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Pesquisa : D12.776.543.750.720.600.285 [Categoria DeCS]
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Id: lil-538256
Autor: Scripes, Nicole de Angelis; Macioszek, Marcelo Abbá; Bahls, Larissa Danielle; Aoki, Mateus Nóbrega; Watanabe, Maria Angelica Ehara; Mazzuco, Tânia Longo.
Título: Expressão de genes relacionados à função adrenocortical no estado de caquexia neoplásica / Expression of genes related to the adrenocortical function in the neoplastic cachexia process
Fonte: Acta sci., Health sci;31(2):133-141, jul.-dez. 2009. ilus, tab, graf.
Idioma: pt.
Resumo: A glândula adrenal tem papel fundamental na resposta neuroendócrina, especialmente em situações em que há comprometimento da homeostasia. No processo de caquexia neoplásica, há prejuízo da homeostasia por alterações nutricionais e metabólicas do câncer em estágio avançado, envolvendo a resposta do eixo hipotálamo-hipófise-adrenal. Neste trabalho, foi utilizado um modelo animal de caquexia induzida pelo tumor de Walker-256 em ratos Wistar. Os animais (n=4) foram sacrificados dez dias após a inoculação de células tumorais e a glândula adrenal foi removida. O RNA foi extraído para o estudo da expressão de genes relacionados ao controle da esteroidogênese por RT-PCR semiquantitativa. A análise dos dados demonstrou expressão significativamente reduzida dos genes MC2R (receptor tipo 2 para melacortina), 3ßHSD I (3β-hidroxiesteroidedesidrogenas e tipo I) e TSPO (proteína translocadora) em animais com caquexia neoplásica(valores de P=0,037; 0,0097 e 0,052, respectivamente), revelando falência do córtex da adrenal.

The adrenal gland plays a crucial role in the neuroendocrine response, especially in situations where homeostasis is disturbed. In the neoplastic cachexiaprocess, there is homeostasis impairment by nutritional and metabolic alterations of advanced-stage cancer, involving hypothalamus-pituitary-adrenal axis response. In this assignment, an experimental model of cachexia induced by Walker-256 tumor was performed in Wistar rats. Animals (n=4) were sacrificed 10 days after inoculation of tumor cells, and the adrenal glands were excised. The RNA was isolated for the study of geneexpression related to the steroidogenesis control by semi-quantitative RT-PCR. Dataanalysis showed a significant reduced expression of MC2R (melancortin type 2 receptor), 3ßHSD I (3-beta-hydroxysteroid dehydrogenase type I) and TSPO (translocator protein)genes in animals with neoplastic cachexia (P=0.037, 0.0097 and 0.052, respectively), revealing adrenal cortex failure.
Descritores: Glândulas Suprarrenais
ABATTOIRS-HIDROXIESTEROIDE DESIDROGENASES
Caquexia
Homeostase
Translocases Mitocondriais de ADP e ATP
Receptores da Corticotropina
Limites: Animais
Ratos
Responsável: BR513.1 - Biblioteca Central


  2 / 7 LILACS  
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Texto completo SciELO Brasil
Texto completo
Id: lil-350398
Autor: Rodrigues, Adriane M; Suplicy, Henrique L; Radominski, Rosana B.
Título: Controle neuroendócrino do peso corporal: implicaçöes na gênese da obesidade / Neuroendocrine control of food intake: implications in the genesis of obesity
Fonte: Arq. bras. endocrinol. metab;47(4):398-409, ago. 2003. ilus, tab.
Idioma: pt.
Resumo: O peso corporal é regulado por uma interaçäo complexa entre hormônios e neuropeptídeos, sob o controle principal de núcleos hipotalâmicos. Mutaçöes nos genes de hormônios e neuropeptídeos, de seus receptores ou de elementos regulatórios, têm sido descritas na espécie humana, mas säo tidas como raras, näo explicando as formas mais comuns de obesidade. No entanto, o estudo destas mutaçöes tem propiciado um grande avanço nos conhecimentos sobre a base genética e a fisiopatologia da obesidade, possibilitando o estudo e abrindo perspectivas para o desenvolvimento de novas modalidades terapêuticas. Recentemente, demonstrou-se que mutaçöes no receptor 4 da melanocortina podiam ser encontradas em até 5 por cento dos casos de obesidade severa, representando até o presente momento a forma mais prevalente de obesidade monogênica na espécie humana. Nesta revisäo, säo discutidas as diversas mutaçöes descritas nos seres humanos de elementos da rede neuroendócrina de controle do peso corporal, bem como as implicaçöes dos mesmos na gênese da obesidade
Descritores: Peso Corporal
Leptina
Mutação/genética
Obesidade
-Pró-Opiomelanocortina
Receptores da Corticotropina
Limites: Humanos
Animais
Responsável: BR1.1 - BIREME


