, 170, 243, 113, and 131 amino acids, respectively. Of these, GHRH, PACAP, SST and IGF1 precursors exhibited a high structural conservation with respect to its counterparts in other vertebrates. On the other hand, iguana's TRH precursor showed 7 functional copies of mature TRH (pyr-QHP-NH ), as compared to 4 and 6 copies of TRH in avian and mammalian proTRH sequences, respectively. It was found that in addition to its primary production site (brain for GHRH, PACAP, TRH and SST, and liver for IGF1), they were also expressed in other peripheral tissues, i.e. testes and ovaries expressed all the studied mRNAs, whereas TRH and IGF1 mRNAs were observed ubiquitously in all tissues considered. These results show that the main SA components in reptiles of the Squamata Order maintain a good structural conservation among vertebrate phylogeny, and suggest important physiological interactions (endocrine, autocrine and/or paracrine) between them due to their wide peripheral tissue expression.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/genética
Iguanas/genética
Fator de Crescimento Insulin-Like I/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Somatostatina/genética
Hormônio Liberador de Tireotropina/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Hormônio Liberador de Hormônio do Crescimento/química
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/química
Fator de Crescimento Insulin-Like I/metabolismo
Filogenia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/química
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Somatostatina/química
Somatostatina/metabolismo
Hormônio Liberador de Tireotropina/química
Hormônio Liberador de Tireotropina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (RNA, Messenger); 51110-01-1 (Somatostatin); 5Y5F15120W (Thyrotropin-Releasing Hormone); 67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


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[PMID]:28977590
[Au] Autor:Foradori CD; Whitlock BK; Daniel JA; Zimmerman AD; Jones MA; Read CC; Steele BP; Smith JT; Clarke IJ; Elsasser TH; Keisler DH; Sartin JL
[Ad] Endereço:Department of Anatomy, Physiology & Pharmacology, Auburn University, Auburn, Alabama 36849.
[Ti] Título:Kisspeptin Stimulates Growth Hormone Release by Utilizing Neuropeptide Y Pathways and Is Dependent on the Presence of Ghrelin in the Ewe.
[So] Source:Endocrinology;158(10):3526-3539, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although kisspeptin is the primary stimulator of gonadotropin-releasing hormone secretion and therefore the hypothalamic-pituitary-gonadal axis, recent findings suggest kisspeptin can also regulate additional neuroendocrine processes including release of growth hormone (GH). Here we show that central delivery of kisspeptin causes a robust rise in plasma GH in fasted but not fed sheep. Kisspeptin-induced GH secretion was similar in animals fasted for 24 hours and those fasted for 72 hours, suggesting that the factors involved in kisspeptin-induced GH secretion are responsive to loss of food availability and not the result of severe negative energy balance. Pretreatment with the neuropeptide Y (NPY) Y1 receptor antagonist, BIBO 3304, blocked the effects of kisspeptin-induced GH release, implicating NPY as an intermediary. Kisspeptin treatment induced c-Fos in NPY and GH-releasing hormone (GHRH) cells of the arcuate nucleus. The same kisspeptin treatment resulted in a reduction in c-Fos in somatostatin (SS) cells in the periventricular nucleus. Finally, blockade of systemic ghrelin release or antagonism of the ghrelin receptor eliminated or reduced the ability of kisspeptin to induce GH release, suggesting the presence of ghrelin is required for kisspeptin-induced GH release in fasted animals. Our findings support the hypothesis that during short-term fasting, systemic ghrelin concentrations and NPY expression in the arcuate nucleus rise. This permits kisspeptin activation of NPY cells. In turn, NPY stimulates GHRH cells and inhibits SS cells, resulting in GH release. We propose a mechanism by which kisspeptin conveys reproductive and hormone status onto the somatotropic axis, resulting in alterations in GH release.
