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[PMID]:27796263
[Au] Autor:Panzer K; Ekhaguere OA; Darbro B; Cook J; Shchelochkov OA
[Ti] Título:Uniparental Isodisomy of Chromosome 1 Unmasking an Autosomal Recessive 3-Beta Hydroxysteroid Dehydrogenase Type II-Related Congenital Adrenal Hyperplasia.
[So] Source:J Clin Res Pediatr Endocrinol;9(1):70-73, 2017 Mar 01.
[Is] ISSN:1308-5735
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:Steroid 3-beta hydroxysteroid dehydrogenase type II (3ß-HSD2) deficiency is a rare autosomal recessive form of congenital adrenal hyperplasia (CAH). We report the genetic basis of 3ß-HSD2 deficiency arising from uniparental isodisomy (UPD) of chromosome 1. We describe a term undervirilized male whose newborn screen indicated borderline CAH. The patient presented on the 7 day of life in salt-wasting adrenal crisis. Steroid hormone testing revealed a complex pattern suggestive of 3ß-HSD deficiency. Chromosomal microarray and single nucleotide polymorphism analysis revealed complete UPD of chromosome 1. Sanger sequencing of revealed a previously described missense mutation, c.424G>A (p.E142K) in homozygous state, thus confirming the diagnosis of 3ß-HSD2 deficiency. We provide evidence of the existence of an uncommon mechanism for gene-related CAH arising from UPD of chromosome 1.
[Mh] Termos MeSH primário: Hiperplasia Suprarrenal Congênita/genética
Cromossomos Humanos Par 1/genética
Genes Recessivos
Progesterona Redutase/genética
Dissomia Uniparental
[Mh] Termos MeSH secundário: Hiperplasia Suprarrenal Congênita/enzimologia
Análise Mutacional de DNA
Homozigoto
Seres Humanos
Hibridização in Situ Fluorescente
Recém-Nascido
Masculino
Mutação de Sentido Incorreto
Progesterona Redutase/deficiência
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.4274/jcrpe.3680


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[PMID]:27793677
[Au] Autor:Gomez-Sanchez CE; Qi X; Gomez-Sanchez EP; Sasano H; Bohlen MO; Wisgerhof M
[Ad] Endereço:Endocrinology Division, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS, United States; University of Mississippi Medical Center, Jackson, MS, United States. Electronic address: cgomez-sanchez@umc.edu.
[Ti] Título:Disordered zonal and cellular CYP11B2 enzyme expression in familial hyperaldosteronism type 3.
[So] Source:Mol Cell Endocrinol;439:74-80, 2017 Jan 05.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Three forms of familial primary aldosteronism have been recognized. Familial Hyperaldosteronism type 1 (FH1) or dexamethasone suppressible hyperaldosteronism, FH2, the most common form of as yet unknown cause(s), and FH3. FH3 is due to activating mutations of the potassium channel gene KCNJ5 that increase constitutive and angiotensin II-induced aldosterone synthesis. In this study we examined the cellular distribution of CYP11B2, CYP11B1, CYP17A1 and KCNJ5 in adrenals from two FH3 siblings using immunohistochemistry and immunofluorescence and obtained unexpected results. The adrenals were markedly enlarged with loss of zonation. CYP11B2 was expressed sporadically throughout the adrenal cortex. CYP11B2 was most often expressed by itself, relatively frequently with CYP17A1, and less frequently with CYP11B1. KCNJ5 was co-expressed with CYP11B2 and in some cells with CYP11B1. This aberrant co-expression of enzymes likely explains the abnormally high secretion rate of the hybrid steroid, 18-oxocortisol.
[Mh] Termos MeSH primário: Citocromo P-450 CYP11B2/metabolismo
Hiperaldosteronismo/enzimologia
Hiperaldosteronismo/patologia
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/enzimologia
Glândulas Suprarrenais/patologia
Criança
Pré-Escolar
Feminino
Imunofluorescência
Seres Humanos
Imuno-Histoquímica
Masculino
Progesterona Redutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase); EC 1.14.15.4 (Cytochrome P-450 CYP11B2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:27476613
[Au] Autor:Güven A; Polat S
[Ad] Endereço:Göztepe Training and Research Hospital, Clinic of Pediatric Endocrinology, Istanbul, Turkey E-mail: aylaguven@yahoo.com.
