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Relevant bibliographies by topics / Steroidogenesis

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Academic literature on the topic 'Steroidogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 December 2024

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Journal articles on the topic "Steroidogenesis"

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Baronio, Ortolano, Menabò, Cassio, Baldazzi, Di Natale, Tonti, Vestrucci, and Balsamo. "46,XX DSD due to Androgen Excess in Monogenic Disorders of Steroidogenesis: Genetic, Biochemical, and Clinical Features." International Journal of Molecular Sciences 20, no. 18 (September 17, 2019): 4605. http://dx.doi.org/10.3390/ijms20184605.

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The term ‘differences of sex development’ (DSD) refers to a group of congenital conditions that are associated with atypical development of chromosomal, gonadal, or anatomical sex. Disorders of steroidogenesis comprise autosomal recessive conditions that affect adrenal and gonadal enzymes and are responsible for some conditions of 46,XX DSD where hyperandrogenism interferes with chromosomal and gonadal sex development. Congenital adrenal hyperplasias (CAHs) are disorders of steroidogenesis that mainly involve the adrenals (21-hydroxylase and 11-hydroxylase deficiencies) and sometimes the gonads (3-beta-hydroxysteroidodehydrogenase and P450-oxidoreductase); in contrast, aromatase deficiency mainly involves the steroidogenetic activity of the gonads. This review describes the main genetic, biochemical, and clinical features that apply to the abovementioned conditions. The activities of the steroidogenetic enzymes are modulated by post-translational modifications and cofactors, particularly electron-donating redox partners. The incidences of the rare forms of CAH vary with ethnicity and geography. The elucidation of the precise roles of these enzymes and cofactors has been significantly facilitated by the identification of the genetic bases of rare disorders of steroidogenesis. Understanding steroidogenesis is important to our comprehension of differences in sexual development and other processes that are related to human reproduction and fertility, particularly those that involve androgen excess as consequence of their impairment.

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Bouguen, Guillaume, Laurent Dubuquoy, Pierre Desreumaux, Thomas Brunner, and Benjamin Bertin. "Intestinal steroidogenesis." Steroids 103 (November 2015): 64–71. http://dx.doi.org/10.1016/j.steroids.2014.12.022.

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Tesic, Biljana, Dragana Samardzija Nenadov, Tamara Tomanic, Svetlana Fa Nedeljkovic, Stevan Milatovic, Bojana Stanic, Kristina Pogrmic-Majkic, and Nebojsa Andric. "DEHP Decreases Steroidogenesis through the cAMP and ERK1/2 Signaling Pathways in FSH-Stimulated Human Granulosa Cells." Cells 12, no. 3 (January 22, 2023): 398. http://dx.doi.org/10.3390/cells12030398.

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DEHP is an endocrine disruptor that interferes with the function of the female reproductive system. Several studies suggested that DEHP affects steroidogenesis in human and rodent granulosa cells (GC). Some studies have shown that DEHP can also affect the FSH-stimulated steroidogenesis in GC; however, the mechanism by which DEHP affects hormone-challenged steroidogenesis in human GC is not understood. Here, we analyzed the mechanism by which DEHP affects steroidogenesis in the primary culture of human cumulus granulosa cells (hCGC) stimulated with FSH. Cells were exposed to DEHP and FSH for 48 h, and steroidogenesis and the activation of cAMP and ERK1/2 were analyzed. The results show that DEHP decreases FSH-stimulated STAR and CYP19A1 expression, which is accompanied by a decrease in progesterone and estradiol production. DEHP lowers cAMP production and CREB phosphorylation in FSH but not cholera toxin- and forskolin-challenged hCGC. DEHP was not able to decrease steroidogenesis in cholera toxin- and forskolin-stimulated hCGC. Furthermore, DEHP decreases FSH-induced ERK1/2 phosphorylation. The addition of EGF rescued ERK1/2 phosphorylation in FSH- and DEHP-treated hCGC and prevented a decrease in steroidogenesis in the FSH- and DEHP-treated hCGC. These results suggest that DEHP inhibits the cAMP and ERK1/2 signaling pathways, leading to the inhibition of steroidogenesis in the FSH-stimulated hCGC.

