Emerging Potential of In Vitro Diagnostic Devices: Applications and Current Status
Debarshi Kar Mahapatra, Sanjay Kumar Bharti in Medicinal Chemistry with Pharmaceutical Product Development, 2019
Hormonal inequity in a biological system is a specific indicator for onset of numerous diseases. Different test methods are there for detecting hormone level (estrogen, cortisol, testosterone and progesterone) in human serum or urine. However, rapid diagnostic test kits have also gained approval for this purpose. A suitable example for this is “The FREND TM Free T4 Test System,” an IVD for the diagnosis of thyroid disorder. It quantitatively determines the level of free thyroxine (FT4). It is based on the principle of competitive immune assay (indirect). Researchers developed Cortisol biosensors for screening Cushing’s syndrome. These IVDs are also-called immune sensors, as Ag-Ab interactions is the principle behind it. Many immune sensors also use enzyme for getting specific reaction results. Like, alkaline phosphatase (AP) enzyme [28], dithiobis (succinimidyl proprionate) were used to measure salivary cortisol concentration. Similarly salivary testosterone can be detected by an SPR biosensor in less than 13 min. Testosterone is the primary male sex hormone which also exists in women allowing the secretion of estrogen [29]. This device was developed by Mitchell and Lowe [30] by conjugating oligoethylene glycol with testosterone by forming a covalent bond and coated on the sensing surface by immobilization technique.
The Pathophysiology of Male Infertility
Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh in Male Infertility in Reproductive Medicine, 2019
Spermatogenesis and steroidogenesis are under endocrine regulation via the pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [8]. The hypothalamus is known to be the center of information processing as per external and internal cues. Via the pulsatile release of gonadotropin-releasing hormone (GnRH), it stimulates the secretion by anterior pituitary, LH and FSH, which binds to receptors on the Leydig cells, and Sertoli cells, respectively. Leydig cells reside within the interstitial compartments and produce testosterone. Sertoli cells lie along the lining of the seminiferous tubules, supporting the germ cells to develop through the stages of spermatogenesis. Sertoli cells have receptors for both FSH and testosterone and produce estradiol at low levels. Another contribution of the Sertoli cells is the productions of glycoprotein hormones (inhibin, activin, and follistatin) that modulate FSH secretion [9]. Testosterone is the main androgen that sends feedback to the hypothalamus and pituitary, regulates spermatogenesis directly, monitors sexual behavior, and serves as the primary male sex hormone that aids primary and secondary sex development.
Effects of sex steroids on brain cells
Barry G. Wren in Progress in the Management of the Menopause, 2020
Hormonal modifications in the growth of neuronal processes may result in changes in the pattern of neuronal connectivity. It is well established that during the critical period gonadal steroids influence the formation of synaptic contacts among neurons, resulting in specific sex differences in neuronal connectivity. Furthermore, the effect of sex hormones on synapses is not restricted to the developmental period. Synapses are plastic structures that may be modified in the adult brain in response to changing physiological conditions, including modifications in hormone levels18, 19. Gonadal hormones influence synapse formation in areas of the central nervous system involved in the control of reproductive behavior, such as the ventromedial hypothalamic nucleus, lateral septum and the amygdala, and in areas involved in the control of the release of pituitary hormones, such as the hypothalamic arcuate nucleus and the preoptic area. In addition, gonadal hormones may affect neuronal connectivity in cognitive areas, such as the hippocampal formation and the cerebral cortex18, 37, 39.
Aromatase inhibitors for the treatment of endometriosis: a systematic review about efficacy, safety and early clinical development
Published in Expert Opinion on Investigational Drugs, 2020
Simone Garzon, Antonio Simone Laganà, Fabio Barra, Jvan Casarin, Antonella Cromi, Ricciarda Raffaelli, Stefano Uccella, Massimo Franchi, Fabio Ghezzi, Simone Ferrero
The role of estrogens is further supported by epidemiological and clinical studies, which demonstrated a strong association between endometriosis and reproductive life, with the regression of endometriotic implants and associated symptomatology after menopause [2–4]. Indeed, the primary source of estrogens is represented by the ovaries, which cyclically produce estrogens during reproductive life. Luteinizing hormone stimulates the theca production of androgens from cholesterol, which diffuse to the granulosa cell layer of the follicle. In the granulosa cells, the follicle-stimulating hormone regulates the expression of the aromatase P450 enzyme, which is responsible for the transformation of androgens into estrogens [54]. Aromatase is a mono-oxygenase enzyme complex that aromatizes androstenedione and testosterone into estrone and estradiol, respectively, through three hydroxylation reactions. The A ring of the androgens is rearranged in a phenolic A ring, characteristic of estrogens [55]. In the ovaries, hormone production involves mainly the aromatization of testosterone into estradiol, which is the principal and more active female sex hormone. The estradiol reaches the endometriotic implants through the blood circulation or by direct spillage in the peritoneal cavity at ovulation [56]. The estrogen dependence of endometriosis and this primary source of estrogens explains the efficacy of all the pharmacotherapeutic options inhibiting and suppressing the ovarian function by blocking gonadotropins release [29,34–36].
Association between testosterone with type 2 diabetes in adult males, a meta-analysis and trial sequential analysis
Published in The Aging Male, 2020
Jianzhong Zhang, Xiao Li, Zhonglin Cai, Hongjun Li, Bin Yang
Testosterone is the primary male sex hormone and an anabolic steroid. In males, testosterone plays an important role in the development of male reproductive tissues such as penis, testes and prostate, as well as promoting secondary sexual characteristics. In addition, testosterone is involved in health and well-being, and the prevention of osteoporosis [5,6]. Insufficient levels of testosterone in men may lead to abnormalities including erectile dysfunction, lower urinary tract symptoms, inflammatory diseases and increased cardiovascular risk factors [7–9]. The corresponding is that testosterone supplement therapy can improve glycemic control, urinary and sexual function, voiding symptoms, and quality of life [10–15]. Although the importance of testosterone in maintaining cardiovascular health is still controversial [16], maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control [8].
An update on the available and emerging pharmacotherapy for adults with testosterone deficiency available in the USA
Published in Expert Opinion on Pharmacotherapy, 2021
Eliyahu Kresch, Mehul Patel, Thiago Fernandes Negris Lima, Ranjith Ramasamy
Testosterone is the primary male sex hormone which plays an integral role in many facets of physiology including embryologic development, spermatogenesis, and development and maintenance of secondary sexual characteristics throughout puberty and adulthood. Testosterone deficiency (TD) is defined as insufficient production of testosterone combined with symptoms of low serum total testosterone such as decreased muscle mass, osteoporosis, poor erythropoiesis, diminished energy, low libido, and erectile function [1–6]. Etiologically, TD can be separated into primary and secondary TD. Primary TD occurs when there are problems with testosterone production at the level of the testes, whereas secondary TD involves defects in the production of gonadotropin hormones from the hypothalamus or pituitary [7]. Although this review focuses mainly on the treatment of TD from a primary etiology, the principles and medications can be used with any patient that presents with TD. Diagnosing TD can be challenging because of the heterogeneity of symptoms experienced by different individuals but the current definition relies on two criteria: having a low serum testosterone defined by two separate early morning testosterone levels <300 ng/dL as well as manifestations of the aforementioned symptoms.Figure 1Table 1
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