[Ti] Título:Testicular Adrenal Rest Tumor in Two Brothers with a Novel Mutation in the 3-Beta-Hydroxysteroid Dehydrogenase-2 Gene.
[So] Source:J Clin Res Pediatr Endocrinol;9(1):85-90, 2017 Mar 01.
[Is] ISSN:1308-5735
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:Testicular adrenal rest tumors (TART) occur frequently in adolescents and adults with 21-hydroxylase deficiency. There have been no reports of TART in children with 3ß-hydroxysteroid dehydrogenase deficiency (HSD3ß). Biopsy proven TART was diagnosed in a 3 -year-old male patient and also in his 22-month-old sibling. Hormonal and anthropometric measurements were performed during glucocorticoid and fludrocortisone treatment. The mutational analysis was performed by direct DNA sequencing of the complete coding region of the HSD3ß2 gene. Initially, both siblings were treated with high doses of hydrocortisone and fludrocortisone. TART regressed with dexamethasone treatment in both patients. However, growth velocity decreased and weight gain increased in both patients. Dexamethasone was changed to high-dose hydrocortisone (>20 mg/m /d). Sequencing analyses revealed a novel homozygous p.W355R (c.763 T>C) mutation at exon 4 of the HSD3ß2 gene in both siblings. These two patients are, to our knowledge, the first known cases of TARTs with a novel mutation in the HSD3ß2 gene detected during childhood. High-dose hydrocortisone treatment is more reliable for TART in children.
[Mh] Termos MeSH primário: Tumor de Resto Suprarrenal/genética
Mutação de Sentido Incorreto
Progesterona Redutase/genética
Irmãos
Neoplasias Testiculares/genética
[Mh] Termos MeSH secundário: Tumor de Resto Suprarrenal/diagnóstico
Tumor de Resto Suprarrenal/tratamento farmacológico
Sequência de Bases
Pré-Escolar
Análise Mutacional de DNA
Éxons/genética
Saúde da Família
Feminino
Homozigoto
Seres Humanos
Lactente
Masculino
Linhagem
Neoplasias Testiculares/diagnóstico
Neoplasias Testiculares/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160802
[St] Status:MEDLINE
[do] DOI:10.4274/jcrpe.3306


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[PMID]:27128796
[Au] Autor:Myat TS; Tetsuka M
[Ad] Endereço:Division of Animal Production, The United Graduate School of Agricultural Sciences, Iwate University, Morioka, Iwate, Japan.
[Ti] Título:Gossypol inhibits LH-induced steroidogenesis in bovine theca cells.
[So] Source:Anim Sci J;88(1):63-71, 2017 Jan.
[Is] ISSN:1740-0929
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Gossypol, a polyphenolic aldehyde found in cottonseed, has been shown to perturb steroidogenesis in granulosa and luteal cells of rats, pigs and cattle. However, little is known about the direct effect of gossypol on theca cell functions in any species. The present study was conducted to investigate the effect of gossypol on the steroidogenesis and the expression of genes involved in it in cultured bovine theca cells. Theca cells were isolated from healthy preovulatory follicles and were cultured in the presence of luteinizing hormone (LH) for up to 7 days. During the culture period, main steroid products of the theca cells shifted from androstenedione (A4) at day 1 to progesterone (P4) from day 2 onward. At days 1 and 7, theca cells were treated with gossypol (0-25 µg/mL) for 24 h. Gossypol inhibited LH-stimulated theca cell A4 and P4 production in a dose-dependent manner at both occasions. The viability of theca cells was not affected by gossypol at any doses used. Gossypol down-regulated expressions of steroidogenic enzymes CYP11A1, HSD3B1 and CYP17A1, but not that of LHR. These results indicate that gossypol inhibits thecal steroidogenesis through down-regulating gene expressions of steroidogenic enzymes but without affecting cell viability in cattle.
