Base de dados : MEDLINE
Pesquisa : D06.472.699.327.740 [Categoria DeCS]
Referências encontradas : 3098 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 310 ir para página                         

  1 / 3098 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27595593
[Au] Autor:Zhang R; Asai M; Mahoney CE; Joachim M; Shen Y; Gunner G; Majzoub JA
[Ad] Endereço:Division of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Loss of hypothalamic corticotropin-releasing hormone markedly reduces anxiety behaviors in mice.
[So] Source:Mol Psychiatry;22(5):733-744, 2017 May.
[Is] ISSN:1476-5578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A long-standing paradigm posits that hypothalamic corticotropin-releasing hormone (CRH) regulates neuroendocrine functions such as adrenal glucocorticoid release, whereas extra-hypothalamic CRH has a key role in stressor-triggered behaviors. Here we report that hypothalamus-specific Crh knockout mice (Sim1CrhKO mice, created by crossing Crhflox with Sim1Cre mice) have absent Crh mRNA and peptide mainly in the paraventricular nucleus of the hypothalamus (PVH) but preserved Crh expression in other brain regions including amygdala and cerebral cortex. As expected, Sim1CrhKO mice exhibit adrenal atrophy as well as decreased basal, diurnal and stressor-stimulated plasma corticosterone secretion and basal plasma adrenocorticotropic hormone, but surprisingly, have a profound anxiolytic phenotype when evaluated using multiple stressors including open-field, elevated plus maze, holeboard, light-dark box and novel object recognition task. Restoring plasma corticosterone did not reverse the anxiolytic phenotype of Sim1CrhKO mice. Crh-Cre driver mice revealed that PVHCrh fibers project abundantly to cingulate cortex and the nucleus accumbens shell, and moderately to medial amygdala, locus coeruleus and solitary tract, consistent with the existence of PVHCrh-dependent behavioral pathways. Although previous, nonselective attenuation of CRH production or action, genetically in mice and pharmacologically in humans, respectively, has not produced the anticipated anxiolytic effects, our data show that targeted interference specifically with hypothalamic Crh expression results in anxiolysis. Our data identify neurons that express both Sim1 and Crh as a cellular entry point into the study of CRH-mediated, anxiety-like behaviors and their therapeutic attenuation.
[Mh] Termos MeSH primário: Ansiedade/metabolismo
Hormônio Liberador da Corticotropina/deficiência
Hipotálamo/metabolismo
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/metabolismo
Tonsila do Cerebelo/metabolismo
Animais
Corticosterona/sangue
Hormônio Liberador da Corticotropina/isolamento & purificação
Hormônio Liberador da Corticotropina/metabolismo
Feminino
Glucocorticoides/metabolismo
Sistema Hipotálamo-Hipofisário/metabolismo
Camundongos
Camundongos Endogâmicos ICR
Camundongos Mutantes
Neurônios/metabolismo
Hormônios Liberadores de Hormônios Hipofisários/metabolismo
Sistema Hipófise-Suprarrenal/metabolismo
RNA Mensageiro/metabolismo
Receptores de Hormônio Liberador da Corticotropina/genética
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Receptores de Glucocorticoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Pituitary Hormone-Releasing Hormones); 0 (RNA, Messenger); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Receptors, Glucocorticoid); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE
[do] DOI:10.1038/mp.2016.136


