Base de dados : MEDLINE
Pesquisa : A05.360.444.849.513 [Categoria DeCS]
Referências encontradas : 6518 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 652 ir para página                         

  1 / 6518 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29385186
[Au] Autor:Eladak S; Moison D; Guerquin MJ; Matilionyte G; Kilcoyne K; N'Tumba-Byn T; Messiaen S; Deceuninck Y; Pozzi-Gaudin S; Benachi A; Livera G; Antignac JP; Mitchell R; Rouiller-Fabre V; Habert R
[Ad] Endereço:Univ. Paris Diderot, Sorbonne Paris Cité, Laboratory of Development of the Gonads, Unit of Genetic Stability, Stem Cells and Radiation, Fontenay-aux-Roses, France.
[Ti] Título:Effects of environmental Bisphenol A exposures on germ cell development and Leydig cell function in the human fetal testis.
[So] Source:PLoS One;13(1):e0191934, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Using an organotypic culture system termed human Fetal Testis Assay (hFeTA) we previously showed that 0.01 µM BPA decreases basal, but not LH-stimulated, testosterone secreted by the first trimester human fetal testis. The present study was conducted to determine the potential for a long-term antiandrogenic effect of BPA using a xenograft model, and also to study the effect of BPA on germ cell development using both the hFETA and xenograft models. METHODS: Using the hFeTA system, first trimester testes were cultured for 3 days with 0.01 to 10 µM BPA. For xenografts, adult castrate male nude mice were injected with hCG and grafted with first trimester testes. Host mice received 10 µM BPA (~ 500 µg/kg/day) in their drinking water for 5 weeks. Plasma levels of total and unconjugated BPA were 0.10 µM and 0.038 µM respectively. Mice grafted with second trimester testes received 0.5 and 50 µg/kg/day BPA by oral gavage for 5 weeks. RESULTS: With first trimester human testes, using the hFeTA model, 10 µM BPA increased germ cell apoptosis. In xenografts, germ cell density was also reduced by BPA exposure. Importantly, BPA exposure significantly decreased the percentage of germ cells expressing the pluripotency marker AP-2γ, whilst the percentage of those expressing the pre-spermatogonial marker MAGE-A4 significantly increased. BPA exposure did not affect hCG-stimulated androgen production in first and second trimester xenografts as evaluated by both plasma testosterone level and seminal vesicle weight in host mice. CONCLUSIONS: Exposure to BPA at environmentally relevant concentrations impairs germ cell development in first trimester human fetal testis, whilst gonadotrophin-stimulated testosterone production was unaffected in both first and second trimester testis. Studies using first trimester human fetal testis demonstrate the complementarity of the FeTA and xenograft models for determining the respective short-term and long term effects of environmental exposures.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Poluentes Ambientais/toxicidade
Células Intersticiais do Testículo/efeitos dos fármacos
Fenóis/toxicidade
Espermatozoides/efeitos dos fármacos
Testículo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Xenoenxertos
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Gravidez
Primeiro Trimestre da Gravidez
Segundo Trimestre da Gravidez
Radioimunoensaio
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Testículo/citologia
Testículo/embriologia
Testosterona/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Environmental Pollutants); 0 (Phenols); 3XMK78S47O (Testosterone); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191934


  2 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28985536
[Au] Autor:Li L; Li X; Chen X; Chen Y; Liu J; Chen F; Ge F; Ye L; Lian Q; Ge RS
[Ad] Endereço:Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou, Zhejiang 325027, China.
[Ti] Título:Perfluorooctane sulfonate impairs rat Leydig cell development during puberty.
[So] Source:Chemosphere;190:43-53, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Perfluorooctane sulfonate (PFOS) possibly delays male sexual development. However, its effects on pubertal Leydig cell development are unclear. The objective of the present study was to investigate the effects of in vivo PFOS exposure on rat Leydig cell development during puberty. Immature male Sprague Dawley rats were gavaged 5 or 10 mg/kg PFOS on postnatal day 35 for 21 days. Compared to the control (0 mg/kg), PFOS lowered serum testosterone levels without altering luteinizing hormone and follicle-stimulating hormone levels on postnatal day 56. PFOS in vivo downregulated mRNA or protein levels of Leydig cells (Lhcgr, Cyp11a1, and Cyp17a1). PFOS in vitro inhibited androgen secretion in immature Leydig cells at ≥ 50 nM, most possibly via downregulating Hsd17b3 mRNA level. At ≥ 500 nM, PFOS downregulated Lhcgr, inhibited BCL-2 and increased BAX levels to cause Leydig cell apoptosis. In conclusion, PFOS at a lower dose directly inhibited pubertal development of Leydig cells.
