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Anatomy and physiology
Published in Suzanne Everett, Handbook of Contraception and Sexual Health, 2020
Three hormones are the principal regulators of the male reproductive system: hypothalamic hormone, anterior pituitary hormones and testicular hormones. Anterior pituitary hormones control spermatogenesis and androgen production, and these are called follicle-stimulating hormone or luteinizing hormone.
Influence of Environmental Agents on Male Reproductive Failure
Published in Vilma R. Hunt, Kathleen Lucas-Wallace, Jeanne M. Manson, Work and the Health of Women, 2020
The function of the testis is controlled by at least two pituitary hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The testis controls the output of these two pituitary hormones by negative feedback, as the concentrations of both hormones in the pituitary and blood are elevated after castration (Figure 2). LH stimulates Leydig cells in the testis to synthesize steroid hormones, principally testosterone. When testosterone levels in the blood are low, the pituitary releases LH, which stimulates Leydig cells in the testis to make more testosterone. Thus, an inverse relationship exists between levels of testosterone and LH, and LH release by the pituitary is controlled by levels of circulating testosterone.84 (Figure 2).
Hypothalamic Neuroendocrine Regulation
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
The study of hypothalamic regulation had its beginning with the work of Scharrer, Scharrer, and Bargmann and their descriptions of neurosecretory neurons using the Gomori chrome alum hematoxylin stain methods.3,4 In the 40 years since, the chemical neuroanatomical research of the hypothalamus has established a detailed description of the hypothalamic cell types and their processes. The distribution of peptidergic and monaminergic cells and their processes were studied first.5 Until recently, the investigations concentrated on the posterior pituitary and the anterior hypophysiotropic pituitary hormones.
The Role of testosterone treatment in patients with metabolic disorders
Published in Expert Review of Clinical Pharmacology, 2021
Giovanni Corona, Giulia Rastrelli, Linda Vignozzi, Arcangelo Barbonetti, Alessandra Sforza, Edoardo Mannucci, Mario Maggi
The testis, the male gonad, is characterized by the production of gametes [spermatozoa] and hormones, from the tubular and interstitial compartments, respectively. Two pituitary hormones mainly control testicular activity: follicular stimulating hormone [FSH] and luteinizing hormone [LH]. The main hormones released by the testis are androgens, and, in particular, testosterone [T], which circulates only in a minor fraction as unbound to some proteins, including albumin and sex hormone-binding globulin [SHBG]. SHBG binds T with high affinity, most probably preventing biological action. In fact, according to the free hormone hypothesis, only unbound [free] T [FT] is able to bind with the androgen receptor [AR]. T concentrations show wide fluctuations over an entire lifespan, with elevated levels in the first postnatal period [mini-puberty] that decline thereafter before surging again during puberty. Several population-based studies have documented that in adult men T levels show a progressive decline as a function of age [1,2]. However, the apparent age-associated decline in serum T is attributable to a range of chronic conditions, which are more frequent with increasing age, including obesity and metabolic derangements. In fact, T levels can remain within the normal range in older healthy men [2]. Obesity-associated reduction of SHBG could partially explain the apparent decline in total T observed in aged subjects [2].
Lead optimization of 4-(thio)-chromenone 6-O-sulfamate analogs using QSAR, molecular docking and DFT – a combined approach as steroidal sulfatase inhibitors
Published in Journal of Receptors and Signal Transduction, 2021
The role of estrogens in breast cancer involves two different mechanisms i) Estrogens synthesized in the ovaries and a Luteinizing Hormone Releasing Hormone (LHRH) agonist suppresses the function of pituitary hormone to promote estrogen synthesis in pre-menopausal women, ii) In post-menopausal women, androgen secreted from adrenal glands synthesize estrogens [9,10]. In recent years, studies have been carried out to predict the mechanism by which estrogens are biosynthesized; intensive research is being done in identifying a novel target that prevents the synthesis of estrogens. In mammary gland an enzyme Steroidal Sulfatase (STS) plays a major role in the biosynthesis of estrogen. STS catalyzes the conversion of biologically inactive steroid sulfates (steroid-3-sulfate) into biologically active unsulfated derivatives (3-hydroxy steroid). The three major advantage of targeting STS are i) at molecular level, 87% of breast cancer patients showed higher expression of STS mRNA levels in malignant tissues [11] ii) the activity of STS in cancer tissue is several hundred times more than that of aromatase pathway [12] iii) 5-androstenediol, a steroid circulates in postmenopausal women binds to ER and stimulates the growth of ER + breast cancer cells. Thus, STS would be a more promising target in discovering novel candidate for the treatment of breast cancer.
Association between reproductive health and nonionizing radiation exposure
Published in Electromagnetic Biology and Medicine, 2021
The seminiferous tubules are disturbed by RF exposure that reduced the testosterone serum concentration as the Leydig cell population decrease. Testosterone is secreted by Leydig cells where Leydig cells are stimulated by luteinizing hormone (LH) to produce and maintain testosterone functions. Testosterone is accountable for the LH secretion feedback control at both the hypothalamus hormone and pituitary hormone. This pituitary hormone helps in the testosterone secretion by the Leydig cells (Dohle 2010). Another analysis of rats by Ozguner et al. (2005) found that there is no considerable difference in FSH, LH, or interstitial histology but testosterone was substantially decreased in the group of EMR relative to the control group (p < 0.05). The study suggested that natural levels of FSH and LH could be explained by reduced anterior pituitary penetration to EMR contributing to low testosterone responding to the excessive release of FSH and LH (Ozguner et al. 2005). A substantial reduction in accessory sex glands was observed in rats when accessory sex glands androgen-dependent secretory activity exposed to cell phone radiation (Salama et al. 2009). Results were linked by the authors to potential differences in receptors of testosterone, or oxidative stress on male accessory glands (Salama et al. 2009).