  2 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27611700
[Au] Autor:Van den Berghe G
[Ad] Endereço:Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven University and Hospitals, Leuven, Belgium.
[Ti] Título:On the Neuroendocrinopathy of Critical Illness. Perspectives for Feeding and Novel Treatments.
[So] Source:Am J Respir Crit Care Med;194(11):1337-1348, 2016 Dec 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Typical for critical illnesses are substantial alterations within the hypothalamic-anterior pituitary-peripheral hormonal axes that are proportionate to the risk of poor outcome. These neuroendocrine responses to critical illness follow a biphasic pattern. The acute phase (first hours to days) is characterized by an increased release of anterior pituitary hormones, whereas altered target-organ sensitivity and hormone metabolism result in low levels of the anabolic peripheral effector hormones and contribute to the substantially elevated levels of the catabolic hormone cortisol. The prolonged phase of critical illness is hallmarked by a uniform suppression of the neuroendocrine axes, predominantly of central/hypothalamic origin, which contributes to the low (or insufficiently high in the case of cortisol) circulating levels of the target-organ hormones. Several of the acute-phase adaptations to critical illness are due to or accentuated by the concomitant fasting. Accepting the lack of macronutrients as well as the neuroendocrine responses to such fasting in the acute phase of critical illness has shown to beneficially affect outcome. In contrast, the neuroendocrine alterations that occur in the chronic phase of illness while patients are fully fed contribute to bone and skeletal muscle wasting and impose risk of adrenocortical atrophy. The combined administration of those hypothalamic releasing factors, which have been identified as suppressed or deficient during prolonged critical illness, may be a promising strategy to enhance recovery. The potential impact of treatment with such hypothalamic releasing factors on recovery from critical illness as well as on long-term rehabilitation should be investigated in future randomized controlled clinical trials.
[Mh] Termos MeSH primário: Estado Terminal/terapia
Comportamento Alimentar
Neuroendocrinologia/métodos
Sistemas Neurossecretores/patologia
Hormônios Liberadores de Hormônios Hipofisários/uso terapêutico
[Mh] Termos MeSH secundário: Seres Humanos
Sistemas Neurossecretores/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Pituitary Hormone-Releasing Hormones)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE


  3 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:26118248
[Au] Autor:Tachè Y
[Ti] Título:HANS SELYE AND THE STRESS RESPONSE: FROM "THE FIRST MEDIATOR" TO THE IDENTIFICATION OF THE HYPOTHALAMIC CORTICOTROPIN-RELEASING FACTOR.
[So] Source:Ideggyogy Sz;67(3-4):95-8, 2014 Mar 30.
[Is] ISSN:0019-1442
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:Selye pioneered the stress concept that is ingrained in the vocabulary of daily life. This was originally build on experimental observations that divers noxious agents can trigger a similar triad of endocrine (adrenal enlargement), immune (involution of thymus) and gut (gastric erosion formation) responses as reported in a letter to Nature in 1936. Subsequently, he articulated the underlying mechanisms and hypothesized the existence of a "first mediator" in the hypothalamus able to orchestrate this bodily changes. However he took two generations to identify this mediator. The Nobel Laureate, Roger Guillemin, a former Selye's PhD student, demonstrated in 1955 the existence of a hypothalamic factor that elicited adrenocorticotropic hormone release from the rat pituitary and named it corticotropin releasing factor (CRF). In 1981, Wylie Vale, a former Guillemin's Ph Student, characterized CRF as 41 amino acid and cloned the CRF1 and CRF2 receptors. This paves the way to experimental studies establishing that the activation of the CRF signaling pathways in the brain plays a key role in mediating the stress-related endocrine, behavioral, autonomic and visceral responses. The unraveling of the biochemical coding of stress is rooted in Selye legacy continues to have increasing impact on the scientific community.
[Mh] Termos MeSH primário: Hormônio Liberador da Corticotropina/história
Síndrome de Adaptação Geral/história
Hipotálamo
Sistema Imunitário
Úlcera Péptica/história
Hormônios Liberadores de Hormônios Hipofisários/história
Estresse Fisiológico
Timo
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/metabolismo
Glândulas Suprarrenais/patologia
Hormônio Adrenocorticotrópico/história
Animais
Atrofia
Hormônio Liberador da Corticotropina/metabolismo
Síndrome de Adaptação Geral/metabolismo
Síndrome de Adaptação Geral/patologia
História do Século XX
Seres Humanos
Hipertrofia
Hipotálamo/metabolismo
Sistema Imunitário/metabolismo
Úlcera Péptica/etiologia
Úlcera Péptica/patologia
Hormônios Liberadores de Hormônios Hipofisários/metabolismo
Ratos
Transdução de Sinais
Estresse Fisiológico/imunologia
Timo/metabolismo
Timo/patologia
[Pt] Tipo de publicação:BIOGRAPHY; HISTORICAL ARTICLE; JOURNAL ARTICLE
[Ps] Nome de pessoa como assunto:Selye H; Guillemin R; Vale W
[Nm] Nome de substância:
0 (Pituitary Hormone-Releasing Hormones); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:150629
[Lr] Data última revisão:
150629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150630
[St] Status:MEDLINE