[Mh] Termos MeSH primário: Androstenodiona/biossíntese
Gossipol/farmacologia
Hormônio Luteinizante/farmacologia
Progesterona/biossíntese
Células Tecais/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Células Cultivadas
Enzima de Clivagem da Cadeia Lateral do Colesterol/genética
Enzima de Clivagem da Cadeia Lateral do Colesterol/metabolismo
Óleo de Sementes de Algodão
Relação Dose-Resposta a Droga
Regulação para Baixo/efeitos dos fármacos
Feminino
Expressão Gênica/efeitos dos fármacos
Complexos Multienzimáticos/genética
Complexos Multienzimáticos/metabolismo
Progesterona Redutase/genética
Progesterona Redutase/metabolismo
Esteroide 17-alfa-Hidroxilase/genética
Esteroide 17-alfa-Hidroxilase/metabolismo
Esteroide Isomerases/genética
Esteroide Isomerases/metabolismo
Células Tecais/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3 beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 0 (Cottonseed Oil); 0 (Multienzyme Complexes); 409J2J96VR (Androstenedione); 4G7DS2Q64Y (Progesterone); 9002-67-9 (Luteinizing Hormone); EC 1.1.1.145 (Progesterone Reductase); EC 1.14.14.19 (CYP17A1 protein, human); EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase); EC 1.14.15.6 (Cholesterol Side-Chain Cleavage Enzyme); EC 5.3.3.- (Steroid Isomerases); KAV15B369O (Gossypol)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170316
[Lr] Data última revisão:
170316
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160430
[St] Status:MEDLINE
[do] DOI:10.1111/asj.12596


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[PMID]:27832956
[Au] Autor:Sechman A; Batoryna M; Antos PA; Hrabia A
[Ad] Endereço:Department of Animal Physiology and Endocrinology, University of Agriculture in Krakow, Al. Mickiewicza 24/28, 30-059 Krakow, Poland. Electronic address: rzsechma@cyf-kr.edu.pl.
[Ti] Título:Effects of PCB 126 and PCB 153 on secretion of steroid hormones and mRNA expression of steroidogenic genes (STAR, HSD3B, CYP19A1) and estrogen receptors (ERα, ERß) in prehierarchical chicken ovarian follicles.
[So] Source:Toxicol Lett;264:29-37, 2016 Dec 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to assess the in vitro effects of dioxin-like PCB 126 and non-dioxin-like PCB 153 on basal and ovine LH (oLH)-stimulated testosterone (T) and estradiol (E2) secretion and expression of steroidogenic genes (STAR, HSD3B and CYP19A1) and estrogen receptors α (ERα) and ß (ERß) in white (WF) and yellowish (YF) prehierarchical follicles of the hen ovary. Steroid concentrations in a medium and gene expression in follicles following 6h of exposition were determined by RIA and real-time qPCR, respectively. Both PCBs increased basal and oLH-stimulated T secretion by the WF follicles. PCB 126 reduced basal E2 secretion by the WF follicles. PCB 153 elevated but PCB 126 reduced oLH-stimulated E2 secretion by the prehierarchical follicles. PCB 126 increased basal STAR and HSD3B and reduced CYP19A1 mRNA expression in these follicles. PCB 153 increased basal expression of STAR and HSD3B in YF follicles, but diminished HSD3B mRNA levels in the WF. The studied PCBs had an opposite effect on basal and oLH-stimulated CYP19A1 mRNA expression in prehierarchical follicles. Both PCBs modulated basal and inhibited oLH-stimulated ERα and ERß gene expression in the prehierarchical follicles. In conclusion, data of the current study demonstrate the congener-specific effects of PCBs on sex steroid secretion by prehierarchical follicles of the chicken ovary, which are at least partly related to STAR, HSD3B and CYP19A1 gene expression. It is suggested that PCBs, by influencing follicular steroidogenesis and expression of estrogen receptors, may impair development and selection of yellowish follicles to the preovulatory hierarchy.