[Mh] Termos MeSH primário: Grelina/metabolismo
Hormônio do Crescimento/efeitos dos fármacos
Kisspeptinas/farmacologia
Neuropeptídeo Y/metabolismo
Células Secretoras de Somatostatina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Núcleo Arqueado do Hipotálamo/efeitos dos fármacos
Núcleo Arqueado do Hipotálamo/metabolismo
Arginina/análogos & derivados
Arginina/farmacologia
Atropina/farmacologia
Jejum/metabolismo
Feminino
Imunofluorescência
Hormônio do Crescimento/secreção
Hormônio Liberador de Hormônio do Crescimento
Antagonistas Muscarínicos/farmacologia
Oligopeptídeos/farmacologia
Proteínas Proto-Oncogênicas c-fos/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de Grelina/antagonistas & inibidores
Receptores de Neuropeptídeo Y/antagonistas & inibidores
Ovinos
Carneiro Doméstico
Células Secretoras de Somatostatina/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GHRP-6, Lys(3)-); 0 (Ghrelin); 0 (Kisspeptins); 0 (Muscarinic Antagonists); 0 (Neuropeptide Y); 0 (Oligopeptides); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Ghrelin); 0 (Receptors, Neuropeptide Y); 7C0697DR9I (Atropine); 9002-72-6 (Growth Hormone); 9034-39-3 (Growth Hormone-Releasing Hormone); 94ZLA3W45F (Arginine); O35HK034KO (BIBO 3304)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00303


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[PMID]:28939282
[Au] Autor:Cuervo D; Loli C; Fernández-Álvarez M; Muñoz G; Carreras D
[Ad] Endereço:Laboratorio de Control del Dopaje, Agencia Española de Protección de la Salud en el Deporte, Ministerio de Educación, Cultura y Deporte, Gobierno de España, c/El Greco s/n, 28040, Madrid, Spain. Electronic address: dario.cuervo@aepsad.gob.es.
[Ti] Título:Determination of doping peptides via solid-phase microelution and accurate-mass quadrupole time-of-flight LC-MS.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1065-1066:134-144, 2017 Oct 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A complete analytical protocol for the determination of 25 doping-related peptidic drugs and 3 metabolites in urine was developed by means of accurate-mass quadrupole time-of-flight (Q-TOF) LC-MS analysis following solid-phase extraction (SPE) on microplates and conventional SPE pre-treatment for initial testing and confirmation, respectively. These substances included growth hormone releasing factors, gonadotropin releasing factors and anti-diuretic hormones, with molecular weights ranging from 540 to 1320Da. Optimal experimental conditions were stablished after investigation of different parameters concerning sample preparation and instrumental analysis. Weak cation exchange SPE followed by C18 HPLC chromatography and accurate mass detection provided the required sensitivity and selectivity for all the target peptides under study. 2mg SPE on 96-well microplates can be used in combination with full scan MS detection for the initial testing, thus providing a fast, cost-effective and high-throughput protocol for the processing of a large batch of samples simultaneously. On the other hand, extraction on 30mg SPE cartridges and subsequent target MS/MS determination was the protocol of choice for confirmatory purposes. The methodology was validated in terms of selectivity, recovery, matrix effect, precision, sensitivity (limit of detection, LOD), cross contamination, carryover, robustness and stability. Recoveries ranged from 6 to 70% (microplates) and 17-95% (cartridges), with LODs from 0.1 to 1ng/mL. The suitability of the method was assessed by analyzing different spiked or excreted urines containing some of the target substances.
[Mh] Termos MeSH primário: Doping nos Esportes
Peptídeos/urina
Extração em Fase Sólida/métodos
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Antidiuréticos/isolamento & purificação
Antidiuréticos/urina
Cromatografia Líquida de Alta Pressão/métodos
Hormônio Liberador de Gonadotropina/isolamento & purificação
Hormônio Liberador de Gonadotropina/urina
Hormônio Liberador de Hormônio do Crescimento/isolamento & purificação
Hormônio Liberador de Hormônio do Crescimento/urina
Seres Humanos
Limite de Detecção
Peptídeos/isolamento & purificação
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidiuretic Agents); 0 (Peptides); 33515-09-2 (Gonadotropin-Releasing Hormone); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE


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[PMID]:28623445
[Au] Autor:Ohara E; Tokuyama H; Kitamoto T; Kitahara A; Hayashi A; Hayashi H; Takemoto M; Yokote K
[Ad] Endereço:Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba, 260-8670, Japan.