  4 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24211830
[Au] Autor:Rivier C
[Ad] Endereço:The Salk Institute, The Clayton Foundation Laboratories for Peptide Biology, La Jolla, CA 92037, USA. Electronic address: crivier@salk.edu.
[Ti] Título:Role of hypothalamic corticotropin-releasing factor in mediating alcohol-induced activation of the rat hypothalamic-pituitary-adrenal axis.
[So] Source:Front Neuroendocrinol;35(2):221-33, 2014 Apr.
[Is] ISSN:1095-6808
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcohol stimulates the hypothalamic-pituitary-adrenal (HPA) axis through brain-based mechanisms in which endogenous corticotropin-releasing factor (CRF) plays a major role. This review first discusses the evidence for this role, as well as the possible importance of intermediates such as vasopressin, nitric oxide and catecholamines. We then illustrate the long-term influence exerted by alcohol on the HPA axis, such as the ability of a first exposure to this drug during adolescence, to permanently blunt neuroendocrine responses to subsequent exposure of the drug. In view of the role played by CRF in addiction, it is likely that a better understanding of the mechanisms through which this drug stimulates the HPA axis may lead to the development of new therapies used in the treatment of alcohol abuse, including clinically relevant CRF antagonists.
[Mh] Termos MeSH primário: Álcoois/farmacologia
Hormônio Liberador da Corticotropina/metabolismo
Sistema Hipotálamo-Hipofisário/metabolismo
Hormônios Liberadores de Hormônios Hipofisários/metabolismo
Sistema Hipófise-Suprarrenal/metabolismo
[Mh] Termos MeSH secundário: Alcoolismo/tratamento farmacológico
Animais
Seres Humanos
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Alcohols); 0 (Pituitary Hormone-Releasing Hormones); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:140324
[Lr] Data última revisão:
140324
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131112
[St] Status:MEDLINE


  5 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:22578217
[Au] Autor:Yu G; Sharp BM
[Ad] Endereço:Department of Pharmacology, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
[Ti] Título:Nicotine modulates multiple regions in the limbic stress network regulating activation of hypophysiotrophic neurons in hypothalamic paraventricular nucleus.
[So] Source:J Neurochem;122(3):628-40, 2012 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nicotine intake affects CNS responses to stressors. We reported that nicotine self-administration (SA) augmented the hypothalamo-pituitary-adrenal (HPA) stress response, in part because of the altered neurotransmission and neuropeptide expression within hypothalamic paraventricular nucleus (PVN). Limbic-PVN interactions involving medial prefrontal cortex, amygdala, and bed nucleus of the stria terminalis (BST) greatly impact the HPA stress response. Therefore, we investigated the effects of nicotine SA on stress-induced neuronal activation in limbic-PVN network, using c-Fos protein immunohistochemistry and retrograde tracing. Nicotine decreased stress-induced c-Fos in prelimbic cortex (PrL), anteroventral BST (avBST), and peri-PVN, but increased c-Fos induction in medial amygdala (MeA), locus coeruleus, and PVN. Fluoro-gold (FG) was injected into avBST or PVN, as GABAergic neurons in avBST projecting to PVN corticotrophin-releasing factor neurons relay information from both PrL glutamatergic and MeA GABAergic neurons. The stress-induced c-Fos expression in retrograde-labeled FG+ neurons was decreased in PrL by nicotine, but increased in MeA, and also reduced in avBST. Therefore, within limbic-PVN network, nicotine SA exerts selective regional effects on neuronal activation by stress. These findings expand the mechanistic framework by demonstrating altered limbic-BST-PVN interactions underlying the disinhibition of PVN corticotrophin-releasing factor neurons, an essential component of the amplified HPA response to stress by nicotine.
[Mh] Termos MeSH primário: Neurônios/efeitos dos fármacos
Nicotina/administração & dosagem
Agonistas Nicotínicos/administração & dosagem
Núcleo Hipotalâmico Paraventricular/patologia
Hormônios Liberadores de Hormônios Hipofisários/metabolismo
Estresse Psicológico/patologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Condicionamento Operante/efeitos dos fármacos
Eletrochoque/efeitos adversos
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Sprague-Dawley
Autoadministração
Estilbamidinas/metabolismo
Estresse Psicológico/etiologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt); 0 (Nicotinic Agonists); 0 (Pituitary Hormone-Releasing Hormones); 0 (Proto-Oncogene Proteins c-fos); 0 (Stilbamidines); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1209
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120515
[St] Status:MEDLINE
[do] DOI:10.1111/j.1471-4159.2012.07785.x