[Mh] Termos MeSH primário: Galinhas
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Folículo Ovariano/metabolismo
Bifenilos Policlorados/toxicidade
RNA Mensageiro/genética
Esteroides/metabolismo
[Mh] Termos MeSH secundário: Animais
Aromatase/metabolismo
Receptor alfa de Estrogênio/biossíntese
Receptor beta de Estrogênio/biossíntese
Feminino
Fase Folicular/efeitos dos fármacos
Folículo Ovariano/efeitos dos fármacos
Folículo Ovariano/crescimento & desenvolvimento
Progesterona Redutase/metabolismo
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (RNA, Messenger); 0 (Steroids); 3XMK78S47O (Testosterone); DFC2HB4I0K (Polychlorinated Biphenyls); EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase); EC 1.14.14.1 (Aromatase); TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl); ZRU0C9E32O (2,4,5,2',4',5'-hexachlorobiphenyl)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170202
[Lr] Data última revisão:
170202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161112
[St] Status:MEDLINE


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[PMID]:27683264
[Au] Autor:Roche J; Ramé C; Reverchon M; Mellouk N; Cornuau M; Guerif F; Froment P; Dupont J
[Ad] Endereço:Unité de Physiologie de la Reproduction et des Comportements, Institut National de la Recherche Agronomique, Nouzilly, France.
[Ti] Título:Apelin (APLN) and Apelin Receptor (APLNR) in Human Ovary: Expression, Signaling, and Regulation of Steroidogenesis in Primary Human Luteinized Granulosa Cells.
[So] Source:Biol Reprod;95(5):104, 2016 Nov.
[Is] ISSN:1529-7268
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apelin (APLN) is a recently discovered adipokine involved in the regulation of various metabolic functions. Its receptor, APLNR, is expressed in reproductive tissues, however, its role in human ovarian cells is unknown. In this study, we identified APLN and APLNR in human ovarian follicles and analyzed their expression in granulosa cells and follicular fluid obtained from obese and nonobese patients, with or without polycystic ovary syndrome (PCOS). We also investigated the effect of APLN on steroidogenesis in cultured human luteinized granulosa cells (hGCs) from nonobese patients without PCOS. Using RT-PCR and immunoblotting, we found that APLN and APLNR were expressed in hGCs and cumulus and theca cells. We confirmed these data immunohistochemically and observed that APLNR and APLN are present in human oocytes at different stages of follicular development. In patients with PCOS, we observed that follicular fluid APLN concentration and granulosa cell APLN and APLNR mRNA expression was higher than that observed in control patients. In cultured hGCs from nonobese patients without PCOS, insulin-like growth factor 1 (IGF1) increased APLNR expression, and recombinant human APLN (APLN-13 and APLN-17) increased both basal and IGF1-induced steroid secretion. These effects on steroid production were reversed when cultured in the presence of ML221, an APLNR antagonist, which was associated with an increased 3beta-hydrosteroid dehydrogenase (HSD3B) protein concentration. We showed that these effects were dependent on the activation of the AKT and MAPK3/1 pathways using pharmacological inhibitors. Our results show that APLN and APLNR are present in human ovarian cells and APLN increases IGF1-induced steroidogenesis in granulosa cells through an increase in HSD3B protein expression and activation of the MAPK3/1 and Akt pathways. Therefore, APLN and APLNR may play a role in human follicular development and the pathogenesis of PCOS.
