This review summarizes current knowledge on the mechanisms that control aromatase activity in the quail preoptic area, a brain region that plays a key role in the control of reproduction. Aromatase and aromatase mRNA synthesis in the preoptic area are enhanced by testosterone and its metabolite estradiol, but estradiol receptors of the alpha subtype are not regularly colocalized with aromatase. Estradiol receptors of the beta subtype are present in the preoptic area but it is not yet known whether these receptors are colocalized with aromatase. The regulation by estrogen of aromatase activity may be, in part, trans-synaptically mediated, in a manner that is reminiscent of the ways in which steroids control the activity of gonadotropic hormone releasing hormone neurons. Aromatase-immunoreactive neurons are surrounded by dense networks of vasotocin-immunoreactive and tyrosine hydroxylase-immunoreactive fibers and punctate structures. These inputs are in part steroid-sensitive and could therefore mediate the effects of steroids on aromatase activity. In vivo pharmacological experiments indicate that catecholaminergic depletions significantly affect aromatase activity presumably by modulating aromatase transcription. In addition, in vitro studies on brain homogenates or on preoptic-hypothalamic explants show that aromatase activity can be rapidly modulated by a variety of dopaminergic compounds. These effects do not appear to be mediated by the membrane dopamine receptors and could involve changes in the phosphorylation state of the enzyme. Together, these results provide converging evidence for a direct control of aromatase activity by catecholamines consistent with the anatomical data indicating the presence of a catecholaminergic innervation of aromatase cells. These dopamine-induced changes in aromatase activity are observed after several hours or days and presumably result from changes in aromatase transcription but rapid non-genomic controls have also been identified. The potential significance of these processes for the physiology of reproduction is critically evaluated.
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BMJ Case Rep
January 2025
Diabetes and Endocrinology, Children's Health Ireland at Crumlin, Dublin 12, Ireland.
A boy in mid-childhood presented with right-sided gynaecomastia, which was excised. He represented and, on review by endocrinology, Tanner staging showed stage 2 left-sided glandular breast tissue and some features of virilisation. His testicular volumes remained prepubertal (3 mL).
View Article and Find Full Text PDFJ Environ Manage
January 2025
Molecular and Cellular Endocrinology Laboratory, Department of Zoology, Visva-Bharati University, Santiniketan, 731235, India. Electronic address:
Nonylphenol (NP), a non-ionic surfactant and potent endocrine disruptor, is known for its environmental persistence, biotic accumulation potential and toxicity. Nonetheless, mechanisms underlying NP modulation of female fertility with potential impact on embryogenesis in the unexposed offspring remain elusive. This study investigates the effects and toxic mechanisms of maternal exposure to NP at varying concentrations (50 and 100 μg/L) on zebrafish (Danio rerio), specifically focusing on ovarian health, reproductive parameters, and early developmental potential in the F1 generation.
View Article and Find Full Text PDFCureus
December 2024
Internal Medicine and Family Medicine, Larkin Community Hospital Palm Springs Campus, Miami, USA.
The purpose of this review is to explore the relationship between weight loss (WL), specifically reductions in body mass index (BMI), and increases in testosterone levels. Obesity and excess body fat are linked to reduced testosterone levels, which can lead to metabolic dysfunctions, reduced libido, and diminished muscle mass. To attain this purpose, this review will summarize current evidence on how weight reduction interventions, including dietary changes, exercise, and bariatric surgery, affect testosterone production in overweight and obese individuals.
View Article and Find Full Text PDFMillions of women worldwide have breast cancer, a common and possibly fatal illness according to WHO Reports. A genetic mutation usually causes breast adenocarcinomas. Only 5-10% of cancers are induced by genetic mutations that develop with age, and the "wear and tear" of general life causes 85-90% of breast cancers.
View Article and Find Full Text PDFBreast
January 2025
Department of Medical Oncology, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.
Tamoxifen is an estrogen-receptor (ER) antagonist, used as adjuvant treatment of ER-positive breast cancer. It is converted by CYP2D6 into endoxifen, its most active metabolite. Patients with endoxifen plasma concentrations <16 nM face a higher risk of recurrence.
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