  6 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:22159036
[Au] Autor:Liu JL; Srikant CB; Chowdhury S
[Ti] Título:Is 11ß-HSD1 expressed in islet ß-cells and regulated by corticotropin-releasing hormone?
[So] Source:Proc Natl Acad Sci U S A;108(51):E1390; author reply E1391, 2011 Dec 20.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenases/fisiologia
Sistema Hipotálamo-Hipofisário/metabolismo
Ilhotas Pancreáticas/metabolismo
Hormônios Liberadores de Hormônios Hipofisários/fisiologia
Sistema Hipófise-Suprarrenal/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Pituitary Hormone-Releasing Hormones); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
[Em] Mês de entrada:1203
[Cu] Atualização por classe:150129
[Lr] Data última revisão:
150129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111214
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1116146109


  7 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:21825133
[Au] Autor:Schmid J; Ludwig B; Schally AV; Steffen A; Ziegler CG; Block NL; Koutmani Y; Brendel MD; Karalis KP; Simeonovic CJ; Licinio J; Ehrhart-Bornstein M; Bornstein SR
[Ad] Endereço:Department of Medicine III, University Hospital Carl Gustav Carus, 01307 Dresden, Germany.
[Ti] Título:Modulation of pancreatic islets-stress axis by hypothalamic releasing hormones and 11beta-hydroxysteroid dehydrogenase.
[So] Source:Proc Natl Acad Sci U S A;108(33):13722-7, 2011 Aug 16.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Corticotropin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH), primarily characterized as neuroregulators of the hypothalamic-pituitary-adrenal axis, directly influence tissue-specific receptor-systems for CRH and GHRH in the endocrine pancreas. Here, we demonstrate the expression of mRNA for CRH and CRH-receptor type 1 (CRHR1) and of protein for CRHR1 in rat and human pancreatic islets and rat insulinoma cells. Activation of CRHR1 and GHRH-receptor significantly increased cell proliferation and reduced cell apoptosis. CRH stimulated both cellular content and release of insulin in rat islet and insulinoma cells. At the ultrastructural level, CRHR1 stimulation revealed a more active metabolic state with enlarged mitochondria. Moreover, glucocorticoids that promote glucose production are balanced by both 11b-hydroxysteroid dehydrogenase (11ß-HSD) isoforms; 11ß-HSD-type-1 and 11ß-HSD-type-2. We demonstrated expression of mRNA for 11ß-HSD-1 and 11ß-HSD-2 and protein for 11ß-HSD-1 in rat and human pancreatic islets and insulinoma cells. Quantitative real-time PCR revealed that stimulation of CRHR1 and GHRH-receptor affects the metabolism of insulinoma cells by down-regulating 11ß-HSD-1 and up-regulating 11ß-HSD-2. The 11ß-HSD enzyme activity was analyzed by measuring the production of cortisol from cortisone. Similarly, activation of CRHR1 resulted in reduced cortisol levels, indicating either decreased 11ß-HSD-1 enzyme activity or increased 11ß-HSD-2 enzyme activity; thus, activation of CRHR1 alters the glucocorticoid balance toward the inactive form. These data indicate that functional receptor systems for hypothalamic-releasing hormone agonists exist within the endocrine pancreas and influence synthesis of insulin and the pancreatic glucocorticoid shuttle. Agonists of CRHR1 and GHRH-receptor, therefore, may play an important role as novel therapeutic tools in the treatment of diabetes mellitus.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenases/fisiologia
Sistema Hipotálamo-Hipofisário/metabolismo
Ilhotas Pancreáticas/metabolismo
Hormônios Liberadores de Hormônios Hipofisários/fisiologia
Sistema Hipófise-Suprarrenal/metabolismo
[Mh] Termos MeSH secundário: Animais
Hormônio Liberador da Corticotropina
Seres Humanos
Insulina/biossíntese
Insulinoma/patologia
RNA Mensageiro
Ratos
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Receptores de Neuropeptídeos/metabolismo
Receptores de Hormônios Reguladores de Hormônio Hipofisário/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CRF receptor type 1); 0 (Insulin); 0 (Pituitary Hormone-Releasing Hormones); 0 (RNA, Messenger); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Receptors, Neuropeptide); 0 (Receptors, Pituitary Hormone-Regulating Hormone); 0 (somatotropin releasing hormone receptor); 9015-71-8 (Corticotropin-Releasing Hormone); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
[Em] Mês de entrada:1111
[Cu] Atualização por classe:150204
[Lr] Data última revisão:
150204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110810
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1110965108