[Mh] Termos MeSH primário: Células da Granulosa/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Células Lúteas/metabolismo
Luteinização/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Apelina
Receptores de Apelina
Estradiol/metabolismo
Feminino
Células da Granulosa/efeitos dos fármacos
Seres Humanos
Fator de Crescimento Insulin-Like I/farmacologia
Células Lúteas/efeitos dos fármacos
Complexos Multienzimáticos/metabolismo
Síndrome do Ovário Policístico/metabolismo
Progesterona/metabolismo
Progesterona Redutase/metabolismo
Transdução de Sinais/efeitos dos fármacos
Esteroide Isomerases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3 beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 0 (APLN protein, human); 0 (APLNR protein, human); 0 (Apelin); 0 (Apelin Receptors); 0 (Intercellular Signaling Peptides and Proteins); 0 (Multienzyme Complexes); 0 (Receptors, G-Protein-Coupled); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); 67763-96-6 (Insulin-Like Growth Factor I); EC 1.1.1.145 (Progesterone Reductase); EC 5.3.3.- (Steroid Isomerases)
[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:160930
[St] Status:MEDLINE


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[PMID]:27623070
[Au] Autor:Rege J; Karashima S; Lerario AM; Smith JM; Auchus RJ; Kasa-Vubu JZ; Sasano H; Nakamura Y; White PC; Rainey WE
[Ad] Endereço:Department of Molecular and Integrative Physiology (J.R., S.K., W.E.R.), University of Michigan, Ann Arbor, Michigan 48109; Department of Internal Medicine (A.M.L., R.J.A.), University of Michigan, Ann Arbor, Michigan 48109; Division of Pediatric Endocrinology (J.M.S.), Specially for Children, Austi
[Ti] Título:Age-dependent Increases in Adrenal Cytochrome b5 and Serum 5-Androstenediol-3-sulfate.
[So] Source:J Clin Endocrinol Metab;101(12):4585-4593, 2016 Dec.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Adrenal production of dehydroepiandrosterone sulfate (DHEA-S) increases throughout childhood owing to expansion of the zona reticularis (ZR). ZR features cells with a steroidogenic phenotype distinct from that of the adjacent zona fasciculata, with higher expression of cytochrome b type A (CYB5A) and steroid sulfotransferase type 2A1 but decreased 3ß-hydroxysteroid dehydrogenase type 2 (HSD3B2). In addition to DHEA-S, three adrenal Δ5-steroid sulfates could provide additional tools to define adrenal maturation. OBJECTIVE: This study sought to simultaneously measure serum levels of four adrenal Δ5-steroid sulfates, pregnenolone sulfate (Preg-S), 17α-hydroxypregnenolone sulfate (17OHPreg-S), DHEA-S, and 5-androstenediol-3-sulfate (Adiol-S) as a function of age and relate their production to the age-dependent adrenal localization of CYB5A. PARTICIPANTS AND METHODS: Δ5-steroid sulfates were quantified by liquid chromatography-tandem mass spectrometry in sera from 247 normal children (129 males,118 females) age 1.5-18 y and 42 adults (20 males, 22 females). Immunofluorescence localized HSD3B2 and CYB5A in normal adrenal glands from subjects age 2-35 y. Finally, HAC15 adrenocortical cells were transduced with lentiviral short hairpin RNA to suppress CYB5A expression. RESULTS: Of the Δ5-steroid sulfates quantified, DHEA-S was most abundant. Adiol-S increased in parallel with DHEA-S. Steroid ratios (17OHPreg-S/DHEA-S) suggested increases in 17,20-lyase activity during childhood. Immunofluorescence analysis showed age-related increases in ZR CYB5A immunoreactivity. Furthermore, silencing CYB5A in HAC15 adrenocortical cells significantly reduced DHEA-S and Adiol-S production. CONCLUSION: Adiol-S shows a similar age-related increase to that of DHEA-S. This likely results from the childhood expansion of CYB5A-expressing ZR, which enhances 17,20-lyase activity and the production of DHEA-S and Adiol-S.
[Mh] Termos MeSH primário: 17-alfa-Hidroxipregnenolona/sangue
Androstenodiol/sangue
Citocromos b5/metabolismo
Sulfato de Desidroepiandrosterona/sangue
Desenvolvimento Humano/fisiologia
Pregnenolona/sangue
Progesterona Redutase/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Glândulas Suprarrenais
Adulto
Fatores Etários
Técnicas de Cultura de Células
Criança
Pré-Escolar
Feminino
Seres Humanos
Lactente
Masculino
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CYB5A protein, human); 04Y4D91RG0 (pregnenolone sulfate); 387-79-1 (17-alpha-Hydroxypregnenolone); 57B09Q7FJR (Dehydroepiandrosterone Sulfate); 73R90F7MQ8 (Pregnenolone); 9035-39-6 (Cytochromes b5); 95PS51EMXY (Androstenediol); EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE


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[PMID]:27575027
[Au] Autor:Hearn JWD; AbuAli G; Reichard CA; Reddy CA; Magi-Galluzzi C; Chang KH; Carlson R; Rangel L; Reagan K; Davis BJ; Karnes RJ; Kohli M; Tindall D; Klein EA; Sharifi N
[Ad] Endereço:Department of Radiation Oncology, Taussig Cancer Institute, Cleveland, OH, USA; Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.
[Ti] Título:HSD3B1 and resistance to androgen-deprivation therapy in prostate cancer: a retrospective, multicohort study.
[So] Source:Lancet Oncol;17(10):1435-1444, 2016 Oct.
[Is] ISSN:1474-5488
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: HSD3B1 (1245A>C) has been mechanistically linked to castration-resistant prostate cancer because it encodes an altered enzyme that augments dihydrotestosterone synthesis from non-gonadal precursors. We postulated that men inheriting the HSD3B1 (1245C) allele would exhibit resistance to androgen-deprivation therapy (ADT). METHODS: In this multicohort study, we determined HSD3B1 genotype retrospectively in men treated with ADT for post-prostatectomy biochemical failure and correlated genotype with long-term clinical outcomes. We used data and samples from prospectively maintained prostate cancer registries at the Cleveland Clinic (Cleveland, OH, USA; primary study cohort) and the Mayo Clinic (Rochester, MN, USA; post-prostatectomy and metastatic validation cohorts). In the post-prostatectomy cohorts, patients of any age were eligible if they underwent prostatectomy between Jan 1, 1996, and Dec 31, 2009 (at the Cleveland Clinic; primary cohort), or between Jan 1, 1987, and Dec 31, 2011 (at the Mayo Clinic; post-prostatectomy cohort) and were treated with ADT for biochemical failure or for non-metastatic clinical failure. In the metastatic validation cohort, patients of any age were eligible if they were enrolled at Mayo Clinic between Sept 1, 2009, and July 31, 2013, with metastatic castration-resistant prostate cancer. The primary endpoint was progression-free survival according to HSD3B1 genotype. We did prespecified multivariable analyses to assess the independent predictive value of HSD3B1 genotype on outcomes. FINDINGS: We included and genotyped 443 patients: 118 in the primary cohort (who underwent prostatectomy), 137 in the post-prostatectomy validation cohort, and 188 in the metastatic validation cohort. In the primary study cohort, median progression-free survival diminished as a function of the number of variant alleles inherited: 6·6 years (95% CI 3·8-not reached) in men with homozygous wild-type genotype, 4·1 years (3·0-5·5) in men with heterozygous variant genotype, and 2·5 years (0·7 to not reached) in men with homozygous variant genotype (p=0·011). Relative to the homozygous wild-type genotype, inheritance of two copies of the variant allele was predictive of decreased progression-free survival (hazard ratio [HR] 2·4 [95% CI 1·1-5·3], p=0·029), as was inheritance of one copy of the variant allele (HR 1·7 [1·0-2·9], p=0·041). Findings were similar for distant metastasis-free survival and overall survival. The effect of the HSD3B1 genotype was independently confirmed in the validation cohorts. INTERPRETATION: Inheritance of the HSD3B1 (1245C) allele that enhances dihydrotestosterone synthesis is associated with prostate cancer resistance to ADT. HSD3B1 could therefore potentially be a powerful genetic biomarker capable of distinguishing men who are a priori likely to fare favourably with ADT from those who harbour disease liable to behave more aggressively, and who therefore might warrant early escalated therapy. FUNDING: Prostate Cancer Foundation, National Institutes of Health, US Department of Defense, Howard Hughes Medical Institute, American Cancer Society, Conquer Cancer Foundation of the American Society of Clinical Oncology, Cleveland Clinic Research Programs Committee and Department of Radiation Oncology, Gail and Joseph Gassner Development Funds.
[Mh] Termos MeSH primário: Antagonistas de Androgênios/uso terapêutico
Complexos Multienzimáticos/genética
Progesterona Redutase/genética
Neoplasias da Próstata/tratamento farmacológico
Esteroide Isomerases/genética
[Mh] Termos MeSH secundário: Idoso
Estudos de Coortes
Genótipo
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Prostatectomia
Neoplasias da Próstata/genética
Neoplasias da Próstata/mortalidade
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3 beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 0 (Androgen Antagonists); 0 (Multienzyme Complexes); EC 1.1.1.145 (Progesterone Reductase); EC 5.3.3.- (Steroid Isomerases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


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[PMID]:27387444
[Au] Autor:Nakamura I; Kusakabe M; Swanson P; Young G
[Ad] Endereço:School of Aquatic and Fishery Sciences, University of Washington, Seattle, WA 98105, USA; Atmosphere and Ocean Research Institute, University of Tokyo, Chiba 277-8564, Japan.
[Ti] Título:Regulation of sex steroid production and mRNAs encoding gonadotropin receptors and steroidogenic proteins by gonadotropins, cyclic AMP and insulin-like growth factor-I in ovarian follicles of rainbow trout (Oncorhynchus mykiss) at two stages of vitellogenesis.
[So] Source:Comp Biochem Physiol A Mol Integr Physiol;201:132-140, 2016 Nov.
[Is] ISSN:1531-4332
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:At the completion of vitellogenesis, the steroid biosynthetic pathway in teleost ovarian follicles switches from estradiol-17ß (E2) to maturational progestin production, associated with decreased follicle stimulating hormone (Fsh) and increased luteinizing hormone (Lh) signaling. This study compared effects of gonadotropins, human insulin-like growth factor-I (IGF1), and cAMP/protein kinase A signaling (forskolin) on E2 production and levels of mRNAs encoding steroidogenic proteins and gonadotropin receptors using midvitellogenic (MV) and late/postvitellogenic (L/PV) ovarian follicles of rainbow trout. Fsh, Lh and forskolin, but not IGF1, increased testosterone and E2 production in MV and L/PV follicles. Fsh increased steroidogenic acute regulatory protein (star; MV), 3ß-hydroxysteroid dehydrogenase/Δ(5-4) isomerase (hsd3b; MV) and P450 aromatase (cyp19a1a; MV) transcript levels. Lh increased star mRNA levels (MV, L/PV) but reduced cyp19a1a transcripts in L/PV follicles. At both follicle stages, IGF1 reduced levels of hsd3b transcripts. In MV follicles, IGF1 decreased P450 side-chain cleavage enzyme (cyp11a1) transcripts but increased cyp19a1a transcripts. In MV follicles only, forskolin increased star and hsd3b transcripts. Forskolin reduced MV follicle cyp11a1 transcripts and reduced cyp19a1a transcripts in follicles at both stages. Fsh and Lh reduced fshr transcripts in L/PV follicles. Lh also reduced lhcgr transcripts (L/PV). IGF1 had no effect on gonadotropin receptor transcripts. Forskolin reduced MV follicle fshr transcript levels and reduced lhcgr transcripts in L/PV follicles. These results reveal hormone- and stage-specific transcriptional regulation of steroidogenic protein and gonadotropin receptor genes and suggest that the steroidogenic shift at the completion of vitellogenesis involves loss of stimulatory effects of Fsh and Igfs on cyp19a1a expression and inhibition of cyp19a1a transcription by Lh.
