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Relevant bibliographies by topics / Testicular steroidogenesis

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Academic literature on the topic 'Testicular steroidogenesis'

Author: Grafiati

Published: 19 February 2023

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Journal articles on the topic "Testicular steroidogenesis"

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Rommerts, F. F. G., K. Teerds, A. P. N. Themmen, and M. van Noort. "Multiple regulation of testicular steroidogenesis." Journal of Steroid Biochemistry 27, no. 1-3 (January 1987): 309–16. http://dx.doi.org/10.1016/0022-4731(87)90322-0.

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Sarawi, Wedad S., Ahlam M. Alhusaini, Laila M. Fadda, Hatun A. Alomar, Awatif B. Albaker, Hanan K. Alghibiwi, Amjad S. Aljrboa, Areej M. Alotaibi, Iman H. Hasan, and Ayman M. Mahmoud. "Nano-Curcumin Prevents Copper Reproductive Toxicity by Attenuating Oxidative Stress and Inflammation and Improving Nrf2/HO-1 Signaling and Pituitary-Gonadal Axis in Male Rats." Toxics 10, no. 7 (June 30, 2022): 356. http://dx.doi.org/10.3390/toxics10070356.

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Copper is essential for several cellular processes and is an important catalytic factor for many proteins. However, excess copper can provoke oxidative stress and reproductive toxicity. This study evaluated the effect of liposomal nano-curcumin (N-CUR) and CUR on testicular oxidative injury, inflammation, and apoptosis, and altered steroidogenesis and Nrf2/HO-1 signaling induced by copper sulfate (CuSO4). Rats received CuSO4 and N-CUR or CUR via oral gavage for 7 days. CuSO4 induced histopathological changes and altered pituitary-gonadal axis manifested by decreased serum gonadotropins and testosterone. Testicular steroidogenesis genes (StAR, 3β-HSD, CYP17A1, and 17β-HSD) and androgen receptor (AR) were downregulated in rats that received CuSO4. N-CUR and CUR prevented testicular tissue injury, increased circulating FSH, LH, and testosterone, and upregulated testicular steroidogenesis genes and AR. Additionally, N-CUR and CUR decreased testicular MDA, NO, NF-κB, iNOS, TNF-α, Bax, and caspase-3 while enhanced Bcl-2, Nrf2, and the antioxidants GSH, HO-1, SOD, and catalase. In conclusion, N-CUR and CUR prevented CuSO4-induced reproductive toxicity in male rats by suppressing oxidative injury and inflammatory response and boosting steroidogenesis, sex hormones, and Nrf2/HO-1 signaling. N-CUR was more effective in ameliorating tissue injury, oxidative stress, inflammation, and apoptosis and enhancing steroidogenesis and Nrf2/HO-1 than the native form.

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Bakhtyukov, Andrey A., Kira V. Derkach, Maxim A. Gureev, Dmitry V. Dar’in, Viktor N. Sorokoumov, Irina V. Romanova, Irina Yu Morina, Anna M. Stepochkina, and Alexander O. Shpakov. "Comparative Study of the Steroidogenic Effects of Human Chorionic Gonadotropin and Thieno[2,3-D]pyrimidine-Based Allosteric Agonist of Luteinizing Hormone Receptor in Young Adult, Aging and Diabetic Male Rats." International Journal of Molecular Sciences 21, no. 20 (October 11, 2020): 7493. http://dx.doi.org/10.3390/ijms21207493.

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Low-molecular-weight agonists of luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor (LHCGR), which interact with LHCGR transmembrane allosteric site and, in comparison with gonadotropins, more selectively activate intracellular effectors, are currently being developed. Meanwhile, their effects on testicular steroidogenesis have not been studied. The purpose of this work is to perform a comparative study of the effects of 5-amino-N-tert-butyl-4-(3-(1-methylpyrazole-4-carboxamido)phenyl)-2-(methylthio)thieno[2,3-d] pyrimidine-6-carboxamide (TP4/2), a LHCGR allosteric agonist developed by us, and hCG on adenylyl cyclase activity in rat testicular membranes, testosterone levels, testicular steroidogenesis and spermatogenesis in young (four-month-old), aging (18-month-old) and diabetic male Wistar rats. Type 1 diabetes was caused by a single streptozotocin (50 mg/kg) injection. TP4/2 (20 mg/kg/day) and hCG (20 IU/rat/day) were administered for 5 days. TP4/2 was less effective in adenylyl cyclase stimulation and ability to activate steroidogenesis when administered once into rats. On the 3rd–5th day, TP4/2 and hCG steroidogenic effects in young adult, aging and diabetic rats were comparable. Unlike hCG, TP4/2 did not inhibit LHCGR gene expression and did not hyperstimulate the testicular steroidogenesis system, moderately increasing steroidogenic proteins gene expression and testosterone production. In aging and diabetic testes, TP4/2 improved spermatogenesis. Thus, during five-day administration, TP4/2 steadily stimulates testicular steroidogenesis, and can be used to prevent androgen deficiency in aging and diabetes.