  3 / 7 LILACS  
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Texto completo SciELO Brasil
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Id: lil-270221
Autor: Elias, L. L. K; Clark, A. J. L.
Título: The expression of the ACTH receptor
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;33(10):1245-8, Oct. 2000.
Idioma: en.
Conferência: Apresentado em: International Meeting on Adrenal Disease: Basic and Clinical Aspects, 1, Ribeiräo Preto, Aug. 31-Sept. 2, 1999.
Resumo: Adrenal glucocorticoid secretion is regulated by adrenocorticotropic hormone (ACTH) acting through a specific cell membrane receptor (ACTH-R). The ACTH-R is a member of the G protein superfamily-coupled receptors and belongs to the subfamily of melanocortin receptors. The ACTH-R is mainly expressed in the adrenocortical cells showing a restricted tissue specificity, although ACTH is recognized by the other four melanocortin receptors. The cloning of the ACTH-R was followed by the study of this gene in human diseases such as familial glucocorticoid deficiency (FGD) and adrenocortical tumors. FGD is a rare autosomal recessive disease characterized by glucocorticoid deficiency, elevated plasma ACTH levels and preserved renin/aldosterone secretion. This disorder has been ascribed to an impaired adrenal responsiveness to ACTH due to a defective ACTH-R, a defect in intracellular signal transduction or an abnormality in adrenal cortical development. Mutations of the ACTH-R have been described in patients with FGD in segregation with the disease. The functional characterization of these mutations has been prevented by difficulties in expressing human ACTH-R in cells that lack endogenous melanocortin receptor activity. To overcome these difficulties we used Y6 cells, a mutant variant of the Y1 cell line, which possesses a non-expressed ACTH-R gene allowing the functional study without any background activity. Our results demonstrated that the several mutations of the ACTH-R found in FGD result in an impaired cAMP response or loss of sensitivity to ACTH stimulation. An ACTH-binding study showed an impairment of ligand binding with loss of the high affinity site in most of the mutations studied.
Descritores: Receptores da Corticotropina/genética
Receptores da Corticotropina/metabolismo
-Mutação
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


  4 / 7 LILACS  
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Texto completo SciELO Brasil
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Id: lil-270218
Autor: Latronico, A. C.
Título: Role of ACTH receptor in adrenocortical tumor formation
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;33(10):1249-52, Oct. 2000.
Idioma: en.
Conferência: Apresentado em: International Meeting on Adrenal Disease: Basic and Clinical Aspects, 1, Ribeiräo Preto, Aug. 31-Sept. 2, 1999.
Resumo: Adrenocorticotrophin (ACTH) is the major regulatory hormone of steroid synthesis and secretion by adrenocortical cells. The actions of ACTH are mediated by its specific membrane receptor (ACTH-R). The human ACTH-R gene was recently cloned, allowing systematic determination of its sequence, expression and function in adrenal tumorigenesis. The presence of oncogenic mutations of the ACTH-R gene in adrenocortical tumors has been reported. Direct sequencing of the entire coding region of the ACTH-R gene of sporadic adrenocortical adenomas and carcinomas did not reveal constitutive activating mutations, indicating that this mechanism is not frequent in human adrenocortical tumorigenesis. Recent studies demonstrated allelic loss of the ACTH-R gene in a subset of sporadic adrenocortical tumors using a PstI polymorphism located in the promoter region of the ACTH-R gene. Loss of heterozygosity of the ACTH-R was analyzed in 20 informative patients with a variety of benign and malignant adrenocortical tumors. Three of them showed loss of heterozygosity of the ACTH-R gene. In addition, Northern blot experiments demonstrated reduced expression of ACTH-R mRNA in these three tumors with loss of heterozygosity, suggesting the functional significance of this finding at the transcriptional level. Deletion of the ACTH-R gene seems to be involved in a subset of human adrenocortical tumors, contributing to cellular dedifferentiation.
Descritores: Neoplasias do Córtex Suprarrenal/genética
Receptores da Corticotropina/fisiologia
-Perda de Heterozigosidade
Mutação
Receptores da Corticotropina/genética
RNA Mensageiro
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