  8 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:21735696
[Au] Autor:Jarzabek-Bielecka G; Warchol-Biedermann K; Sowinska E; Wachowiak-Ochmanska K
[Ad] Endereço:Pracownia Ginekologii Wieku Rozwojowego i Seksuologii Kliniki Ginekologii Katedry Perinatologii i Ginekologii Uniwersytetu Medycznego w Poznaniu. grajarz@o2.pl
[Ti] Título:[Precocious puberty].
[Ti] Título:Przedwczesne dojrzewanie plciowe..
[So] Source:Ginekol Pol;82(4):281-6, 2011 Apr.
[Is] ISSN:0017-0011
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Precocious puberty is an early sexual maturation before the age of 8 in case of girls and 9 in boys. There are two types: isosexual precocious puberty--characteristic are appropriate for the child's genetic and gonadal sex; and heterosexual precocious puberty--sexual characteristic are inappropriate for the genetic sex (feminizing syndrome in boys or virilizing syndrome in girls). Precocious puberty is an important problem in childhood gynecology pediatrics, endocrinology and psychology.
[Mh] Termos MeSH primário: Puberdade Precoce/diagnóstico
Puberdade Precoce/terapia
Caracteres Sexuais
Maturidade Sexual
[Mh] Termos MeSH secundário: Androgênios/secreção
Criança
Feminino
Seres Humanos
Sistema Hipotálamo-Hipofisário/metabolismo
Masculino
Menarca
Hormônios Liberadores de Hormônios Hipofisários/uso terapêutico
Puberdade Precoce/classificação
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Androgens); 0 (Pituitary Hormone-Releasing Hormones)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110709
[St] Status:MEDLINE