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Marak, Chuckles Ch, Brilliant N. Marak, Ved Prakash Singh, Guruswami Gurusubramanian, and Vikas Kumar Roy. "Effect of Cycas pectinata Seed Extract on Testicular Steroidogenesis in a Mouse Model." Andrologia 2023 (February 9, 2023): 1–15. http://dx.doi.org/10.1155/2023/5446928.

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The seed of Cycas pectinata is widely used in traditional practices in the Northeastern region of India for diverse purposes along with improving testicular functions. Thus, it may be hypothesized that the phytochemicals of C. pectinata seed could modulate testicular steroidogenesis. Therefore, we have investigated the effects of C. Pectinata seed extract (CPE) on testicular steroidogenesis by using in vivo and in vitro approaches. We have also performed the molecular docking of phytochemicals with some steroidogenic markers based on the identified phytochemicals from our previous study. The in vivo treatment of CPE increased the circulating estrogen and decreased circulating testosterone. The in vitro treatment of CPE also showed increased secretion of estrogen which can be suggested due to an increase in the aromatase (CYP19A1) activity. Our results also showed that the expression and localization of CYP19A1 were elevated by the CPE. The treatment of CPE also showed an accumulation of cholesterol in the testis, which could enhance testicular steroidogenesis. The other steroidogenic markers like 3βHSD, StAR, and LHR were upregulated by the CPE. Twelve compounds exhibited binding energy in the range of -10.0 to -8.0 kcal/mol with CYP19A1. Our data from in vitro, in vivo, and docking studies, showed that phytochemicals of CPE could modulate testicular steroidogenesis.

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Alam, Mohammad Shah, Seiichiroh Ohsako, Takashi Matsuwaki, Xiao Bo Zhu, Naoki Tsunekawa, Yoshiakira Kanai, Hideko Sone, Chiharu Tohyama, and Masamichi Kurohmaru. "Induction of spermatogenic cell apoptosis in prepubertal rat testes irrespective of testicular steroidogenesis: a possible estrogenic effect of di(n-butyl) phthalate." REPRODUCTION 139, no. 2 (February 2010): 427–37. http://dx.doi.org/10.1530/rep-09-0226.

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Although di(n-butyl) phthalate (DBP), a suspected endocrine disruptor, induces testicular atrophy in prepubertal male rats, whether it exerts estrogenic activity in vivo remains a matter of debate. In the present study, we explored the estrogenic potency of DBP using 3-week-old male rats, and then examined the relationship between estrogen-induced spermatogenic cell apoptosis and testicular steroidogenesis. Daily exposure to DBP for 7 days caused testicular atrophy due to loss of spermatogenic cells, whereas testicular steroidogenesis was almost the same with the control values. A single exposure of DBP decreased testicular steroidogenesis in addition to decreasing the level of serum LH at 3 h after DBP treatment, with an extremely high incidence of apoptotic spermatogenic cells at 6 h after administration. To elucidate the estrogenic activity of DBP, we carried out an inhibition study using pure antiestrogen ICI 182,780 (ICI) in a model of spermatogenic cell apoptosis induced by DBP or estradial-3-benzoate (EB). Although both the DBP- and EB-treated groups showed a significant increase in spermatogenic cell apoptosis, ICI pretreatment significantly decreased the number of apoptotic spermatogenic cells in these two groups. In contrast, testicular steroidogenesis and serum FSH were significantly reduced in all the treated groups, even in the DBP+ICI and EB+ICI groups. Taken together, these findings led us to conclude that estrogenic compounds such as DBP and EB induce spermatogenic cell apoptosis in prepubertal rats, probably by activating estrogen receptors in testis, and that reduction in testicular steroidogenic function induced by estrogenic compounds is not associated with spermatogenic cell apoptosis.

