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Congenital Adrenal Hyperplasia
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Biochemical pathways of adrenal steroidogenesis consist of three major routes that all start with cholesterol: mineralocorticoids (end product: aldosterone), glucocorticoids (end product: cortisol), and sex steroids (end product: testosterone) (Figure 52.1). Multiple proteins/enzymes are required for these biochemical pathways, including steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage (CYP11A1), 3β-hydroxysteroid dehydrogenase type 2 (HSD3B2), 17α-hydroxylase/17,20-lyase (CYP17A1), cytochrome b5 (CYB5A), 21-hydroxylase (CYP21A2), 11β-hydroxylase (CYP11B1), aldosterone synthase (CYP11B2), and 17β-hydroxysteroid dehydrogenase type 5 (AKR1C3) (Figure 52.1). Although mutations in the underlying genes encoding any of these proteins/enzymes may cause disruptions in steroidogenesis, potentially leading to CAH, those affecting 21 hydroxylase (P450c21), 11ß hydroxylase (P450c11β) and 17α-hydroxylase/17,20-lyase (P450c17), stand out most (Table 52.1). In fact, mutations in the CYP21A2 (6p21.3), CYP11B1 (8q24.3), and CYP17A1 (10q21-q22) genes encoding P450c21, P450c11β, and P450c17 account for approximately 90%, 5%, and 5% of CAH cases, respectively (Table 52.1) [7–10].
Testosterone signaling in spermatogenesis, male fertility and infertility
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
Arijit Chakraborty, Vertika Singh, Kiran Singh, Rajender Singh
Testicular Leydig cells synthesize the male sex steroid hormones, which are low molecular weight compounds derived from cholesterol, under the regulation of LH. While Leydig cells are capable of de novo synthesis of cholesterol from acetyl coenzyme A, the main source of cholesterol comes from lipoprotein particles transported through the blood into the Leydig cells. Steroid synthesis commences with the transportation of cytosolic cholesterol from the outer membrane to the inner membrane of the mitochondria, which also serves as the rate-limiting step in the process of steroidogenesis. A number of proteins assist in the transportation of the hydrophobic cholesterol, which is unable to simply diffuse through the membrane on its own. The most important of these proteins is the steroidogenic acute regulatory protein StAR (4), consisting of a family of 37 kDa (precursor) and 30 kDa (mature) mitochondrial proteins (5). It mainly detects the response of Leydig cells against tropic hormones and other external stimuli and helps in transporting free cholesterol inside mitochondria of the Leydig cells, stimulating steroidogenesis.
Radioiodinated Cholesterol as A Radiotracer in Biochemical Studies
Published in William C. Eckelman, Lelio G. Colombetti, Receptor-Binding Radiotracers, 2019
Raymond E. Counsell, Nancy Korn
Steroid hormone synthesis in the adrenals and gonads is controlled to a large extent by the pituitary hormones, namely: adrenocorticotrophic hormone (ACTH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Although, the precise mechanisms whereby these trophic hormones exert their control of steroidogenesis is not fully understood, they have been observed to modulate a variety of steps in the pathway.
Human ovarian granulosa cells use clathrin-mediated endocytosis for LDL uptake: immunocytochemical and electron microscopic study
Published in Ultrastructural Pathology, 2023
Aynur Abdulova, Merjem Purelku, Hakan Sahin, Gamze Tanrıverdi
Steroidogenesis is a complex process between multiple enzymes and substrates by which cholesterol is converted into steroid hormones. Cholesterol is stored in lipid droplets (LDs) as cholesterol esters (CEs) within the steroidogenic tissue. The cholesterol that is required for steroidogenesis which is being initiated in response to a hormonal stimulus is provided by the mobilization of these stored CEs within the cells.3 There are two different forms of cholesterol which are known as high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Studies are focused on the fact that granulosa cells use the LDL-receptor (LDLR)-mediated endocytic pathway for steroid biosynthesis. LDLR is an important protein that functions to mediate the uptake of LDL cholesterol, which is a specific substrate for steroid hormone production.3–5 Many different endocytic pathways have been described in eukaryotic cells, but the main pathway for LDL transport has been reported to be the clathrin-mediated endocytosis pathway.6,7 However, no study that clarifies LDL internalization in human granulosa cells and whether the clathrin-mediated endocytic pathway is functional in this process has yet been published.
Evaluating the histomorphological and biochemical changes induced by Tributyltin Chloride on pituitary-testicular axis of adult albino rats and the possible ameliorative role of hesperidin
Published in Ultrastructural Pathology, 2023
Sahar F. Shaban, Maha A. Khattab, Samar H. Abd El Hameed, Shaimaa A. Abdelrahman
Regarding hormonal levels of FSH, LH and testosterone, there were significant decreases of the mean values of group II in comparison with group I. The decrease in FSH and LH in this study might be evidenced by histological and immunohisto-chemical results which appeared in TBT treated group in pars distalis of pituitary gland. These results were supported by Sena et al.46 and Barbosa et al.47 who attributed the decrease in pituitary FSH and LH levels in TBT-treated female rats, to the apoptosis in GNRH neuronal cells in the hypothalamus which led to decrease in GNRH mRNA expression and consequently, disrupting hypothalamic hypophyseal gonadal axis. Faralla et al.48 explained that decreased levels of LH can affect steroidogenesis as it maintains the fully differentiated structure and function of Leydig cells. Decreased Testosterone levels in group II might be indirectly due to decrease LH or due to the direct effect of TBT on Leydig cells. TBT directly affects Leydig cells development and proliferation. Moreover, it can affect the enzymes responsible for steroidogenesis.49–52
Oxytocin modulates steroidogenesis-associated genes and estradiol levels in the placenta
Published in Systems Biology in Reproductive Medicine, 2023
Sung-Min An, Min Jae Kim, Jea Sic Jeong, So Young Kim, Da Som Kim, Beum-Soo An, Seung Chul Kim
Steroid hormones are primarily produced by a biological process called steroidogenesis, which is the process by which cholesterol is converted into several other steroid hormones. Humans and various mammals use cholesterol to synthesize steroid hormones in the reproductive glands and placenta (Payne and Hales 2004). During pregnancy, multiple steroid hormones released by the placenta perform a variety of roles, including placental trophoblast differentiation, expansion and maturation of the placental vessels, and uterine endovascular invasion by the placental trophoblast (extravillous cytotrophoblast) (Pepe and Albrecht 2008). One study demonstrated that CTB isolated form human placentas are capable of differentiating and fusing spontaneously to form functional STB as well as producing steroid hormones (Kliman et al. 1986). In addition, various studies have conducted research on synthesis of steroid hormones using JEG-3 cells (Samson et al. 2009; Cao et al. 2017; Karahoda et al. 2021). Since the process of synthesizing steroid hormones in the placenta has a large impact on the mother and fetus during pregnancy, in-depth studies on placental steroidogenesis are inevitable.