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Whitehouse, B. J. "Benzodiazepines and steroidogenesis." Journal of Endocrinology 134, no. 1 (July 1992): 1–3. http://dx.doi.org/10.1677/joe.0.1340001.

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Bornstein, S. R., H. Rutkowski, and I. Vrezas. "Cytokines and steroidogenesis." Molecular and Cellular Endocrinology 215, no. 1-2 (February 2004): 135–41. http://dx.doi.org/10.1016/j.mce.2003.11.022.

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Miller, Walter L. "Steroidogenesis: Unanswered Questions." Trends in Endocrinology & Metabolism 28, no. 11 (November 2017): 771–93. http://dx.doi.org/10.1016/j.tem.2017.09.002.

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Biason-Lauber, A., M. Boscaro, F. Mantero, and G. Balercia. "Defects of steroidogenesis." Journal of Endocrinological Investigation 33, no. 10 (February 24, 2010): 756–66. http://dx.doi.org/10.1007/bf03346683.

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HUANG, BU‐MIIN, DOUGLAS M. STOCCO, and REID L. NORMAN. "The Cellular Mechanisms of Corticotropin‐Releasing Hormone (CRH)‐Stimulated Steroidogenesis in Mouse Leydig Cells Are Similar to Those for LH." Journal of Andrology 18, no. 5 (September 10, 1997): 528–34. http://dx.doi.org/10.1002/j.1939-4640.1997.tb01968.x.

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ABSTRACT: Previous reports have demonstrated that corticotropin‐releasing hormone (CRH) treatment of primary cultures of mouse Leydig cells and MA‐10 mouse Leydig tumor cells results in a dose‐dependent stimulation of steroidogenesis, probably by acting through the cAMP/protein kinase A second messenger pathway. Based on this observation, the mechanism of CRH‐stimulated steroidogenesis is now further investigated and compared to trophic hormone stimulation. Both cell types were treated with human chorionic gonadotropin (hCG) or CRH in the absence and presence of the following agents: the translation inhibitor cycloheximide, the transcription inhibitor actinomycin D, the protonophore carbonyl cyanide m‐chlorophenylhydrozone (mCCCP), which disrupts the mitochondrial electrochemical gradient or the phorbol ester, phorbol‐12‐myristate 13‐acetate (PMA), a stimulator of protein kinase C. Cortico‐releasing hormone‐stimulated steroidogenesis was completely blocked by cycloheximide in both cell types, indicating that CRH‐stimulated steroidogenesis in mouse Leydig cells requires ongoing protein synthesis. Actinomycin D had profound inhibitory effects on CRH‐stimulated steroidogenesis in MA‐10 cells, and this inhibition was greater than that seen in mouse primary Leydig cells. mCCCP severely inhibited CRH‐stimulated steroid production in both cell types, indicating that an electrochemical gradient across the inner mitochondrial membrane is required for CRH‐stimulated steroidogenesis. In addition, PMA inhibited hCG‐ and CRH‐stimulated steroidogenesis in MA‐10 cells and CRH‐stimulated steroidogenesis in primary Leydig cells, suggesting that activation of the protein kinase C pathway can influence protein kinase A stimulated steroidogenesis. Results of these studies suggest that the mouse Leydig cell steroidogenic response to CRH shares many similarities to that of the LH response.

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Choi, M. S. K., and B. A. Cooke. "Calmidazolium is a potent stimulator of steroidogenesis via mechanisms not involving cyclic AMP, calcium or protein synthesis." Biochemical Journal 281, no. 1 (January 1, 1992): 291–96. http://dx.doi.org/10.1042/bj2810291.

