Topic
Testosterone
About: Testosterone is a research topic. Over the lifetime, 23258 publications have been published within this topic receiving 808079 citations. The topic is also known as: 4-androsten-17beta-ol-3-one & 4-Androsten-3-one-17b-ol.
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TL;DR: It is postulated that the conjugating activity of UGT enzymes is the main mechanism for modulating the action of steroids and protecting the androgen-sensitive tissues from deleteriously high concentrations of DHT, ADT and 3alpha-DIOL.
Abstract: In humans, 3beta-hydroxysteroid dehydrogenase (3beta-HSD), 17beta-HSD and 5alpha-reductase activities in androgen target tissues, such as the prostate and skin, convert dehydroepiandrosterone, androstenedione and testosterone into the most potent natural androgen dihydrotestosterone (DHT). This androgen is converted mainly in situ into two phase I metabolites, androsterone (ADT) and androstane-3alpha,17beta-diol (3alpha-DIOL), which might be back converted to DHT. Here, we discuss the recent findings regarding the characterization of specific UDP-glucuronosyltransferases (UGTs), UGT2B7, B15 and B17, responsible for the glucuronidation of these metabolites. The tissue distribution and cellular localization of the UGT2B transcripts and proteins in humans clearly indicate that these enzymes are synthesized in androgen-sensitive tissues. It is postulated that the conjugating activity of UGT enzymes is the main mechanism for modulating the action of steroids and protecting the androgen-sensitive tissues from deleteriously high concentrations of DHT, ADT and 3alpha-DIOL.
241 citations
01 Jan 1981
TL;DR: In this article, the antifertility effects of a potent gonadotropin-releasing hormone agonist (LHRHA) D-Trp -Pro -N-ethylamide-LHRH in 8 normal men who received daily subcutaneous injections for 6-10 weeks were studied.
Abstract: We studied the antifertility effects of a potent gonadotropin-releasing hormone agonist (LHRHA) D-Trp -Pro -N-ethylamide-LHRH in 8 normal men who received daily subcutaneous injections for 6-10 weeks. Plasma testosterone levels fell substantially in all 8. Plasma 17-hydroxyprogesterone and serum estradiol-17beta levels decreased concordantly with plasma testosterone. Impotence developed in 5 men between the 6th and 7th weeks of treatment with resolution in each case within 2 weeks of cessation of treatment. Serum gonadotropin levels also fell during treatment briefly rebounding above basal levels when therapy ended. Sperm density and motility fell to a nadir during the 7th-18th weeks after therapy. In 6 subjects sperm levels fell to 6x10 sperm/milliliter or less and in the other 2 they decreased 70 and 86% respectively below basal mean values. Sperm density returned to pretreatment levels in all men during the 10-14 weeks of recovery. These results are consistent with LHRHA-induced pituitary "desensitization" but do not exclude a direct inhibitory effect of LHRHA on testicular steroidogenesis and spermatogenesis. (authors)
240 citations
TL;DR: It is suggested that androgen deficiency is associated with IR, T2D, MetS, and with increased deposition of visceral fat, which serves as an endocrine organ, producing inflammatory cytokines and thus promoting endothelial dysfunction and vascular disease.
Abstract: A considerable body of evidence exists suggesting a link among reduced testosterone plasma levels, type 2 diabetes (T2D), and insulin resistance (IR). Hypogonadal men are at higher risk for T2D. Here we evaluate the relationships between testosterone, metabolic syndrome (MetS), T2D, and IR and discuss the relationships among androgen deficiency and these factors, especially as it ultimately relates to the development of cardiovascular disease and erectile dysfunction (ED). Thus, a comprehensive literature search was carried out using PubMed, and relevant articles pertinent to androgen deficiency, T2D, IR, MetS, and ED were reviewed and discussed. Low testosterone precedes elevated fasting insulin, glucose, and hemoglobin A1c (HbA1C) values and may even predict the onset of diabetes. Treatment of prostate cancer patients with surgical or medical castration exacerbates IR and glycemic control, strengthening the link between testosterone deficiency and onset of T2D and IR. Androgen therapy of hypogonadal men improves insulin sensitivity, fasting glucose, and HbA1c levels. We suggest that androgen deficiency is associated with IR, T2D, MetS, and with increased deposition of visceral fat, which serves as an endocrine organ, producing inflammatory cytokines and thus promoting endothelial dysfunction and vascular disease.
240 citations
TL;DR: The reproductive capacity of mice lacking Bmal1 (Arntl, Mop3), one of the central circadian clock genes, is investigated, and expression of the steroidogenic acute regulatory protein (StAR) gene and protein, which regulates the rate-limiting step of steroidogenesis, was decreased in testes from B mal1 KO mice.
Abstract: Although it is well established that the circadian clock regulates mammalian reproductive physiology, the molecular mechanisms by which this regulation occurs are not clear. The authors investigated the reproductive capacity of mice lacking Bmal1 (Arntl, Mop3), one of the central circadian clock genes. They found that both male and female Bmal1 knockout (KO) mice are infertile. Gross and microscopic inspection of the reproductive anatomy of both sexes suggested deficiencies in steroidogenesis. Male Bmal1 KO mice had low testosterone and high luteinizing hormone serum concentrations, suggesting a defect in testicular Leydig cells. Importantly, Leydig cells rhythmically express BMAL1 protein, suggesting peripheral control of testosterone production by this clock protein. Expression of steroidogenic genes was reduced in testes and other steroidogenic tissues of Bmal1 KO mice. In particular, expression of the steroidogenic acute regulatory protein (StAR) gene and protein, which regulates the rate-limiting ste...
240 citations
TL;DR: Kiss1 neurons have emerged as primary transducers of internal and environmental cues to regulate the neuroendocrine reproductive axis and may regulate the negative feedback effect of gonadal steroids on GnRH and gonadotropin secretion in both sexes.
Abstract: Neurons that produce gonadotropin-releasing hormone (GnRH) reside in the basal forebrain and drive reproductive function in mammals. Understanding the circuitry that regulates GnRH neurons is fundamental to comprehending the neuroendocrine control of puberty and reproduction in the adult. This review focuses on a family of neuropeptides encoded by the Kiss1 gene, the kisspeptins, and their cognate receptor, GPR54, which have been implicated in the regulation of GnRH secretion. Kisspeptins are potent secretagogues for GnRH, and the Kiss1 gene is a target for regulation by gonadal steroids (e.g., estradiol and testosterone), metabolic factors (e.g., leptin), photoperiod, and season. Kiss1 neurons in the arcuate nucleus may regulate the negative feedback effect of gonadal steroids on GnRH and gonadotropin secretion in both sexes. The expression of Kiss1 in the anteroventral periventricular nucleus (AVPV) is sexually dimorphic, and Kiss1 neurons in the AVPV may participate in the generation of the preovulatory GnRH/luteinizing hormone (LH) surge in the female rodent. Kiss1 neurons have emerged as primary transducers of internal and environmental cues to regulate the neuroendocrine reproductive axis.
240 citations