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Kostic, TS, SA Andric, D. Maric, SS Stojilkovic, and R. Kovacevic. "Involvement of inducible nitric oxide synthase in stress-impaired testicular steroidogenesis." Journal of Endocrinology 163, no. 3 (December 1, 1999): 409–16. http://dx.doi.org/10.1677/joe.0.1630409.

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The immobilization stress induces an acute inhibition of testicular steroidogenesis that is mediated by the nitric oxide (NO) signaling pathway. Here we compared the effects of 2-h immobilization stress on in vivo and in vitro rat steroidogenesis at two time points, 0 h and 6 h after the end of the stress session. As expected, serum androgens and human chorionic gonadotropin (hCG)-stimulated progesterone and testosterone production by testicular tissue were inhibited at 0 h, and also at the 6-h time point. Both the acute and sustained inhibitions of in vitro steroidogenesis were accompanied by a significant increase in nitrite, a stable oxidation product of NO. To clarify which subtype of NO synthase (NOS) (constitutive (cNOS) or inducible (iNOS)) participates in down-regulation of testicular steroidogenesis, aminoguanidine hydrochloride (AG), a selective iNOS inhibitor, was employed. Intratesticular injection of AG prevented the sustained, but not the acute, stress-induced decrease in serum testosterone. When added in vitro, it also prevented the sustained decrease in steroid production and increase in nitrite production by testicular tissue, both in a dose-dependent manner and with EC microM. Furthermore, AG added in vivo and in vitro effectively blocked the sustained decrease in 3beta-hydroxysteroid dehydrogenase (3betaHSD) and 17alpha-hydroxylase/C17-20 lyase (P450c17) activities. In all concentrations employed, AG did not affect serum androgens and in vitro steroid and nitrite production in unstressed animals. These results indicate that the NO signaling pathway participates in acute and sustained stress-induced down-regulation of testicular steroidogenesis, presumably through its direct action on 3betaHSD and P450c17. The acute NO production is controlled by cNOS and the sustained production of this messenger is controlled by iNOS.

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Rossato, M., G. Guarneri, T. Lavagnini, D. Padovan, and C. Foresta. "Simvastatin Influences Testicular Steroidogenesis in Human." Hormone and Metabolic Research 25, no. 09 (September 1993): 503–5. http://dx.doi.org/10.1055/s-2007-1002161.

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Kovačević, R., L. Krsmanović, S. Cupać, I. Simonović, S. Stojilković, D. Marić, and R. K. Andjus. "Effects of bromocriptine on testicular steroidogenesis." Journal of Steroid Biochemistry 25 (January 1986): 41. http://dx.doi.org/10.1016/0022-4731(86)90578-9.

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Ahmed, Mona M., Mohamed M. A. Hussein, Taisir Saber, and Yasmina M. Abd-Elhakim. "Palliative Effect of Resveratrol against Nanosized Iron Oxide-Induced Oxidative Stress and Steroidogenesis-Related Genes Dysregulation in Testicular Tissue of Adult Male Rats." International Journal of Environmental Research and Public Health 19, no. 13 (July 4, 2022): 8171. http://dx.doi.org/10.3390/ijerph19138171.

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The nano-sized iron oxide (Fe2O3-NPs) is one of the most used engineered nanomaterials worldwide. This study investigated the efficacy of natural polyphenol resveratrol (RSV) (20 mg/kg b.wt, orally once daily) to alleviate the impaired sperm quality and testicular injury resulting from Fe2O3-NPs exposure (3.5 or 7 mg/kg b.wt, intraperitoneally once a week) for eight weeks. Spermiograms, sexual hormonal levels, oxidative stress indicators, and lipid peroxidation biomarker were assessed. Moreover, the steroidogenesis-related genes mRNA expressions were evaluated. The results showed that RSV substantially rescued Fe2O3-NPs-mediated sperm defects. Additionally, the Fe2O3-NPs-induced depressing effects on sperm motility and viability were markedly counteracted by RSV. Moreover, RSV significantly restored Fe2O3-NPs-induced depletion of testosterone, follicle-stimulated hormone, luteinizing hormone, and testicular antioxidant enzymes but reduced malondialdehyde content. Furthermore, the Fe2O3-NPs-induced downregulation of steroidogenesis-related genes (3 β-HSD, 17 β-HSD, and Nr5A1) was significantly counteracted in the testicular tissue of RSV-treated rats. These findings concluded that RSV could limit the Fe2O3-NPs-induced reduced sperm quality and testicular injury most likely via their antioxidant activity and steroidogenesis-related gene expression modulation.

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Park, Eunsook, Yeawon Kim, Hyun Joo Lee, and Keesook Lee. "Differential Regulation Of Steroidogenic Enzyme Genes by TRα Signaling in Testicular Leydig Cells." Molecular Endocrinology 28, no. 6 (June 1, 2014): 822–33. http://dx.doi.org/10.1210/me.2013-1150.

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Abstract Thyroid hormone signaling has long been implicated in mammalian testicular function, affecting steroidogenesis in testicular Leydig cells. However, its molecular mechanism is not well understood. Here, we investigated the molecular action of thyroid hormone receptor-α (TRα) on mouse testicular steroidogenesis. TRα/thyroid hormone (T3) signaling differentially affected the expression of steroidogenic enzyme genes, mainly regulating their promoter activity. TRα directly regulated the promoter activity of the cytochrome P450 17α-hydroxylase/C17–20 lyase gene, elevating its expression in the presence of T3. TRα also indirectly regulated the expression of steroidogenic enzyme genes, such as steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase, by modulating the transactivation of Nur77 on steroidogenic enzyme gene promoters through protein-protein interaction. TRα enhanced Nur77 transactivation by excluding histone deacetylases from Nur77 in the absence of T3, whereas liganded TRα inhibited Nur77 transactivation, likely due to interfering with the recruitment of coactivator such as the steroid receptor coactivator-1 to Nur77. Together, these findings suggest a role of TRα/T3 in testicular steroidogenesis and may provide molecular mechanisms for the differential regulation of steroidogenic enzyme genes by thyroid hormone.

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Dissertations / Theses on the topic "Testicular steroidogenesis"

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Gunnarsson, David. "Reproductive toxicology of endocrine disruptors : effects of cadmium, phthalates and phytoestrogens on testicular steroidogenesis." Doctoral thesis, Umeå : Department of Molecular Biology, Umeå University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1876.

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Romano, Renata Marino. "Efeitos da exposição pré-púbere ao herbicida glifosato no desenvolvimento reprodutivo de ratos Wistar machos." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/10/10131/tde-14032008-113544/.

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O glifosato-Roundup é um herbicida amplamente utilizado em diversas culturas agrícolas. Sua toxicidade reprodutiva está relacionada com a inibição da proteína StAR e da enzima aromatase, causando in vitro redução significativa da produção de testosterona e estradiol. Este trabalho teve como objetivo verificar esse efeito in vivo, utilizando-se ratos Wistar machos pré-púberes como modelo experimental. Utilizou-se 68 machos tratados dos 23 aos 53 dias de idade com as doses de 0, 5, 50 e 250 mg/kg de peso vivo por gavagem uma vez ao dia. Foram avaliados a progressão da puberdade, o desenvolvimento corporal, a produção hormonal de testosterona, estradiol e corticosterona, morfologia testicular e da glândula adrenal, função renal e hepática e histopatologia renal e hepática. As análises estatísticas utilizadas foram a análise de variâncias de uma via ANOVA, de duas vias MANOVA ou Kruskall-Walis e pós-testes de Tukey-Kramer, Fisher ou de Dun. O herbicida glyphosate-Roundup alterou de forma significativa a progressão da puberdade de forma dose dependente, bem como se observou a redução na produção de testosterona e alterações na morfologia dos túbulos seminíferos. A morfologia da glândula adrenal e a produção de corticosterona não foram afetadas pelas doses utilizadas nesse estudo. Observou-se comprometimento da função renal e alterações patológicas nesse órgão. Não foram evidenciadas alterações hepáticas. O crescimento corporal dos animais não foi influenciado pelo tratamento. Pode-se concluir que esse herbicida é um potente disruptor endócrino in vivo, causando distúrbios no desenvolvimento reprodutivo e na produção hormonal dos animais.
The glyphosate-Roundup is a widely pesticide used in several culturas agrícolas. Its reproductive toxicity is associated to inhibition of StAR protein and aromatase enzime that cause in vitro significantly reduction in testosterone and estradiol production. The objective of this study was to evaluate the in vivo effects of inhibition of StAR protein and aromatase enzyme, using prepubertal male Wistar rats like experimental model. 68 animals were exposed once a day by gavage to glyphosate-Roundup in following doses: 0, 5, 50 or 250 mg/kg of body weight. The end points were puberty progression, body development, testosterone, estradiol and corticosterona productions and testicular and adrenal morphology, renal and liver function and histopatology. The statistical analysis used were one-way ANOVA, multi-way ANOVA or Kruskall-Walis and posthoc tests of Tukey-Kramer, Fisher or Dun. The herbicide glyphosate-Roundup changed significantly the puberty progression in dose-dependent manner, as well reduction in testosterone production and alterations in testicular morphology. There were not observed alterations in adrenal morphology or corticosterone production in the doses used in this study. The renal function and histopatology were altered in treated groups while liver function wasn\'t. The body development was not influenced by the exposure. In conclusion, glyphosate-Roundup is a potent endocrine disruptor in vivo that cause problems in reproductive development and hormonal synthesis in exposure animals.

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Sinclair, Philip Alexander. "Testicular steroidogenesis in the neonatal intact male pig and its relationship to the development of boar taint." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/MQ55714.pdf.

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Feek, Colin Michael. "Adrenal → gonad interactions in the male rat : studies on the influence of the adrenal gland on testicular steroidogenesis." Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/18875.

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Muller, Ashley George. "The effects of nanomaterials, in the presence and absence of serum proteins, on testicular cell metabolic processes and steroidogenesis." Thesis, University of the Western Cape, 2014. http://hdl.handle.net/11394/4143.

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Magister Scientiae (Medical Bioscience) - MSc(MBS)
The aim of this study is to be the first to ascertain the effects of silver nanoparticles on testosterone production. The Ag NPs used for this study have the following characteristics; purity ≥ 99.5%; 66.7 % of particles have a diameter between 20-40 nm in aqueous solution. Three month old male Balb/C mice were sacrificed and testicular cell cultures were prepared. The cells were subsequently treated with various concentrations of Ag NPs (with or without luteinizing hormone (LH)-treatment) and incubated for 4 hours. Testosterone secretion in the culture supernantant was then determined using a testosterone ELISA kit. Ag NPs (at 20 μg/ml) significantly (p < 0.001) decreased LH-stimulated testosterone production as compared to the control. This study showed that Ag NPs adversely affect testosterone synthesis in vitro and can therefore pose a risk for male reproduction.

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ARGYRIOU, ANASTASSIOS. "Etude de la steroidogenese dans le testicule de l'homme jeune." Paris 6, 1988. http://www.theses.fr/1988PA066026.

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TAHRI-JOUTEI, ABDERRAFIH. "Hormones neurohypophysaires et fonction testiculaire : controle de la steroidogenese leydigienne par l'arginine vasopressine." Paris 6, 1989. http://www.theses.fr/1989PA066477.

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In vitro, l'arginine vasopressine (avp) module directement et de facon dose-dependante la stereoidogenese des cellules de leydig de souris. Cette action se traduit, selon les conditions experimentales, par un double effet stimulateur ou inhibiteur sur la production de testosterones. L'effet de l'avp est dependant d'une synthese proteique. La stimulation de la production de testosterone resulte de l'activation d'une etape enzymatique precedant la formation de la progesterone, alors que la diminution de la production de testosterone stimulee par hcg est associee a une reduction des activites enzymatiques 17 alpha-hydroxylase/17,20-lyase, sans modification apparente de la formation d'amp cyclique. Les etudes de la liaison de l'avp-#3h a la cellule de leydig revelent l'existence d'une seule classe de sites du sous-type v#1 de forte affinite (k#d de l'ordre du nanomolaire) et de faible capacite (9600 sites/cellule). La regulation de la capacite androgenique de la cellule de leydig par l'avp est sous l'influence d'un controle hormonal qui depend sans doute, a la fois de l'etat de la maturation de la gonade et de son etat fonctionnel

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MARIE, ERIC-MONVIEU. "Steroidogenese testiculaire et spermatogenese chez l'homme jeune : apports au diagnostic de la fertilite." Caen, 1994. http://www.theses.fr/1994CAEN2012.

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Les gonadotropines (lh, fsh) et la testosterone conditionnent la maturation des cellules germinales et le maintien de la spermatogenese chez les mammiferes. L'objectif de notre travail a ete de rechercher l'existence eventuelle de correlations entre le taux de testosterone intratesticulaire et ceux d'autres steroides, avec l'aspect de la biopsie (analyse histologique semi-quantitative) et les taux hormonaux seriques chez l'homme sain (patients en etat de mort cerebrale) et infertile (patients consultants pour infertilite excretoire ou secretoire). Les parametres seriques ne sont pas differents; par contre, les taux de testosterone et d'estradiol intratesticulaires sont plus eleves chez les sujets infertiles que chez les sujets en coma depasse. Si la testosterone a un role reel dans la spermatogenese, la pregnenolone et l'estradiol semblent importants. Chez les sujets infertiles, les taux eleves de testosterone tissulaire pourraient etre lies a un emballement de la fonction steroidogene en relation avec une dominance de la voie des steroides en delta 4 qui conduirait a une elevation de l'estradiol susceptible d'inhiber la spermatogenese

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Martinot, Emmanuelle. "Etude du rôle du récepteur nucléaire FXRα dans la physiologie et la physiopathologie testiculaire." Thesis, Clermont-Ferrand 2, 2015. http://www.theses.fr/2015CLF22644/document.

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Fxrα est le récepteur nucléaire des acides biliaires, exprimé majoritairement dans le foie, l'intestin, les reins et les glandes surrénales. L'intérêt pour ce dernier est devenu croissant au cours des dernières années, de part le rôle central qu'il joue dans le contrôle de l'homéostasie du cholestérol, des acides biliaires, des triglycérides ou encore du glucose. Plus récemment, Fxrα ainsi que ses ligands, les acides biliaires, ont été localisés dans le testicule, soulevant la question du rôle potentiel de Fxrα dans cet organe, et plus généralement dans la fonction de reproduction mâle. Mais les études menées à ce sujet restent jusqu'à présent peu nombreuses, et focalisées sur son implication dans le contrôle du métabolisme des stéroïdes : l'activation in vivo de Fxrα par un agoniste synthétique conduit ainsi chez l'adulte à court terme à une répression de la stéroïdogenèse. Outre son rôle dans le contrôle de l'activité endocrine des cellules de Leydig, l'impact de l'activation in vivo de Fxrα sur la physiologie plus globale du testicule n'a jamais été abordé à ce jour. De telles études seraient pourtant pertinentes étant donné que Fxrα est ciblé pour le traitement de pathologies métaboliques telles que la dyslipidémie ou le diabète. Dans ce contexte, l'objectif de ce travail de thèse était d'étudier le rôle de Fxrα dans la physiologie et la pathophysiologie du testicule, en s'appuyant sur l'analyse d'un modèle murin dont le gène codant Fxrα a été invalidé. Nos résultats démontrent que : 1) la perte de Fxrα prédispose le testicule à une sur-mortalité des cellules germinales dans un contexte pathologique de cholestase ; 2) la sur-activation de la signalisation Fxrα au cours de la puberté conduit à un défaut de la différenciation germinale, associée à une altération de la fonction endocrine du testicule ; 3) outre la régulation de la stéroïdogenèse dans les cellules de Leydig, Fxrα participe au contrôle des fonctions sertoliennes et de la prolifération et / ou différenciation des cellules germinales souches. L'ensemble de ces données définissent Fxrα comme un nouvel acteur impliqué dans le contrôle de la physiologie testiculaire et devraient être prises en considération quant-à l'utilisation de molécules agonistes et / ou antagonistes de Fxrα dans le cadre du traitement de pathologies métaboliques
Fxrα is the bile acid nuclear receptor, predominantly expressed in liver, intestine, kidney and adrenal glands. In recent years, interest in Fxrα has been increasing due to its central role in the control of cholesterol, bile acids, triglycerides or glucose homeostasis. More recently, Fxrα and its ligands, bile acids, have been detected in the testis pointing out its potential involvement in this tissue and more widely in the male reproductive functions. However, the few studies on this topic focused essentially on Fxrα involvement in the control of steroids metabolism. Indeed, activation of Fxrα in vivo with a synthetic agonist leads to short-term steroidogenesis repression in the adult. In vivo the impact of alteration of Fxrα signaling on the global testis physiology has never been explored so far. Such studies would be pertinent considering that Fxrα is a target for the treatment of metabolic diseases such as dyslipidemia or diabetes. In this context, the aim of my work was to study the implication of Fxrα in testis physiology and physiopathology by analyzing a knock out mouse model for Fxrα. Our results show that: 1) the loss of Fxrα increase germ cell mortality in the testis in a disease context of cholestasis ; 2) over-activation of Fxrα signaling during puberty leads to germ cell differentiation defects, associated with an alteration of testis endocrine function ; 3) besides steroidogenesis control in Leydig cell, Fxrα is involved in Sertoli cell functions and spermatogonial stem cell proliferation and/or differentiation. Taken together, these data define Fxrα as a new actor involved in the control of testis physiology, and should be taken into consideration regarding the use of Fxrα agonistic or antagonistic ligands for the treatment of metabolic diseases