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This study reports an unexpected effect of calmidazolium on steroidogenesis. In contrast with previous work, which established that calmidazolium inhibits hormone-stimulated testosterone production in rat Leydig cells, the present study demonstrates that this compound is a potent stimulator of steroidogenesis when added by itself; this stimulation (approx. 10-fold in a 2 h incubation), was obtained over a narrow dose range (e.g.1-10 microM) in mouse and rat Leydig cells and in rat adrenocortical cells. The same concentrations of calmidazolium decreased basal cyclic AMP to undetectable levels in rat Leydig cells. Also, cyclic AMP stimulated with luteinizing hormone (LH), cholera toxin and forskolin was inhibited by calmidazolium (ED50 2 microM). In contrast with the actions of LH and cyclic AMP analogues on steroidogenesis, the effect of calmidazolium was not inhibited by removal of extracellular Ca2+, or by the addition of La3+ (a Ca(2+)-entry blocker), or the addition of cycloheximide (an inhibitor of protein translation). However, like dibutyryl cyclic AMP, calmidazolium-stimulated steroidogenesis was inhibited by aminoglutethimide, an inhibitor of cholesterol side-chain cleavage. Another calmodulin inhibitor, trifluoperazine, did not stimulate steroidogenesis. It is concluded that calmidazolium has a similar effect on steroidogenesis to LH, but by-passes the requirements for cyclic AMP, Ca2+, and protein synthesis. Calmidazolium is therefore a potentially important probe for elucidating the mechansims of control of steroidogenesis.

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de Mattos, Karine, Kenley Joule Pierre, and Jacques J. Tremblay. "Hormones and Signaling Pathways Involved in the Stimulation of Leydig Cell Steroidogenesis." Endocrines 4, no. 3 (August 1, 2023): 573–94. http://dx.doi.org/10.3390/endocrines4030041.

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Leydig cells, located in the testis interstitial space, are the primary source of testosterone in males. Testosterone plays critical roles in both reproductive and metabolic functions and therefore is essential for male health. Steroidogenesis must be properly regulated since dysregulated hormone production can lead to infertility and metabolic disorders. Leydig cell steroidogenesis relies on the coordinated interaction of various factors, such as hormones and signaling molecules. While luteinizing hormone (LH) is the main regulator of Leydig cell steroidogenesis, other molecules, including growth hormones (GH), prolactin, growth factors (insulin, IGF, FGF, EGF), and osteocalcin, have also been implicated in the stimulation of steroidogenesis. This review provides a comprehensive summary of the mechanisms and signaling pathways employed by LH and other molecules in the stimulation of Leydig cell steroidogenesis, providing valuable insights into the complex regulation of male reproductive and metabolic health.

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Dissertations / Theses on the topic "Steroidogenesis"

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Mannan, Md Abdul. "Steroidogenesis in the developing ovary." Thesis, Royal Veterinary College (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522681.

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Gyles, Shan Lindsey. "Intracellular signalling mechanisms in steroidogenesis." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269684.

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Barton, Louise Marie. "Polyunsaturated fatty acids and adrenal steroidogenesis." Thesis, Royal Veterinary College (University of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519549.

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Schuliga, Michael, and michael schuliga@deakin edu au. "Steroidogenesis in cultured mammalian glial cells." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20061207.154152.

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A protocol for culturing mammalian type 1 astrocytic cells, using female post-natal rat cerebral cortical tissue, was established and refined for use in steroidogenic metabolic studies incorporating progestin radioisotopes. Cultures were characterised for homogeneity using standard morphological and immunostaining techniques. Qualitative and quantitative studies were conducted to characterise the progesterone (P) metabolic pathways present in astrocytes in vitro. Of particular interest was the formation of the P metabolite, 5á-pregnan-3á-ol-20-one (THP). THP is a GABA(A) receptor agonist, believed to play a vital role in neural functioning and CNS homeostasis. One aim of this study was to observe any modulatory effects selected neuroactive ligands have on the conversion of P into THP, in an attempt to link astrocytic steroidogenesis with neuronal control. In qualitative studies, chromatographic procedures were used to establish the progestin profile of cerebral cortical astrocytes. Tritiated P, DHP (5á-pregnan-3,20-dione) and THP incurbates were preliminary fractionated by either normal phase (NP) or reverse phase (RP) high performance liquid chromatography (HPLC). The radiometabolites associated with each fraction were further chromatographed, before and/or after chemical derivatistation, by the aforemention HPLC procedures and thin layer chromatography (TLC). Steroid radiometabolites were tentatively identified by comparing their chromatographic mobility with authentic steroids. The identity of the main putative 5á-reduced P metabolities, DHP, THP and 5á-pregnan-3á,20á-diol (20áOH-THP) were further confirmed by isotopic dilution analysis. Their conclusive identification, along with the tentative identification of 20á-hydroxypreg-4-en-3-one (20áOH-P) and 20á-hydroxy-5á-pregnan-3-one (20áOH-DHP), verify the localisation of 5á-reductase, 3á-hydroxy steroif oxidoreductase (HSOR), and 20á-HSOR activity in the cultured astrocytes utilised in this study programme. Other minor metabolites detected were tentatively identified, including 5á-pregnan-3á,21-diol-20-one (THDoc), indicating the presence of 21-hydroxylase enzymatic activity. THDoc, like THP, is a GABA(A) receptor agonist. The chemical and physical characterisation of several yet unidentified progestin metabolites, associated with a highly polar RP HPLC fraction (designated RP peak 1*), indicate the presence of one or more extra hydroxylase enzymes. Quantitative analysis included a preliminary study. In this study, the percentage yields of radiometabolites formed in cultures incubated with increasing substrate concentrations of (3)H-P for 24 hours were determined. At the lower concentrations examined (ie 0.5 to 50nM), the metabolites associated with the polar RP HPLC fraction (RP peak 1*) collectively have the highest percentage yield. They are subsequently considered metabolic end products of degradative catabolic P pathways. The percentage yield of THP peaks in the medium concentration ranges (ie 5 to 500nM), whereas DHP remains fairly static at a low level with increasing concentration. Both DHP and THP are considered metabolic pathway intermediates. The percentage yield of 20áOH-THP continues to increase with increasing concentration over 5nM, superseding THP approaching the highest concentration examined (5000nM). This indicated the formation of 20áOH-THP does not occur entirely via THP. 20áOH-THP also possibly serves as the direct intermediate in the formation of the main radiometabolites associated with RP peak 1*. A time/yield study incorporating incubation times from one to 24 hours was also conducted. The full array of radiometabolites (individually or in groups) formed in astrocyte cultures incubated with 50nM tritiated P, DHP of THP, were assayed. Cultures were observed to rapidly convert any DHP into THP, showing astrocytic 3á-HSOR activity is very high. The study also showed 5á-reduction (ie the conversation of P into DHP) is the rate limiting reaction in the two step conversion of P into THP. 5á-Reduction also appears to be a rate limiting step in the formation of 20á-hydroxylated metabolites in astrocytes. Cultures incubated with the tritiated 5á-reduced pregnanes from one to four hours form greater quantities to 20á-hydroxylated radiometabolites compared to cultures incubated with (3)H-P. The time yield/studies also provided further evidence the unidentified polar radiometabolites associated with RP peak 1* are metabolic end products. For the P and DHP incubates, the collective formation of the aforementioned polar radiometabolites initially lags behind the formation of THP. As the formation of the latter begins to plateau with increasing time between four to 24 hours, the net yield of radiometabolites associated with RP peak 1* continues to rise. The time/yield studies also indicate 5á-reduction and perhaps 3á-hydroxylation are pre-requisite steps in the formation of the polar metabolites. Cultures incubated with the 5á-reduced progestins from one to four hours form higher yields of the radiometabolites associated with RP peak 1* compared to cultures incubated with P as substrate. The net yields of the radiometabolites associated with RP peak 1* for cultures incubated with THP were substantially higher compared to cultures incubated with DHP after equivalent times. The effect selected neuroligands have on the yield of radiometabolites formed by cultured astrocytes incubated with 50nM (3)H-P was also examined. Dibutyryl cyclic adenosine monophosphate (DBcAMP), not actually a neuroligand per se, but an analog of the intracellular secondary messenger cAMP, was also utilised in these studies. The inhibitory neurotransmitter ã-amino-nbutyric acid (GABA), DBcAMP and isoproterenol (a â-adrenergic receptor agonist) all quickly induce a transient but substantial increase in 20á-HSOR activity in cultured astrocytes. Cultures pretreated with these three compounds (10, 20 and 1µM respectively) form substantially higher yields of 20á-hydroxylated metabolites, including 20áOH-THP (between 200 to 580% greater), when incubated with 50nM (3)H-P for one to four hours. These increases also coincide with increases in the net yield of metabolites formed (by 16 to 48%). The same pre-treated cultures form significantly lower yields of THP, by 25 to 41%, after one hour. This is most likely due to the increased metabolism of any formed THP into 20áOH-THP. Octopamine (an á-adrenergic agonist) only induces a slight increase in 20á-HSOR activity, having relatively little effect on the yield of 20áOH-THP formed. Pretreatment with octopamine induces a significant increase in the yield of THP for cultures incubated with (3)H-P for four hours (by 24%). The increase in THP formation appears to be due to an increase in 3á-HSOR activity, as judged by the concomitant drop in the yield of the 5á-reduced, 3-keto substrates. An increase in 5á-reductase activity cannot be excluded however. Isoproterenol appears to induce an increase in 5á-reductase activity as isoproterenol appears to induce an increase in 5á-reductase activity as isoproterenol one and four hour incubates have higher yields of DHP. This is in contrast to the other three incubates. After 12 hours, all incubates have higher yields of THP (15-30%).