  5 / 7 LILACS  
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Armelin, H. A
Texto completo
Id: lil-270216
Autor: Lotfi, C. F. P; Lepique, A. P; Forti, F. L; Schwindt, T. T; Eichler, C. B; Santos, M. O; Rebustini, I. T; Hajj, G. N. M; Juliano, L; Armelin, H. A.
Título: Proliferative signaling initiated in ACTH receptors
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;33(10):1133-40, Oct. 2000. ilus.
Idioma: en.
Conferência: Apresentado em: International Meeting on Adrenal Disease: Basic and Clinical Aspects, 1, Ribeiräo Preto, Aug. 31-Sept. 2, 1999.
Resumo: This article reviews recent results of studies aiming to elucidate modes of integrating signals initiated in ACTH receptors and FGF2 receptors, within the network system of signal transduction found in Y1 adrenocortical cells. These modes of signal integration should be central to the mechanisms underlying the regulation of the G0->G1->S transition in the adrenal cell cycle. FGF2 elicits a strong mitogenic response in G0/G1-arrested Y1 adrenocortical cells, that includes a) rapid and transient activation of extracellular signal-regulated kinases-mitogen-activated protein kinases (ERK-MAPK) (2 to 10 min), b) transcription activation of c-fos, c-jun and c-myc genes (10 to 30 min), c) induction of c-Fos and c-Myc proteins by 1 h and cyclin D1 protein by 5 h, and d) onset of DNA synthesis stimulation within 8 h. ACTH, itself a weak mitogen, interacts with FGF2 in a complex manner, blocking the FGF2 mitogenic response during the early and middle G1 phase, keeping ERK-MAPK activation and c-Fos and cyclin D1 induction at maximal levels, but post-transcriptionally inhibiting c-Myc expression. c-Fos and c-Jun proteins are mediators in both the strong and the weak mitogenic responses respectively triggered by FGF2 and ACTH. Induction of c-Fos and stimulation of DNA synthesis by ACTH are independent of PKA and are inhibited by the PKC inhibitor GF109203X. In addition, ACTH is a poor activator of ERK-MAPK, but c-Fos induction and DNA synthesis stimulation by ACTH are strongly inhibited by the inhibitor of MEK1 PD98059.
Descritores: Córtex Suprarrenal/citologia
Receptores da Corticotropina/fisiologia
Transdução de Sinais/fisiologia
-Neoplasias do Córtex Suprarrenal
Ciclo Celular/fisiologia
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Proteína Quinase C/metabolismo
Receptores de Fatores de Crescimento de Fibroblastos/fisiologia
Células Tumorais Cultivadas/fisiologia
Limites: Humanos
Animais
Tipo de Publ: Revisão
Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-260222
Autor: Saavedra G., Victor.
Título: Rol del tejido adiposo / Adipose tissue role
Fonte: Rev. chil. obes;4(2):41-6, 1999.
Idioma: es.
Resumo: Currently the research on adipose tissue has yielded same insights of itïs function. On the embrionary state the differentiation between white adipose tissue and brown adipose tissue and brown adipose tissue signals different functions. The presence of multiple receptors and actions define itïs autocrine, paracline and endocrine roles
Descritores: Adipócitos
Tecido Adiposo/fisiologia
Metabolismo Energético/fisiologia
Receptor de Insulina
Receptores Adrenérgicos alfa
Receptores Adrenérgicos beta
Receptores da Colecistocinina
Receptores da Corticotropina
Receptores de Glucagon
Receptores da Somatotropina
Receptores dos Hormônios Tireóideos
-Tecido Adiposo/embriologia
Tecido Adiposo/crescimento & desenvolvimento
Proteínas/antagonistas & inibidores
Receptores de Glucocorticoides
Limites: Humanos
Responsável: CL2.1 - Biblioteca de Medicina


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Id: lil-186337
Autor: Armelin, Hugo A; Kimura, Eico.
Título: Induction of fos and jun proto-oncogenes by the adrenocorticotropic hormone (ACTH): possible biological implications
Fonte: Ciênc. cult. (Säo Paulo);48(5/6):361-3, Sept.-Dec. 1996. ilus.
Idioma: en.
Projeto: FAPESP; . CNPq.
Resumo: ACTH induces the expression of fos and jun proto-oncogene family members in the mouse Y-1 adrenocortical cell fine. PMA (phorbol-12-myristate-l3-acetate) closely mimics these inductive effects of ACTH. On the other hand, cAMP derivatives are not effective in inducing the fos and jun genes. These results suggest that ACTH receptors are likely to activate signaling routes other than the classical cAMP/protein kinase A in order to induce FOS and JUN proteins. We hypothesize that induction of FOS and JUN proteins is likely to be important in the trophic response of adrenocortical cells to ACTH.
Descritores: Hormônio Adrenocorticotrópico/farmacologia
Proteínas Proto-Oncogênicas c-fos
Proteínas Proto-Oncogênicas c-jun
-AMP Cíclico
Proteínas Quinases
Receptores da Corticotropina/metabolismo
Acetato de Tetradecanoilforbol
Limites: Animais
Camundongos
Responsável: BR1.1 - BIREME



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