[Ti] Título:Laparoscopic Sleeve Gastrectomy Resolves Low GHRP-2-Stimulated Growth Hormone Levels in Obese Patients.
[So] Source:Obes Surg;27(8):2214-2217, 2017 Aug.
[Is] ISSN:1708-0428
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Because growth hormone (GH) secretion is reportedly decreased in obese patients, we examined not only the factors associated with the decreased GH secretion but also GH response to the GH-releasing peptide (GHRP)-2-load test before and after laparoscopic gastrectomy (LSG). The study comprised 28 individuals aged 19-65 years [mean body mass index (BMI), 39.4 ± 9.4 kg/m ]. In the univariate analysis, GH secretion peaks correlated negatively with BMI (r = -0.59, p = 0.001), visceral adipose tissue (r = -0.47, p = 0.005), and subcutaneous adipose tissue (r = -0.40, p = 0.04). In the two obese patients, the response to the GHRP-2-load test markedly improved by weight loss 12 months after LSG. In conclusion, GH secretion was decreased in obese patients and improved by LSG.
[Mh] Termos MeSH primário: Gastrectomia/métodos
Obesidade/sangue
Obesidade/cirurgia
Oligopeptídeos/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Hormônio Liberador de Hormônio do Crescimento/sangue
Hormônio Liberador de Hormônio do Crescimento/secreção
Seres Humanos
Laparoscopia
Masculino
Meia-Idade
Obesidade/metabolismo
Oligopeptídeos/secreção
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligopeptides); 9034-39-3 (Growth Hormone-Releasing Hormone); E6S6E1F19M (growth hormone-releasing peptide-2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170618
[St] Status:MEDLINE
[do] DOI:10.1007/s11695-017-2769-4


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[PMID]:28617838
[Au] Autor:Clemmons DR; Miller S; Mamputu JC
[Ad] Endereço:Division of Endocrinology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
[Ti] Título:Safety and metabolic effects of tesamorelin, a growth hormone-releasing factor analogue, in patients with type 2 diabetes: A randomized, placebo-controlled trial.
[So] Source:PLoS One;12(6):e0179538, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Use of growth hormone is associated with side effects, including insulin resistance. The objective of this study was to determine whether tesamorelin, a stabilized growth hormone-releasing hormone analogue, would alter insulin sensitivity or control of diabetes. DESIGN: A 12-week randomized, placebo-controlled study of 53 patients with type 2 diabetes. Three treatment groups: placebo, 1 and 2 mg tesamorelin. MEASUREMENTS: Fasting glucose, glucose and insulin from oral glucose tolerance test, glycosylated hemoglobin (HbA1c), home blood glucose, insulin-like growth factor-1, and lipids. MAIN OUTCOME MEASURE: Relative insulin response following oral ingestion of glucose. RESULTS: No significant differences were observed between groups in relative insulin response over the 12-week treatment period. At Week 12, fasting glucose, HbA1c and overall diabetes control were not significantly different between groups. In addition, relevant modifications in diabetes medications were similar between groups. Total cholesterol (-0.3±0.6 mmol/L) and non-HDL cholesterol (-0.3±0.5 mmol/L) significantly decreased from baseline to Week 12 in the tesamorelin 2 mg group (p<0.05 vs. placebo). No patient discontinued the study due to loss of diabetes control. CONCLUSIONS: Treatment of type 2 diabetic patients with tesamorelin for 12 weeks did not alter insulin response or glycemic control. TRIAL REGISTRATION: ClinicalTrials.gov NCT01264497.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Diabetes Mellitus Tipo 2
Hemoglobina A Glicada/metabolismo
Hormônio Liberador de Hormônio do Crescimento/análogos & derivados
Resistência à Insulina
Fator de Crescimento Insulin-Like I/metabolismo
Lipídeos/sangue
[Mh] Termos MeSH secundário: Idoso
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/tratamento farmacológico
Feminino
Hormônio Liberador de Hormônio do Crescimento/administração & dosagem
Hormônio Liberador de Hormônio do Crescimento/efeitos adversos
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Glycated Hemoglobin A); 0 (Lipids); 0 (hemoglobin A1c protein, human); 67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone); MQG94M5EEO (tesamorelin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179538


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[PMID]:28438614
[Au] Autor:Kovári B; Vranic S; Marchio C; Sapino A; Cserni G
[Ad] Endereço:Department of Pathology, University of Szeged, 6720 Szeged, Hungary. Electronic address: kovari.bence.p@gmail.com.