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Griffin, Aliesha. "The mitochondrial redox regulation of steroidogenesis." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5803/.

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Mitochondrial steroidogenic cytochrome P450 (CYP) enzymes rely on electron transfer from the redox partner ferredoxin for catalytic activity. Previous in vitro data suggests these co-factors are key regulators of CYP enzyme activity. However, this has never been studied in vivo. Zebrafish have emerged as model to study human steroidogenesis as they have conserved steroidogenic genes, molecular mechanisms and endocrine tissues. This project aimed to establish zebrafish as an in vivo model for endocrine development and its disorders, and to investigate the influence of mitochondrial redox regulation on steroid hormone production. This study involved the identification and characterisation of zebrafish mitochondrial steroidogenic CYP enzymes and their ferredoxin co-factors. Through implementation of recent genomic editing methods including Transcription Activator-Like Effector Nucleases (TALENs) and the Clustered Regulatory Interspaced Short Palindromic Repeat Cas9 nuclease (CRISPR/Cas9) system, and steroid hormone analysis from whole zebrafish extracts by liquid chromatography/tandem mass spectrometry, essential mitochondrial redox components required for zebrafish glucocorticoid production were identified. Overall, this work has helped established zebrafish as a model to study the pathophysiological consequences of steroid hormone disease and provided insights into the mechanism of mitochondrial redox regulation of steroid hormone production.

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Ramnath, Helen Indira. "The effect of chloride ions on steroidogenesis." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267284.

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Hazel, C. M. "Steroidogenesis in the female crab (Carcinus maenas)." Thesis, University of Liverpool, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372692.

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McIlmoil, Stephen. "Regulation of adrenal steroidogenesis by interleukin-6 /." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1976.pdf.

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Hess, Monna Fay. "Steroidogenesis in the equine testis throughout puberty /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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McIlmoil, Stephen A. "Regulation of Adrenal Steroidogenesis by Interleukin-6." BYU ScholarsArchive, 2007. https://scholarsarchive.byu.edu/etd/975.

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Cortisol and dehydroepiandrosterone (DHEA) are steroids produced by the zona fasciculata (ZF) and reticularis (ZR), respectively, of the adrenal cortex. Both steroids are upregulated in response to adrenocorticotropic hormone (ACTH). Cortisol is a glucorticoid that is important in the regulation of inflammation and metabolism. DHEA is an adrenal androgen important in fetal growth and puberty but tends to decrease gradually after puberty in both men and women. DHEA has various effects on metabolism and immune function including inhibiting the effects of cortisol on some tissues. During the acute phase of stress, cortisol and DHEA rise due to an increase in ACTH released from the anterior pituitary. In contrast, during chronic stress, cortisol remains elevated but DHEA and ACTH levels decrease. Likewise, stress causes serum levels of IL-6 to increase. IL-6 increases cortisol release from the human and bovine adrenal cortex. IL-6 also decreases DHEA release from zona reticularis of the bovine adrenal gland. In humans the effect of IL-6 on DHEA production is still uncertain. To determine a possible mechanism of IL-6 on the zona fasciculata and reticularis, human H294R cells and bovine adrenal tissue were incubated in serum free medium containing IL-6, at various concentrations and incubation intervals. At the end of the incubation interval, mRNA or protein was extracted from the cells or tissue. Standard PCR, real time PCR, and western blot assays were used to determine the effects of IL-6 on the enzymes involved in cortisol and DHEA synthesis, steroidogenic factor-1 (SF-1), steroidogenic acute regulatory protein (StAR), and dosage sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX-1). In human H295R cells and bovine zona fasciculata cells IL-6 caused an increase in SF-1, StAR, P450scc, 17α hydroxylase, 3β-hydroxysteroid dehydrogenase type 2 (3β HSD2), 21 hydroxylase, and 11β hydroxylase mRNA and protein. IL-6 caused DAX-1 mRNA and protein to decrease. These effects were manifest in a time dependent manner. Dose response treatments incubated for 60 min increased SF-1, StAR, P450scc, 17α hydroxylase, 3β HSD2, 21 hydroxylase, and 11β hydroxylase but there was not significant change between the different treatments of IL-6. The bovine zona reticularis stimulated with IL-6 showed a decrease in SF-1, StAR, P450scc, 17α hydroxylase, and 3β HSD2 with an increase in DAX-1 mRNA and protein. This response was manifest in a time dependent manner for both mRNA and protein, and the effect was dose-dependent for mRNA but not protein levels within the 60 min time period. These data provide a mechanism by which increased stress, physical or emotional, which increases IL-6 serum level, could increase cortisol and decrease DHEA. This would account for decreased immune function, increased blood pressure, and changes in metabolism.

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Books on the topic "Steroidogenesis"

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Rumsby, Gill, and Gary M. Woodward, eds. Disorders of Steroidogenesis. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-96364-8.

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Yamada Conference on Molecular Steroidogenesis (52nd 1999 Nara, Japan). Molecular steroidogenesis: Proceedings of the Yamada Conference LII on Molecular Steroidogenesis held on August 25-28, 1999, in Nara, Japan. Tokyo, Japan: Universal Academy Press, 2000.

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Berman, Ezra. Altered steroidogenesis in whole-ovary and adrenal culture in cycling rats. [Washington, D.C.?: Environmental Protection Agency, 1993.

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Klaus, Ruckpaul, and Rein Horst, eds. Molecular mechanisms of adrenal steroidogenesis and aspects of regulation and application. London: Taylor & Francis, 1990.

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Ryan, Jean. The effect of varying LH environments on the steroidogenesis in the ovary of patients undergoing in-vitro fertilisation treatment. [S.l: The Author], 1994.

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Horrocks, Peter M. The use of ACTH and steroid profiling in the investigation and management of patients with disorders of adrenocortical steroidogenesis. Birmingham: University of Birmingham., 1987.

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Test No. 456: H295R Steroidogenesis Assay. OECD, 2011. http://dx.doi.org/10.1787/9789264122642-en.

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Ruckpaul, Klaus. Frontiers in Biotransformation - Molecular Mechanisms of Adrenal Steroidogenesis and Aspects. Wiley & Sons, Incorporated, John, 1990.

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Rumsby, Gill, and Gary M. Woodward. Disorders of Steroidogenesis: Guide to Steroid Profiling and Biochemical Diagnosis. Springer, 2019.

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Rumsby, Gill, and Gary M. Woodward. Disorders of Steroidogenesis: Guide to Steroid Profiling and Biochemical Diagnosis. Springer, 2018.

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Book chapters on the topic "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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LaVoie, Holly A. "Luteal Steroidogenesis." In The Life Cycle of the Corpus Luteum, 37–55. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43238-0_3.

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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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Yamazaki, Takeshi, and Yasuhiro Ishihara. "Neurosteroids: Regional Steroidogenesis." In Fifty Years of Cytochrome P450 Research, 153–73. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54992-5_9.

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Woodward, Gary M., and Gill Rumsby. "Overview of Adrenal Physiology and Steroid Biochemistry." In Disorders of Steroidogenesis, 1–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_1.

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Rumsby, Gill. "17β-Hydroxysteroid Dehydrogenase Deficiency." In Disorders of Steroidogenesis, 103–10. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_10.

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Rumsby, Gill. "Steroid 5α-Reductase Deficiency." In Disorders of Steroidogenesis, 111–19. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_11.

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Woodward, Gary M. "11β-Hydroxysteroid Dehydrogenase Deficiency." In Disorders of Steroidogenesis, 121–28. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_12.

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Rumsby, Gill. "Steroid Sulphotransferase and Sulphatase Deficiency." In Disorders of Steroidogenesis, 129–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_13.

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Lam, Francis, and Oliver Clifford-Mobley. "Cholesterol Synthesis Defects." In Disorders of Steroidogenesis, 137–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96364-8_14.

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Conference papers on the topic "Steroidogenesis"

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Krainer, M., J. Sommer, D. Silbert-Wagner, S. Racedo, K. Panzitt, and M. Wagner. "Does the gut microbiome affect intestinal steroidogenesis?" In 52. Jahrestagung & 30. Fortbildungskurs der Österreichischen Gesellschaft für Gastroenterologie & Hepatologie (ÖGGH). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1691870.

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Bakhtyukov, Andrej, Kira Derkach, Lyubov' Bayunova, Inna Zorina, Vikas Roy, Alexej Gryaznov, and Alexander Shpakov. "THE PROCESSES OF STEROIDOGENESIS AND SPERMATOGENESIS IN MALE MICE WITH TYPE 1 DIABETES MELLITUS." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m939.sudak.ns2020-16/88.

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Chang, Kai-Hsiung, and Nima Sharifi. "Abstract 2115: Interrogation of mechanisms that underlie augmented steroidogenesis in castration-resistant prostate cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2115.

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Yenki, Parvin, Hans Adomat, Chi Wing Cheng, and Christopher Ong. "Abstract 1164: Semaphorin 3C promotes de novo steroidogenesis in androgen-deprived prostate cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1164.

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Moll, Jan Matthijs, Johannes Hofland, Wilma Teubel, Corrina M. A. de Ridder, Anne E. Taylor, Ralph Graeser, Wiebke Arlt, Guido W. Jenster, and Wytske M. van Weerden. "Abstract C97: Beyond intratumoural steroidogenesis: abiraterone resistance mediated by AR variants and glucocorticoid receptor signalling." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c97.

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Jacoby, Douglas, and Martin Williams. "Abstract 83: Differential inhibitory effects of galeterone, abiraterone, orteronel and ketoconazole on CYP17A1 and steroidogenesis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-83.

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Ning, Baitang, Dongying Li, Bridgett Knox, and Weida Tong. "Pharmacological Effects of Ketoconazole in the Treatment of Steroidogenesis Suppression via CYP17A1 Inhibition May Involve MicroRNA Regulation." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.218670.

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Bakhtyukov, Andrew, Ivan Lebedev, Kira Derkach, Viktor Sorokoumov, and Alexandr Shpakov. "Effect of metformin treatment on basal and stimulated by gonadotropin and allosteric luteinizing hormone receptor steroidogenesis in diabetic male rats." In II Международная конференция, посвящеенная 100- летию И.А. Држевецкой. СКФУ, 2022. http://dx.doi.org/10.38006/9612-62-6.2022.63.66.

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Lubik, Amy A., Hans Adomat, Emma S. Guns, and Ralph Buttyan. "Abstract 1632: Paracrine Hedgehog as a mediator of stromal cell steroidogenesis that contributes to progression of prostate cancer to castration resistant disease." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1632.

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Reports on the topic "Steroidogenesis"

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Solomon, Keith R., and Kristine Pelton. Disparities in Intratumoral Steroidogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada610224.

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Solomon, Keith R., and Kristine Pelton. Disparities in Intratumoral Steroidogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada586254.

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Shemesh, Mordechai, and William Hansel. Regulation of Steroidogenesis in the Bovine Plancenta. United States Department of Agriculture, April 1992. http://dx.doi.org/10.32747/1992.7599672.bard.

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Grasfeder, Linda. The Role of Estrogen-Related Receptor Alpha in Steroidogenesis in the Breast. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada505074.

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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587723.bard.

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Abstract:

Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.

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