[Mh] Termos MeSH primário: Ácidos Alcanossulfônicos/toxicidade
Fluorcarbonetos/toxicidade
Células Intersticiais do Testículo/efeitos dos fármacos
Maturidade Sexual/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Regulação para Baixo
Células Intersticiais do Testículo/patologia
Hormônio Luteinizante/efeitos dos fármacos
Hormônio Luteinizante/metabolismo
Masculino
Proteínas/efeitos dos fármacos
Proteínas/metabolismo
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Testosterona/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkanesulfonic Acids); 0 (Fluorocarbons); 0 (Proteins); 0 (RNA, Messenger); 3XMK78S47O (Testosterone); 9002-67-9 (Luteinizing Hormone); 9H2MAI21CL (perfluorooctane sulfonic acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  3 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29300865
[Au] Autor:Fan J; Wang K; Zirkin B; Papadopoulos V
[Ad] Endereço:Research Institute of the McGill University Health Centre and Department of Medicine, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
[Ti] Título:CRISPR/Cas9‒Mediated Tspo Gene Mutations Lead to Reduced Mitochondrial Membrane Potential and Steroid Formation in MA-10 Mouse Tumor Leydig Cells.
[So] Source:Endocrinology;159(2):1130-1146, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The outer mitochondrial membrane translocator protein (TSPO) binds cholesterol with high affinity and is involved in mediating its delivery into mitochondria, the rate-limiting step in hormone-induced steroidogenesis. Specific ligand binding to TSPO has been shown to initiate steroid formation. However, recent studies of the genetic deletion of Tspo have provided conflicting results. Here, we address and extend previous studies by examining the effects of Tspo-specific mutations on steroid formation in hormone- and cyclic adenosine monophosphate (cAMP)-responsive MA-10 cells, using the CRISPR/Cas9 system. Two mutant subcell lines, nG1 and G2G, each carrying a Tspo exon2-specific genome modification, and two control subcell lines, G1 and HH, each carrying a wild-type Tspo, were produced. In response to dibutyryl cAMP, the nG1 and G2G cells produced progesterone at levels significantly lower than those produced by the corresponding control cells G1 and HH. Neutral lipid homeostasis, which provides free cholesterol for steroid biosynthesis, was altered significantly in the Tspo mutant cells. Interestingly, the mitochondrial membrane potential (ΔΨm) of the Tspo mutant cells was significantly reduced compared with that of the control cells, likely because of TSPO interactions with the voltage-dependent anion channel and tubulin at the outer mitochondrial membrane. Steroidogenic acute regulatory protein (STAR) expression was induced in nG1 cells, suggesting that reduced TSPO affected STAR synthesis and/or processing. Taken together, these results provide further evidence for the critical role of TSPO in steroid biosynthesis and suggest that it may function at least in part via its regulation of ΔΨm and effects on STAR.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Hormônios Esteroides Gonadais/biossíntese
Células Intersticiais do Testículo/metabolismo
Potencial da Membrana Mitocondrial/genética
Mutagênese Sítio-Dirigida
Mutação
Receptores de GABA/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Tumor de Células de Leydig/genética
Tumor de Células de Leydig/metabolismo
Tumor de Células de Leydig/patologia
Masculino
Camundongos
Mutagênese Sítio-Dirigida/métodos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Esteroides/biossíntese
Neoplasias Testiculares/genética
Neoplasias Testiculares/metabolismo
Neoplasias Testiculares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bzrp protein, mouse); 0 (Gonadal Steroid Hormones); 0 (Phosphoproteins); 0 (Receptors, GABA); 0 (Steroids); 0 (steroidogenic acute regulatory protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03065


  4 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29304246
[Au] Autor:Ma Y; Zhou Y; Zhu YC; Wang SQ; Ping P; Chen XF
[Ad] Endereço:Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China.
[Ti] Título:Lipophagy Contributes to Testosterone Biosynthesis in Male Rat Leydig Cells.
[So] Source:Endocrinology;159(2):1119-1129, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In recent years, autophagy was found to regulate lipid metabolism through a process termed lipophagy. Lipophagy modulates the degradation of cholesteryl esters to free cholesterol (FC), which is the substrate of testosterone biosynthesis. However, the role of lipophagy in testosterone production is unknown. To investigate this, primary rat Leydig cells and varicocele rat models were administered to inhibit or promote autophagy, and testosterone, lipid droplets (LDs), total cholesterol (TC), and FC were evaluated. The results demonstrated that inhibiting autophagy in primary rat Leydig cells reduced testosterone production. Further studies demonstrated that inhibiting autophagy increased the number and size of LDs and the level of TC, but decreased the level of FC. Furthermore, hypoxia promoted autophagy in Leydig cells. We found that short-term hypoxia stimulated testosterone secretion; however, the inhibition of autophagy abolished stimulated testosterone release. Hypoxia decreased the number and size of LDs in Leydig cells, but the changes could be largely rescued by blocking autophagy. In experimental varicocele rat models, the administration of autophagy inhibitors substantially reduced serum testosterone. These data demonstrate that autophagy contributes to testosterone biosynthesis at least partially through degrading intracellular LDs/TC. Our observations might reveal an autophagic regulatory mode regarding testosterone biosynthesis.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Células Intersticiais do Testículo/metabolismo
Lipólise/fisiologia
Testosterona/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Colesterol/metabolismo
Gotículas Lipídicas/metabolismo
Metabolismo dos Lipídeos/fisiologia
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
3XMK78S47O (Testosterone); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03020


  5 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29324782
[Au] Autor:Shawki HH; Oishi H; Usui T; Kitadate Y; Basha WA; Abdellatif AM; Hasegawa K; Okada R; Mochida K; El-Shemy HA; Muratani M; Ogura A; Yoshida S; Takahashi S
[Ad] Endereço:Department of Anatomy and Embryology, Graduate School of Comprehensive Human Science, University of Tsukuba, Tsukuba, Japan.
[Ti] Título:MAFB is dispensable for the fetal testis morphogenesis and the maintenance of spermatogenesis in adult mice.
[So] Source:PLoS One;13(1):e0190800, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor MAFB is an important regulator of the development and differentiation of various organs and tissues. Previous studies have shown that MAFB is expressed in embryonic and adult mouse testes and is expected to act as the downstream target of retinoic acid (RA) to initiate spermatogenesis. However, its exact localization and function remain unclear. Here, we localized MAFB expression in embryonic and adult testes and analyzed its gene function using Mafb-deficient mice. We found that MAFB and c-MAF are the only large MAF transcription factors expressed in testes, while MAFA and NRL are not. MAFB was localized in Leydig and Sertoli cells at embryonic day (E) 18.5 but in Leydig cells, Sertoli cells, and pachytene spermatocytes in adults. Mafb-deficient testes at E18.5 showed fully formed seminiferous tubules with no abnormal structure or differences in testicular somatic cell numbers compared with those of control wild-type mice. Additionally, the expression levels of genes related to development and function of testicular cells were unchanged between genotypes. In adults, the expression of MAFB in Sertoli cells was shown to be stage specific and induced by RA. By generating Mafbfl/fl CAG-CreER™ (Mafb-cKO) mice, in which Cre recombinase was activated upon tamoxifen treatment, we found that the neonatal cKO mice died shortly upon Mafb deletion, but adult cKO mice were alive upon deletion. Adult cKO mice were fertile, and spermatogenesis maintenance was normal, as indicated by histological analysis, hormone levels, and germ cell stage-specific markers. Moreover, there were no differences in the proportion of seminiferous stages between cKO mice and controls. However, RNA-Seq analysis of cKO Sertoli cells revealed that the down-regulated genes were related to immune function and phagocytosis activity but not spermatogenesis. In conclusion, we found that MAFB is dispensable for fetal testis morphogenesis and spermatogenesis maintenance in adult mice, despite the significant gene expression in different cell types, but MAFB might be critical for phagocytosis activity of Sertoli cells.
[Mh] Termos MeSH primário: Fator de Transcrição MafB/metabolismo
Espermatogênese/fisiologia
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Fertilidade/fisiologia
Células Intersticiais do Testículo/citologia
Células Intersticiais do Testículo/metabolismo
Fator de Transcrição MafB/genética
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Proto-Oncogênicas c-maf/metabolismo
RNA Mensageiro/metabolismo
Células de Sertoli/citologia
Células de Sertoli/metabolismo
Espermatócitos/citologia
Espermatócitos/metabolismo
Testículo/anatomia & histologia
Testosterona/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Maf protein, mouse); 0 (MafB Transcription Factor); 0 (Mafb protein, mouse); 0 (Proto-Oncogene Proteins c-maf); 0 (RNA, Messenger); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190800


  6 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28911170
[Au] Autor:Rebourcet D; Darbey A; Monteiro A; Soffientini U; Tsai YT; Handel I; Pitetti JL; Nef S; Smith LB; O'Shaughnessy PJ
[Ad] Endereço:Institute of Biodiversity, Animal Health and Comparative Medicine, University of Glasgow, Glasgow G61 1QH, United Kingdom.
[Ti] Título:Sertoli Cell Number Defines and Predicts Germ and Leydig Cell Population Sizes in the Adult Mouse Testis.
[So] Source:Endocrinology;158(9):2955-2969, 2017 Sep 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sertoli cells regulate differentiation and development of the testis and are essential for maintaining adult testis function. To model the effects of dysregulating Sertoli cell number during development or aging, we have used acute diphtheria toxin-mediated cell ablation to reduce Sertoli cell population size. Results show that the size of the Sertoli cell population that forms during development determines the number of germ cells and Leydig cells that will be present in the adult testis. Similarly, the number of germ cells and Leydig cells that can be maintained in the adult depends directly on the size of the adult Sertoli cell population. Finally, we have used linear modeling to generate predictive models of testis cell composition during development and in the adult based on the size of the Sertoli cell population. This study shows that at all ages the size of the Sertoli cell population is predictive of resulting testicular cell composition. A reduction in Sertoli cell number/proliferation at any age will therefore lead to a proportional decrease in germ cell and Leydig cell numbers, with likely consequential effects on fertility and health.
[Mh] Termos MeSH primário: Células Germinativas/citologia
Células Intersticiais do Testículo/citologia
Células de Sertoli/citologia
Testículo/citologia
[Mh] Termos MeSH secundário: Envelhecimento/fisiologia
Animais
Contagem de Células
Diferenciação Celular
Toxina Diftérica/genética
Genes Transgênicos Suicidas
Células Germinativas/fisiologia
Crescimento e Desenvolvimento/fisiologia
Células Intersticiais do Testículo/fisiologia
Masculino
Camundongos
Camundongos Transgênicos
Fragmentos de Peptídeos/genética
Células de Sertoli/fisiologia
Maturidade Sexual/fisiologia
Espermatogênese/fisiologia
Espermatozoides/citologia
Espermatozoides/fisiologia
Testículo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diphtheria Toxin); 0 (Peptide Fragments); 0 (diphtheria toxin fragment A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00196


  7 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28903063
[Au] Autor:Ghouili F; Martin LJ
[Ad] Endereço:Biology Department, Université de Moncton, Moncton, New-Brunswick E1A 3E9, Canada.
[Ti] Título:Cooperative regulation of Gja1 expression by members of the AP-1 family cJun and cFos in TM3 Leydig and TM4 Sertoli cells.
[So] Source:Gene;635:24-32, 2017 Nov 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Within the testis, connexin43 encoded by Gja1 plays an important role in cell-to-cell communication between Leydig cells as well as between Sertoli cells and spermatogonia. In the adult male, Leydig cells are the principal producers of testosterone sustaining spermatogenesis, while Sertoli cells nourish, protect and support the differentiating germ cells. It has been shown previously that members of the AP-1 family regulate Gja1 expression in myometrial cells, suggesting that such regulatory mechanism may also be relevant within the testis. Thus, we performed cotransfections of AP-1 expression plasmids with different mouse Gja1 promoter/luciferase reporter constructs within TM3 Leydig and TM4 Sertoli cells. We showed that a functional cooperation between cJun and cFos activates Gja1 expression and requires an AP-1 DNA regulatory element located between -132 and -26 bp. In addition, such synergy relies on the recruitment of cFos to this region of the mouse Gja1 promoter. Hence, our data indicate that AP-1 members are important for optimal expression of Gja1 within Sertoli and Leydig cells from the testis.
[Mh] Termos MeSH primário: Comunicação Celular/genética
Conexina 43/genética
Proteínas Oncogênicas v-fos/genética
Fator de Transcrição AP-1/genética
[Mh] Termos MeSH secundário: Animais
Conexina 43/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Células Intersticiais do Testículo/metabolismo
Masculino
Camundongos
Proteínas Oncogênicas v-fos/biossíntese
Regiões Promotoras Genéticas
Células de Sertoli/metabolismo
Espermatogênese/genética
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
Testosterona/genética
Fator de Transcrição AP-1/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (GJA1 protein, mouse); 0 (Oncogene Proteins v-fos); 0 (Transcription Factor AP-1); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


  8 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28772110
[Au] Autor:Bandak M; Jørgensen N; Juul A; Lauritsen J; Oturai PS; Mortensen J; Hojman P; Helge JW; Daugaard G
[Ad] Endereço:Department of Oncology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. Electronic address: mikkel.bandak@regionh.dk.
[Ti] Título:Leydig cell dysfunction, systemic inflammation and metabolic syndrome in long-term testicular cancer survivors.
[So] Source:Eur J Cancer;84:9-17, 2017 Oct.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Twenty to thirty percent of testicular cancer (TC) survivors have elevated serum levels of luteinising hormone (LH) with or without corresponding low testosterone levels (Leydig cell dysfunction) during clinical follow-up for TC. However, it remains to be clarified if this subgroup of TC survivors has an increased long-term risk of systemic inflammation and metabolic syndrome (MetS) when compared with TC survivors with normal Leydig cell function during follow-up. PATIENTS AND METHODS: TC survivors with Leydig cell dysfunction and a control group of TC survivors with normal Leydig cell function during follow-up were eligible for participation in the study. Markers of systemic inflammation and prevalence of MetS were compared between TC survivors with Leydig cell dysfunction and the control group. RESULTS: Of 158 included TC survivors, 28 (18%) had uncompensated Leydig cell dysfunction, 59 (37%) had compensated Leydig cell dysfunction and 71 (45%) had normal Leydig cell function during follow-up. MetS and markers of systemic inflammation were evaluated at a median follow-up of 9.7 years (interquartile range 4.1-17.1) after TC treatment. The prevalence of MetS was significantly lower among patients with compensated Leydig cell dysfunction during follow-up (12% versus 27%, p = 0.04), whereas there was no difference between TC survivors with uncompensated Leydig cell dysfunction and controls (33% versus 27%, p = 0.5). Apart from high-sensitivity C-reactive protein which was higher in TC survivors with uncompensated Leydig cell dysfunction during follow-up, there was no evidence of increased systemic inflammation in patients with Leydig cell dysfunction during clinical follow-up. Total testosterone at follow-up was significantly associated with MetS, whereas there was no association between LH and MetS. CONCLUSION: We did not find evidence that TC survivors with Leydig cell dysfunction during clinical follow-up had increased long-term risk of MetS. Total testosterone at follow-up was significantly associated with MetS. The study is registered at www.clinicaltrials.govNCT02240966.
[Mh] Termos MeSH primário: Inflamação/epidemiologia
Células Intersticiais do Testículo/metabolismo
Hormônio Luteinizante/sangue
Síndrome Metabólica/epidemiologia
Sobreviventes
Neoplasias Testiculares/terapia
Testosterona/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Dinamarca/epidemiologia
Terapia de Reposição Hormonal
Seres Humanos
Inflamação/sangue
Inflamação/diagnóstico
Inflamação/prevenção & controle
Células Intersticiais do Testículo/patologia
Masculino
Síndrome Metabólica/sangue
Síndrome Metabólica/diagnóstico
Síndrome Metabólica/prevenção & controle
Meia-Idade
Prevalência
Fatores de Proteção
Fatores de Risco
Testosterona/deficiência
Testosterona/uso terapêutico
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 3XMK78S47O (Testosterone); 9002-67-9 (Luteinizing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


  9 / 6518 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28697429
[Au] Autor:Lan HC; Wu KY; Lin IW; Yang ZJ; Chang AA; Hu MC
[Ad] Endereço:Institute of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan. Electronic address: blue2010@mail.ndmctsgh.edu.tw.
[Ti] Título:Bisphenol A disrupts steroidogenesis and induces a sex hormone imbalance through c-Jun phosphorylation in Leydig cells.
[So] Source:Chemosphere;185:237-246, 2017 Oct.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bisphenol A (BPA) is a well-known endocrine disrupting chemical (EDC) that is used to manufacture plastic consumer products. It is well known that exposure to BPA can induce defects in gonad development and negatively influences reproductive function in both males and females. In this study, we assessed the effects of BPA on hormone production in Leydig cells, which secrete hormones in the testes and support male fertility. We examined two steroidogenic enzymes, CYP11A1 and CYP19 that involved in sex hormone synthesis in mouse MA-10 Leydig cells. We found that BPA activated CYP gene in both mRNA and protein levels then resulted in alteration of the normal sex hormone ratio. Furthermore, we found that BPA induced c-Jun phosphorylation and contributed to CYP gene expression. Similar results were observed in an animal study. In conclusion, BPA disrupts the hormone environment in testis via steroidogenic gene activation through the JNK/c-Jun signaling pathway.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Disruptores Endócrinos/farmacologia
Hormônios Esteroides Gonadais/metabolismo
Células Intersticiais do Testículo/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Fenóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Aromatase/genética
Aromatase/metabolismo
Feminino
Expressão Gênica
Hormônios Esteroides Gonadais/biossíntese
Masculino
Camundongos
Fosforilação
Proteínas Proto-Oncogênicas c-jun/metabolismo
RNA Mensageiro/metabolismo
Testículo/efeitos dos fármacos
Testículo/metabolismo
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Endocrine Disruptors); 0 (Gonadal Steroid Hormones); 0 (Phenols); 0 (Proto-Oncogene Proteins c-jun); 0 (RNA, Messenger); EC 1.14.14.1 (Aromatase); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


  10 / 6518 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28645613
[Au] Autor:Zhao Y; Li HX; Wang K; Yan BY; Li W
[Ad] Endereço:Reproductive Medical Center, Navy General Hospital, Beijing 100048, China.
[Ti] Título:Regulation of testicular steroidogenesis by Foxa3 via transcriptional modulation of ERα signaling in type 2 diabetes mellitus (T2DM).
[So] Source:Biochem Biophys Res Commun;490(3):786-793, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although both insulin and estrogen receptor α (ERα) are known to exert inhibitory effects on testicular steroidogenesis, it remains unknown whether these pathways regulate testosterone (T) production under certain pathological conditions [e.g., type 2 diabetes mellitus (T2DM)] in a coordinated manner. Here, we found that the expression of forkhead box protein A3 (Foxa3), an essential transcriptional regulator engaged in adipogenesis and energy metabolism, was significantly down-regulated in the Leydig cells (LCs) from T-deficient T2DM mice. Functionally, upon hCG stimulation, Foxa3 recruits to the Esr1 promoter and suppresses the transactivation of Esr1 gene. Disruption of this recruitment by T2DM-elicited hyperinsulinemia led to abnormal activation of ERα pathway, inhibited steroidogenic enzyme genes expression, and thus caused inadequate T production. Therapeutically, insulin-impaired and Foxa3 ablation-compromised steroidogenesis were effectively rescued by a pharmacological inhibitor of the ERα pathway. These findings reveal an obligatory coregulatory role of Foxa3 in the regulation of ERα expression and of the Foxa3/ERα cascade, at least in part, in the pathogenesis of androgen deficiency caused by T2DM.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Receptor alfa de Estrogênio/metabolismo
Fator 3-gama Nuclear de Hepatócito/metabolismo
Células Intersticiais do Testículo/metabolismo
Transdução de Sinais
Testosterona/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/patologia
Regulação para Baixo
Receptor alfa de Estrogênio/genética
Fator 3-gama Nuclear de Hepatócito/genética
Células Intersticiais do Testículo/patologia
Masculino
Camundongos Endogâmicos BALB C
Esteroides/metabolismo
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Foxa3 protein, mouse); 0 (Steroids); 135845-91-9 (Hepatocyte Nuclear Factor 3-gamma); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE



página 1 de 652 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