[Ti] Título:The expression of GHRH and its receptors in breast carcinomas with apocrine differentiation-further evidence of the presence of a GHRH pathway in these tumors.
[So] Source:Hum Pathol;64:164-170, 2017 Jun.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apocrine breast carcinomas were evaluated for the expression of components of the growth hormone-releasing hormone (GHRH) autocrine/paracrine pathway: GHRH and its receptors (GHRH-R), as mammary apocrine carcinomas and epithelium seemed to be uniformly positive for GHRH-R in a pilot study. The apocrine phenotype was determined on the basis of hematoxylin-eosin morphology and a congruent immunohistochemical profile (estrogen receptor negativity, androgen receptor and gross cystic disease fluid protein-15 positivity). Thirty-five formalin-fixed, paraffin-embedded apocrine breast cancers in tissue microarrays and 24 cases using whole-tissue sections were evaluated for GHRH-R and GHRH expression by immunohistochemistry using polyclonal antibodies raised against various domains of GHRH-R and one polyclonal antibody specific for GHRH. GHRH-R positivity was detected in the overwhelming majority (ranging from 90% to 100%) of apocrine breast carcinomas with all but one of the antibodies applied. The expression was usually diffuse with only isolated cases showing positivity in less than 50% of tumor cells. With the PA5-33583 antibody, GHRH-R positivity was seen only in 73% of the cases in at least 50% of the tumor cells. GHRH expression was also present in all but one case tested, with more than 50% of the cells expressing it in 30/34 cases. These results support a high rate of GHRH-R and GHRH expression in apocrine breast carcinomas. Whether these findings can be exploited for the targeted treatment of apocrine breast carcinomas with GHRH antagonists requires further study.
[Mh] Termos MeSH primário: Glândulas Apócrinas/química
Biomarcadores Tumorais/análise
Neoplasias da Mama/química
Carcinoma/química
Hormônio Liberador de Hormônio do Crescimento/análise
Receptores de Neuropeptídeos/análise
Receptores de Hormônios Reguladores de Hormônio Hipofisário/análise
[Mh] Termos MeSH secundário: Glândulas Apócrinas/patologia
Biópsia
Neoplasias da Mama/patologia
Carcinoma/patologia
Diferenciação Celular
Feminino
Seres Humanos
Imuno-Histoquímica
Estudos Retrospectivos
Análise Serial de Tecidos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE


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[PMID]:28428227
[Au] Autor:Aguiar-Oliveira MH; Souza AHO; Oliveira CRP; Campos VC; Oliveira-Neto LA; Salvatori R
[Ad] Endereço:Division of EndocrinologyFederal University of Sergipe, Aracaju, Sergipe, Brazil herminio@infonet.com.br.
[Ti] Título:MECHANISMS IN ENDOCRINOLOGY: The multiple facets of GHRH/GH/IGF-I axis: lessons from lifetime, untreated, isolated GH deficiency due to a GHRH receptor gene mutation.