  9 / 3098 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:21239462
[Au] Autor:Rorato R; Reis WL; Antunes-Rodrigues J; Elias LL
[Ad] Endereço:Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Avenida Bandeirantes 3900, 14049-900 Ribeirao Preto, Sao Paulo, Brazil.
[Ti] Título:Cholecystokinin and hypothalamic corticotrophin-releasing factor participate in endotoxin-induced hypophagia.
[So] Source:Exp Physiol;96(4):439-50, 2011 Apr.
[Is] ISSN:1469-445X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cholecystokinin (CCK) provides a meal-related signal that activates brainstem neurons, which have reciprocal interconnections with the hypothalamic paraventricular nucleus. Neurons that express corticotrophin-releasing factor (CRF) in the hypothalamus possess anorexigenic effects and are activated during endotoxaemia. This study investigated the effects of CCK(1) receptor blockade on lipopolysaccharide (LPS)-induced hypophagia and hypothalamic CRF neuronal activation. Male Wistar rats were pretreated with a specific CCK(1) receptor antagonist (devazepide; 1 mg kg(-1); i.p.) or vehicle; 30 min later they received LPS (100 µg kg(-1); i.p.) or saline injection. Food intake, corticosterone responses and Fos-CRF and Fos-α-melanocyte-stimulating hormone (α-MSH) immunoreactivity in the hypothalamus and Fos-tyrosine hydroxylase immunoreactivity in the nucleus of the solitary tract (NTS) were evaluated. In comparison with saline treatment, LPS administration decreased food intake and increased plasma corticosterone levels, as well as the number of Fos-CRF and Fos- tyrosine hydroxylase double-labelled neurons in vehicle-pretreated rats; no change in Fos-α-MSH immunoreactivity was observed after LPS injection. In saline-treated animals, devazepide pretreatment increased food intake, but it did not modify other parameters compared with vehicle-pretreated rats. Devazepide pretreatment partly reversed LPS-induced hypophagia and Fos-CRF and brainstem neuronal activation. Devazepide did not modify the corticosterone and Fos-α-MSH responses in rats treated with LPS. In conclusion, the present data suggest that LPS-induced hypophagia is mediated at least in part by CCK effects, via CCK(1) receptor, on NTS and hypothalamic CRF neurons.
[Mh] Termos MeSH primário: Colecistocinina/metabolismo
Hormônio Liberador da Corticotropina/metabolismo
Endotoxinas/farmacologia
Hiperfagia/metabolismo
Hipotálamo/metabolismo
Hormônios Liberadores de Hormônios Hipofisários/metabolismo
[Mh] Termos MeSH secundário: Animais
Tronco Encefálico/metabolismo
Corticosterona/sangue
Devazepida/farmacologia
Ingestão de Alimentos/efeitos dos fármacos
Endotoxemia/induzido quimicamente
Endotoxemia/metabolismo
Hiperfagia/induzido quimicamente
Lipopolissacarídeos
Masculino
Neurônios/enzimologia
Neurônios/metabolismo
Núcleo Hipotalâmico Paraventricular/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Wistar
Receptor de Colecistocinina A/antagonistas & inibidores
Receptor de Colecistocinina A/metabolismo
Núcleo Solitário/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
alfa-MSH/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endotoxins); 0 (Lipopolysaccharides); 0 (Pituitary Hormone-Releasing Hormones); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptor, Cholecystokinin A); 581-05-5 (alpha-MSH); 9011-97-6 (Cholecystokinin); 9015-71-8 (Corticotropin-Releasing Hormone); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); JE6P7QY7NH (Devazepide); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1107
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110118
[St] Status:MEDLINE
[do] DOI:10.1113/expphysiol.2010.056465


  10 / 3098 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:20825365
[Au] Autor:Chaldakov GN; Fiore M; Tonchev AB; Aloe L
[Ad] Endereço:Division of Cell Biology, Medical University, Varna, Bulgaria. chaldakov@yahoo.com
[Ti] Título:Neuroadipology: a novel component of neuroendocrinology.
[So] Source:Cell Biol Int;34(10):1051-3, 2010 Oct.
[Is] ISSN:1095-8355
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adipose tissue is a dynamic endocrine and paracrine organ producing a large number of signalling proteins collectively termed adipokines. Some of them are mediators in the cross-talk between adipose tissue and the brain in regulating food intake and energy homoeostasis. However, the hypothalamus is not the only brain target for adipokines, and food intake is not the only biological effect of these signals. Rather, some adipokines support various cognitive functions and exert neurotrophic activity. Current data on adipose-derived neuropeptides, neurotrophic factors, pituitary hormones and hypothalamic releasing factors is highlighted in this review. We propose that adipose tissue is a member of the diffuse neuroendocrine system. Cumulatively, this is conceptualized as neuroadipology, a new example of a link between neurobiology and other topics, such as neuroimmunology and neuroendocrinology. Because adipose tissue is a bona fide endocrine organ, neuroadipology may be considered a new discipline in neuroendocrinology. It may have a wide-ranging potential within a variety of neuronal and metabolic functions in health and disease.
[Mh] Termos MeSH primário: Tecido Adiposo/fisiologia
Neuroendocrinologia
Sistemas Neurossecretores/fisiologia
[Mh] Termos MeSH secundário: Adipocinas/fisiologia
Encéfalo/fisiologia
Cognição
Ingestão de Alimentos
Seres Humanos
Fatores de Crescimento Neural/fisiologia
Neuroimunomodulação
Neuropeptídeos/fisiologia
Hormônios Liberadores de Hormônios Hipofisários/fisiologia
Hormônios Hipofisários/fisiologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Adipokines); 0 (Nerve Growth Factors); 0 (Neuropeptides); 0 (Pituitary Hormone-Releasing Hormones); 0 (Pituitary Hormones)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:120802
[Lr] Data última revisão:
120802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100910
[St] Status:MEDLINE
[do] DOI:10.1042/CBI20100509



página 1 de 310 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde