Topic
Steroid biosynthesis
About: Steroid biosynthesis is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 58977 citations.
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TL;DR: The literature that supports the connection between altered MI/DCI ratios and pathological steroidogenesis observed in PCOS women is reviewed, and the application of inositol-based treatment protocols in managing PCOS symptoms and improving the quality of patients’ life is discussed.
Abstract: The presence of abnormal ovarian ratios of myo-inositol (MI) to D-chiro-inositol (DCI) is a recurrent feature in PCOS. Available evidence suggests that MI and DCI may modulate steroid biosynthesis, likely in an opposite manner. Specifically, MI seems to induce estrogen production, while DCI has a role in the synthesis of androgens. Elevated insulin levels, generally associated with PCOS, alter the physiological MI/DCI ratio, increasing MI-to-DCI conversion through activation of a specific epimerase enzyme. DCI directly increases testosterone biosynthesis in thecal cells and reduces its conversion to estradiol by downregulating aromatase enzyme in granulosa cells. This manuscript reviews the literature that supports the connection between altered MI/DCI ratios and pathological steroidogenesis observed in PCOS women. Furthermore, it discusses the application of inositol-based treatment protocols in managing PCOS symptoms and improving the quality of patients' life.
21 citations
TL;DR: Results demonstrate that inhibition of PTP activity affected both StAR protein and mRNA synthesis and suggest that the activity of hormone-regulated PTPs is a requirement in the LH signaling cascade that results in the up-regulation of StARprotein and, subsequently, increased steroid synthesis.
Abstract: The LH signal transduction pathway features the activation of protein tyrosine phosphatases (PTPs) as one of the components of a cascade that includes other well characterized events such as cAMP-dependent protein kinase A (PKA) activation. Moreover, the action of PTPs is required to increase the rate-limiting step in steroid biosynthesis, namely the cAMP-regulated transfer of cholesterol to the inner mitochondrial membrane. Since both PKA activity and steroidogenic acute regulatory (StAR) protein induction are obligatory steps in this transfer of cholesterol, the present study was performed to investigate the role of PTPs in the regulation of PKA activity and StAR expression in response to LH/chorionic gonadotropin (CG) and 8Br-cAMP in MA-10 cells. While the exposure of MA-10 cells to the PTP inhibitor, phenylarsine oxide (PAO), did not modify PKA activity, it partially inhibited the effect of human CG and cAMP analog on StAR protein levels. Time-course studies demonstrated that PAO inhibited cAMP induction of StAR protein and mRNA. At 30 min, the effect on cAMP-stimulated StAR protein levels was a 35% inhibition, progressing to up to 90% inhibition at 120 min of stimulation. The maximal inhibitory effect on cAMP-induced StAR mRNA level was obtained at 60 min (85%). In summary, these results demonstrate that inhibition of PTP activity affected both StAR protein and mRNA synthesis and suggest that the activity of hormone-regulated PTPs is a requirement in the LH signaling cascade that results in the up-regulation of StAR protein and, subsequently, increased steroid synthesis.
21 citations
TL;DR: Endoplasmic reticulum stress related to glycosylation inhibition and damage to cell membrane integrity might contribute to the toxicity of DT against Foc TR4.
Abstract: Fusarium wilt of banana, a destructive disease that affects banana production, is caused by Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4). In a previous study, we confirmed the strong inhibitory effects of Chinese leek (Allium tuberosum) on the incidence of this disease. Sulfur compounds are the primary antifungal constituents of Chinese leek. Among these, dimethyl trisulfide (DT) was the most abundant and exhibited the strongest inhibition of Foc TR4 growth and development. In the present study, the global gene expression profiles of Foc TR4 isolates treated with DT at 4,000 folds dilution (concentration of 1/4,000, v/v) for 1.5, 6, and 12 h were investigated by using RNA sequencing. The expression patterns of 15 DEGs were validated based on quantitative real-time PCR (qRT-PCR) assay. Untreated sample presented 2,556, 1,691, and 1,150 differentially expressed genes (DEGs) at 1.5, 6, and 12 h after the onset of the experiment, respectively, whereas DT-treated isolates presented 2,823, 3,546, and 6,197 DEGs. Based on Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes enrichment analysis, DEGs involved in endoplasmic reticulum (ER), glycosylation, and steroid biosynthesis were significantly inhibited by DT exposure. The similar expressional patterns of 15 DEGs between RNA-seq and qRT-PCR assays indicated the reliability of the RNA-seq data. Thus, ER stress related to glycosylation inhibition and damage to cell membrane integrity might contribute to the toxicity of DT against Foc TR4. As the results presented here evidenced changes in gene expression associated with DT exposure, which might be used to develop new approaches for controlling FWB.
21 citations
Journal Article•
TL;DR: Nearly a decade's experience with prenatal treatment of CAH indicates that the risk-benefit ratio is favorable for mother and fetus with careful medical supervision of gestationally administered dexamethasone.
Abstract: Congenital adrenal hyperplasia (CAH) is a group of inherited disorders caused by enzyme deficiencies in steroid biosynthesis, which disrupt the conversion of cholesterol to cortisol. The most common form of CAH is 21-hydroxylase deficiency (21-OHD). In its severe form, 21-OHD causes prenatal virilization of external female genitalia. Through molecular genetic analysis of fetal DNA, defects in 21-OH synthesis can be diagnosed in utero. Genital ambiguity in females can be reduced or eliminated with prenatal dexamethasone treatment, which successfully suppresses fetal androgen production. Data from current, large cohort studies show that prenatal diagnosis and treatment are safe and effective.
21 citations
23 May 2002
TL;DR: Steroid Biosynthesis: Enzymology, Integration and Control, and Aromatase: Insights into the Roles of Estrogens Revealed by Natural and Targeted Mutations.
Abstract: Steroid Biosynthesis: Enzymology, Integration and Control. Sterol Biosynthesis. Vitamin D Biosynthesis and its Disorders. Bile Acid Biosynthesis. Cholesterol Metabolism in Steroidogenic Tissues. Steroid 21-Hydroxylase. Steroid 11ss-Hydroxylase Isozymes. 3ss-Hydroxysteroid Dehydrogenase/ Isomerase Deficiency. Human 17a-Hydroxylase/17, 20-Lyase. Aromatase: Insights into the Roles of Estrogens Revealed by Natural and Targeted Mutations. 17ss-Hydroxysteroid Dehydrogenase and 5a-Reductase Deficiencies. Steroid Metabolism in Peripheral Tissues. Animal Models of Impaired Steroidgenesis. Regulation of Gene Expression by the Nuclear Receptor Family. Neurosteroids and Brain Sterols.
21 citations