[Mh] Termos MeSH primário: Proteínas de Peixes/genética
Hormônios Esteroides Gonadais/biossíntese
Oncorhynchus mykiss/genética
Oncorhynchus mykiss/fisiologia
Receptores da Gonadotropina/genética
[Mh] Termos MeSH secundário: Animais
Aromatase/genética
Enzima de Clivagem da Cadeia Lateral do Colesterol/genética
Colforsina/farmacologia
AMP Cíclico/metabolismo
Estradiol/biossíntese
Feminino
Fator de Crescimento Insulin-Like I/metabolismo
Complexos Multienzimáticos/genética
Folículo Ovariano/efeitos dos fármacos
Folículo Ovariano/fisiologia
Fosfoproteínas/genética
Progesterona Redutase/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Esteroide Isomerases/genética
Testosterona/biossíntese
Vitelogênese/genética
Vitelogênese/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3 beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 0 (Fish Proteins); 0 (Gonadal Steroid Hormones); 0 (Multienzyme Complexes); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (Receptors, Gonadotropin); 0 (steroidogenic acute regulatory protein); 1F7A44V6OU (Colforsin); 3XMK78S47O (Testosterone); 4TI98Z838E (Estradiol); 67763-96-6 (Insulin-Like Growth Factor I); E0399OZS9N (Cyclic AMP); EC 1.1.1.145 (Progesterone Reductase); EC 1.14.14.1 (Aromatase); EC 1.14.15.6 (Cholesterol Side-Chain Cleavage Enzyme); EC 5.3.3.- (Steroid Isomerases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160709
[St] Status:MEDLINE


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[PMID]:27118251
[Au] Autor:Indran IR; Lee BH; Yong EL
[Ad] Endereço:Department of Obstetrics & Gynaecology, National University of Singapore, NUHS Tower Block, Level 12, 1E Kent Ridge Road, Singapore 119228, Singapore. Electronic address: phciri@nus.edu.sg.
[Ti] Título:Cellular and Animal Studies: Insights into Pathophysiology and Therapy of PCOS.
[So] Source:Best Pract Res Clin Obstet Gynaecol;37:12-24, 2016 Nov.
[Is] ISSN:1532-1932
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Basic science studies have advanced our understanding of the role of key enzymes in the steroidogenesis pathway and those that affect the pathophysiology of PCOS. Studies with ovarian theca cells taken from women with PCOS have demonstrated increased androgen production due to increased CYP17A1 and HSD3B2 enzyme activities. Furthermore, overexpression of DENND1A variant 2 in normal theca cells resulted in a PCOS phenotype with increased androgen production. Notably, cellular steroidogenesis models have facilitated the understanding of the mechanistic effects of pharmacotherapies, including insulin sensitizers (e.g., pioglitazone and metformin) used for the treatment of insulin resistance in PCOS, on androgen production. In addition, animal models of PCOS have provided a critical platform to study the effects of therapeutic agents in a manner closer to the physiological state. Indeed, recent breakthroughs have demonstrated that natural derivatives such as the dietary medium-chain fatty acid decanoic acid (DA) can restore estrous cyclicity and lower androgen levels in an animal model of PCOS, thus laying the platform for novel therapeutic developments in PCOS. This chapter reviews the current understanding on the pathways modulating androgen biosynthesis, and the cellular and animal models that form the basis for preclinical research in PCOS, and sets the stage for clinical research.
[Mh] Termos MeSH primário: Androgênios/biossíntese
Hiperandrogenismo/metabolismo
Síndrome do Ovário Policístico/metabolismo
Células Tecais/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Adaptadoras de Sinalização de Receptores de Domínio de Morte/metabolismo
Ácidos Decanoicos/uso terapêutico
Modelos Animais de Doenças
Feminino
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Seres Humanos
Hiperandrogenismo/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Técnicas In Vitro
Resistência à Insulina
Metformina/uso terapêutico
Síndrome do Ovário Policístico/tratamento farmacológico
Progesterona Redutase/metabolismo
Esteroide 17-alfa-Hidroxilase/metabolismo
Tiazolidinedionas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Androgens); 0 (DENND1A protein, human); 0 (Death Domain Receptor Signaling Adaptor Proteins); 0 (Decanoic Acids); 0 (Guanine Nucleotide Exchange Factors); 0 (Hypoglycemic Agents); 0 (Thiazolidinediones); 4G9EDB6V73 (decanoic acid); 9100L32L2N (Metformin); EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase); EC 1.14.14.19 (CYP17A1 protein, human); EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160428
[St] Status:MEDLINE



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