[So] Source:Eur J Endocrinol;177(2):R85-R97, 2017 Aug.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Twenty years ago, we described kindred of 105 individuals with isolated GH deficiency (IGHD) in Itabaianinha County, in northeast Brazil, carrying a homozygous mutation in the GH-releasing hormone receptor gene. These subjects exhibit markedly reduced GH responsiveness to stimulatory tests, and anterior pituitary hypoplasia. Serum concentrations of IGF-I, IGF binding protein type 3 and the acid-labile subunit are markedly reduced, with a lesser reduction of IGF-II. The most striking physical findings of these IGHD individuals are the proportionate short stature, doll facies, high-pitched voice and visceral obesity with reduced fat-free mass. There is neither microphallus, nor neonatal hypoglycemia. Puberty is delayed, menopause anticipated, but fertility is preserved in both genders. The reduction in bone sizes is not even, with mean standard deviation scores for height of -7.2, total maxillary length of -6.5, total facial height of -4.3 and cephalic perimeter of -2.7. In addition, the non-osseous growth is not uniform, preserving some organs, like pancreas, liver, kidney, brain and eyes, and compromising others such as thyroid, heart, uterus and spleen. These subjects present higher prevalence of dizziness, mild high-tones sensorineural hearing loss, reduction of vascular retinal branching points, increase of optic disk, genu valgum and increased systolic blood pressure. Biochemically, they have high low density lipoprotein cholesterol and C-reactive protein levels, but maintain increased insulin sensitivity, and do not show premature atherosclerosis. Finally, they have normal immune function, and normal longevity. This review details the findings and summarizes 20 years of clinical research carried out in this unique population.
[Mh] Termos MeSH primário: Nanismo Hipofisário/genética
Hormônio Liberador de Hormônio do Crescimento/genética
Hormônio do Crescimento Humano/genética
Fator de Crescimento Insulin-Like I/genética
Mutação/genética
Receptores de Grelina/genética
[Mh] Termos MeSH secundário: Nanismo Hipofisário/diagnóstico
Nanismo Hipofisário/metabolismo
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Hormônio do Crescimento Humano/metabolismo
Seres Humanos
Fator de Crescimento Insulin-Like I/metabolismo
Receptores de Grelina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Ghrelin); 12629-01-5 (Human Growth Hormone); 67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-16-1047


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[PMID]:28245459
[Au] Autor:Bodart G; Farhat K; Charlet-Renard C; Salvatori R; Geenen V; Martens H
[Ti] Título:The Somatotrope Growth Hormone-Releasing Hormone/Growth Hormone/Insulin-Like Growth Factor-1 Axis in Immunoregulation and Immunosenescence.
[So] Source:Front Horm Res;48:147-159, 2017.
[Is] ISSN:1662-3762
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Most scientific reports debate the thymotropic and immuno-stimulating properties of the somatotrope growth hormone-releasing hormone (GHRH)/growth hormone (GH)/insulin-like growth factor (IGF)-1 axis, but there is still some disagreement about the physiological role of this axis in basal conditions. Moreover, some authors have hypothesized that the physiological role of the somatotrope axis only appears in stressful conditions (such as sepsis or infective and inflammatory diseases). This chapter will provide an extended overview of the expression of the components (signals and receptors) of the somatotrope axis and their properties on cells of the innate and adaptive immune system. It will also summarize some clinical studies suggesting a benefit for a short-term GH treatment in acute immunodeficiencies, and the importance of GH supplementation in adult GH deficiency. A new transgenic mouse model, the hypothalamic GHRH-deficient (Ghrh-/-) mouse, which exhibits a severe deficiency of the somatotrope axis, will be presented since it will be of great help in further deciphering the regulation by the GHRH/GH/IGF-1 axis on both immune development and function. Finally, we will discuss the implication of aging-related somatopause in relation to the general context of Immunosenescence.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/fisiologia
Hormônio do Crescimento/fisiologia
Sistema Imunitário/fisiologia
Imunossenescência
Fator de Crescimento Insulin-Like I/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE
[do] DOI:10.1159/000452913


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[PMID]:28193499
[Au] Autor:Muñoz-Moreno L; Bajo AM; Prieto JC; Carmena MJ
[Ad] Endereço:Department of Systems Biology, Unit of Biochemistry and Molecular Biology, University of Alcalá, Alcalá de Henares 28871, Spain.
[Ti] Título:Growth hormone-releasing hormone (GHRH) promotes metastatic phenotypes through EGFR/HER2 transactivation in prostate cancer cells.