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Habert, René. "Activité androgène du testicule chez le fœtus de rat in vivo et sa régulation." Paris 7, 1986. http://www.theses.fr/1986PA077086.

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Recherche chez le fœtus de rat de l'existence et de l'origine des hormones gonadotropes circulantes et détermination du rôle de ces hormones dans le contrôle de la production testiculaire de testostérone. Mise au point d'un dosage biologique pour l'évaluation de l'activité gonadotrope totale circulante. Étude du rôle de l'hypophyse: évaluation des effets de la décapitation fœtale sur les différents niveaux de l'axe hypophyse. Testicule-tractus génital puis mesure de la réponse du testicule a la stimulation par des gonadotrophines exogenes. Etude de l'action en retour du testicule sur l'axe hypothalamo-hypophysaire. Étude de l'influence des facteurs extrahypophysaires (gonadotrophine placentaire-progestérone)

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Book chapters on the topic "Testicular steroidogenesis"

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Flück, Christa E., and Amit V. Pandey. "Testicular Steroidogenesis." In Endocrinology, 343–71. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44441-3_10.

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Flück, Christa E., and Amit V. Pandey. "Testicular Steroidogenesis." In Endocrinology, 1–29. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-29456-8_10-1.

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Stocco, D. M. "Steroidogenic Acute Regulatory Protein and Steroidogenesis." In Testicular Function: From Gene Expression to Genetic Manipulation, 179–211. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03671-6_10.

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Huhtaniemi, Ilpo, and Jorma Toppari. "Endocrine, Paracrine and Autocrine Regulation of Testicular Steroidogenesis." In Advances in Experimental Medicine and Biology, 33–54. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-0952-7_3.

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Stocco, Douglas M., Barbara J. Clark, Dong Lin, Teruo Sugawara, Jerome F. Strauss, and Walter L. Miller. "Characterization of the Protein Responsible for the Acute Regulation of Steroidogenesis in Mouse Leydig Tumor Cells." In Cellular and Molecular Regulation of Testicular Cells, 311–36. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2374-0_21.

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Liu, Hong, Shumei Lin, Qiufeng Lv, Qunhui Yang, Gaofeng Wu, Jianmin Hu, and Jiancheng Yang. "Taurine Recovers Testicular Steroidogenesis and Spermatogenesis in Streptozotocin-Induced Diabetic Rats." In Advances in Experimental Medicine and Biology, 801–11. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_62.

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Amador, A. G., A. Bartke, and R. W. Steger. "Direct Effects of Hormones of the Hypothalamic-Pituitary-Thyroid Axis on Testicular Steroidogenesis in Hamsters." In Advances in Experimental Medicine and Biology, 613–16. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5395-9_30.

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STOCCO, D., and M. MCPHAUL. "Physiology of Testicular Steroidogenesis." In Knobil and Neill's Physiology of Reproduction, 977–1016. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012515400-0/50025-7.

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Kim, Y., and K. Lee. "The Effect of Thyroid Hormone Signaling on Testicular Steroidogenesis." In Posters I, P2–10—P2–10. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p1.p2-10.

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Hughes, I. A. "Congenital adrenal hyperplasia." In Oxford Textbook of Medicine, 1891–900. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.130702_update_001.

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Abstract:

Congenital adrenal hyperplasia (CAH) results from enzymatic defects in the pathways of adrenal steroidogenesis, with over 90% of cases being due to 21-hydroxylase deficiency caused by autosomal recessive mutations in the CYP21 gene. Classical presentation—this is in the neonatal period with ambiguous genitalia/virilization of a female infant, with phenotype traditionally subdivided according to the presence (75%) or absence of salt wasting, which in affected males is the sole manifestation (and can, if unrecognized, be life-threatening). Delayed presentations can occur, manifest in women as hirsutism, oligomenorrhoea, and infertility and in men as infertility or testicular adrenal rest tumours....

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