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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Estrogens are a family of steroid hormones that are primarily produced and secreted in the ovaries; however, other tissues including the placenta, adrenal cortex, liver, skeletal muscle, and particularly fat can also form estrogens. Small amounts of estrogens are also produced in the testes (29, 148). The primary mechanism of action of estrogens is through gene derepression. Estrogens are formed as a result of the aromatization of the A ring of either androstenedione or testosterone, a reaction catalyzed by the enzyme aromatase. The primary estrogens are estrone, estriol, and estradiol (E2), which has the greatest estrogenic activity.
Hormone Receptors and Endocrine Therapy in Breast Cancer
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Sherry X. Yang, Nancy E. Davidson
Currently, major ER-targeted endocrine strategies include the use of SERMs, aromatase inhibitors (AIs), selective ER down-regulators (SERDs) and luteinizing hormone releasing hormone (LHRH) agonists. SERMs such as tamoxifen directly bind to ER and thus block estrogen from binding to and preventing alteration of the receptor conformation. This results in preferential recruitment of the corepressor proteins rather than the coactivator complex, and, therefore, inhibits the estrogen-stimulated tumor growth [34]. AIs reduce the production of estrogen by blocking the aromatization of androstenedione and testosterone—estrogen precursors in peripheral tissues [35]. SERDs that bind to ER with high affinity are pure anti-estrogen with no agonist effects, leading to partial down-regulation and degradation of the receptor [36–38]. LHRH agonists suppress ovarian production of estrogen in premenopausal women [39, 40]. The FDA-approved ER-targeted drugs for the treatment of breast cancer are listed in Table 5.1.
Adrenal in the adult male
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
Corticosteroids and sex steroids are both vital for mankind: corticosteroids for our survival as individuals and sex steroids for our survival as a species. De novo synthesis of steroid hormones in non-pregnant individuals only occurs in the adrenal cortex and in the gonads. The adrenal cortex secretes the vital glucocorticoids and mineralocorticoids, and also androgens. The latter in turn are converted into minor amounts of estrogens by peripheral aromatization. The gonads are only capable of secreting sex steroids. However, gonadal sex-steroid production is fully sufficient for an adequate reproductive function in both sexes. Why do the adrenals secrete androgens?
The effects of long-term testosterone treatment on endocrine parameters in hypogonadal men: 12-year data from a prospective controlled registry study
Published in The Aging Male, 2022
Aksam Yassin, Farid Saad, Mustafa Alwani, Omar M. Aboumarzouk, Raed M. Al-Zoubi, Joanne Nettleship, Daniel Kelly, Abdulla Al-Ansari
Although TTh improves the QoL of hypogondal men, aromatisation of T, primarily in adipose tissue, can lead to increases in serum estradiol [35]. The extent to which T signals via conversion to estradiol and subsequent activation of the estrogen receptor to undertake tissue-specific actions remains unknown, but the aromatisation to estrogen is responsible for the majority of negative feedback of T on the hypothalamic-pituitary axis [14]. The increased estradiol levels may also have implications for gynecomastia [36], and alterations in inflammatory and immune responses [37,38]. We did observe a dramatic rise in the serum estradiol in the first two years of the TTh, after which a plateau was reached. Nevertheless, the mean serum estradiol concentrations at 12 years following TTh were measured to be within the reference range of 10–40pg/mL for men as outlined by the Endocrine Society [39,40], and thus may have limited clinical consequences. In our previous investigation, we reported a significant reduction in BMI and waist circumference for 411 hypogonadal men on long-term TTh [23]. This reduction in obesity and consequently adipose tissue might contribute to lower aromatization of T and thus plateauing of estradiol levels within the reference range observed here. However, serum estradiol monitoring in hypogonadal men with TTh may still be useful, especially if clinical symptoms develop, and T dose-titration or use of aromatase inhibitors could be required [36]. Moreover, it has been suggested that instead of the effect of estradiol itself, the ratio of T to estradiol may be more clinically informative [41–43].
Dietary Habits and Daily Routines as Prognostic Factors in Endometrial Cancer: A Machine Learning Approach
Published in Nutrition and Cancer, 2022
Ofra Castro Wersäll, Zoia Razumova, Igor Govorov, Miriam Mints
Apart from its beneficial effects on obesity, diabetes, and cardiovascular disorders, regular physical activity reduces the risk of several malignant tumors, including EC (45). According to the meta-analysis by Moore et al., active women had a 30% lower risk of EC compared with non-active women (46). Similar results were obtained in the systematic review, which reported that women who engaged in regular physical activity had a 20-40% lower risk of EC (47). In our study, physical activity did not affect the risk of the EC recurrence, but decreased the risk of death. Again, since older patients usually have concurrent health conditions, the ultimate effect of physical activity is probably the result of various mechanisms. Some examples include the normalization of insulin levels, a decrease in inflammatory markers and reactive oxygen species, modulation of the immune system, and, the most obvious, weight reduction (48–50). The latter usually coincides with the depletion of adipose tissue, which leads to less aromatization, ie., the converting of androgens into bioactive estrogens, which promotes endometrium proliferation.
Advances in targeting estrogen synthesis and receptors in patients with endometriosis
Published in Expert Opinion on Investigational Drugs, 2022
Sara Clemenza, Silvia Vannuccini, Agostino Ruotolo, Tommaso Capezzuoli, Felice Petraglia
Estrogens play a key role in the growth and persistence of endometriotic lesions as well as in genesis of inflammation and pain. E2 synthesis derives from cholesterol through six serial enzymatic conversions [12]. Endometriotic cells can synthesize E2de novo because of the expression of two important proteins involved in estrogen biosynthesis: aromatase and steroidogenic acute regulatory protein (StAR). Aromatase is a member of the cytochrome P450 superfamily and is responsible for the aromatization of androgens into estrogens. StAR is a transport protein that regulates cholesterol transfer within the mitochondria, which is initial step in the production of steroid hormones [13]. Moreover, endometriosis cells do not express 17-hydroxysteroid dehydrogenase type 2 (17HSD2), which normally converts E2 to the less potent estrone [10]. This combination allows the endometriotic implants to be exposed to a high local concentration of bioavailable estrogens [1].