[So] Source:Mol Cell Endocrinol;446:59-69, 2017 May 05.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The involvement of growth hormone-releasing hormone (GHRH) in several relevant processes that contribute to prostate cancer progression was analyzed. Firstly, we evaluated GHRH effects on cell proliferation and adhesion in human cancer prostate cell lines, LNCaP and PC3, by using specific assays (BrdU incorporation and collagen adhesion). The expression levels of the main marker molecules of these processes were measured by RT-PCR, Western blotting and zymography assays. GHRH increased both cell proliferation and proliferating cell nuclear antigen (PCNA) levels in LNCaP cells and in PC3 cells; however, such a rise was faster in the PC3 cells that represent the most aggressive stage of prostate cancer. Furthermore, GHRH significantly reduced cell adhesion and E-cadherin levels in LNCaP and PC3 cells and up-regulated the total and nuclear expression of ß-catenin in PC3 cells. In addition, we assessed cell cycle, cell migration and VEGF secretion in PC3 cells. GHRH augmented the number of cells in G2/M-phase but diminished that corresponding to G1-phase. Cell-cycle specific markers were evaluated since GHRH effects may be related to their differential expression; we observed a decrease of p53, p21, and Bax/Bcl2 ratio. Furthermore, GHRH increased the expression of CD44, c-myc and cyclin D1, MMP-2 and MMP-9 activity, and VEGF secretion. We also observed that EGFR and/or HER2 transactivation is involved in cell adhesion, cell migration and VEGF secretion produced by GHRH. Consequently, present results define GHRH as a proliferative, anti-apoptotic and migratory agent in prostate cancer.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/farmacologia
Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
Receptor do Fator de Crescimento Epidérmico/genética
Receptor ErbB-2/genética
Ativação Transcricional/genética
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Masculino
Metástase Neoplásica
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Fenótipo
Antígeno Nuclear de Célula em Proliferação/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptor ErbB-2/metabolismo
Ativação Transcricional/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/secreção
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Proliferating Cell Nuclear Antigen); 0 (RNA, Messenger); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); 9034-39-3 (Growth Hormone-Releasing Hormone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE


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[PMID]:28076448
[Au] Autor:Decourtye L; Mire E; Clemessy M; Heurtier V; Ledent T; Robinson IC; Mollard P; Epelbaum J; Meaney MJ; Garel S; Le Bouc Y; Kappeler L
[Ad] Endereço:Sorbonne Universités, UPMC Univ Paris 06, INSERM, UMRS 938, Centre de Recherche St-Antoine (CRSA), Paris, France.
[Ti] Título:IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice.
[So] Source:PLoS One;12(1):e0170083, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nutrition during the perinatal period programs body growth. Growth hormone (GH) secretion from the pituitary regulates body growth and is controlled by Growth Hormone Releasing Hormone (GHRH) neurons located in the arcuate nucleus of the hypothalamus. We observed that dietary restriction during the early postnatal period (i.e. lactation) in mice influences postnatal growth by permanently altering the development of the somatotropic axis in the pituitary gland. This alteration may be due to a lack of GHRH signaling during this critical developmental period. Indeed, underfed pups showed decreased insulin-like growth factor I (IGF-I) plasma levels, which are associated with lower innervation of the median eminence by GHRH axons at 10 days of age relative to normally fed pups. IGF-I preferentially stimulated axon elongation of GHRH neurons in in vitro arcuate explant cultures from 7 day-old normally fed pups. This IGF-I stimulating effect was selective since other arcuate neurons visualized concomitantly by neurofilament labeling, or AgRP immunochemistry, did not significantly respond to IGF-I stimulation. Moreover, GHRH neurons in explants from age-matched underfed pups lost the capacity to respond to IGF-I stimulation. Molecular analyses indicated that nutritional restriction was associated with impaired activation of AKT. These results highlight a role for IGF-I in axon elongation that appears to be cell selective and participates in the complex cellular mechanisms that link underfeeding during the early postnatal period with programming of the growth trajectory.
[Mh] Termos MeSH primário: Axônios/efeitos dos fármacos
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/farmacologia
Crescimento Neuronal/efeitos dos fármacos
Neurônios/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Axônios/metabolismo
Axônios/fisiologia
Feminino
Crescimento e Desenvolvimento/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios/metabolismo
Neurônios/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0170083



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