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Premature/Primary Ovarian Insufficiency (POI)
Published in S Paige Hertweck, Maggie L Dwiggins, Clinical Protocols in Pediatric and Adolescent Gynecology, 2022
Christina N. Davis-Kankanamge, Alla Vash-Margita
Mutations in enzymes required in reproductionCarbohydrate-deficient glycoprotein deficiencyGalactose-1-phosphate uridyl transferase (GALT) deficiency (galactosemia)17 α-hydroxylase/17,20-desmolase deficiencyAromatase mutations
Hormones of the Adrenal Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The adrenal cortex secretes two steroids: C19 steroids (androgenic) and C21 steroids (mineralocorticoid and glucocorticoid activity). The steroids are formed from cholesterol. Low-density lipoproteins in blood are absorbed directly by endocytosis. Cholesterol is converted by 20,22 desmolase (a rate-limiting enzyme) to pregnenolone, which is then hydroxylated to 17-OH-pregnenolone and then dehydrogenated to progesterone by 3-β-hydroxysteroid hydrogenase and isomerase in the endoplasmic reticulum.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
ACTH acts on specific receptors in the adrenal cortex, whereupon adenylate cyclase, acting as a second messenger, induces the formation of cAMP inside the cytoplasm of the cells. In the cascade that follows, phosphoprotein kinases phosphorylate proteins. An important step is the subsequent activation of desmolase; this converts cholesterol esters to pregnenolone, upon which all later steps depend.
Oral dehydroepiandrosterone restores ß-endorphin response to OGTT in early and late postmenopause
Published in Gynecological Endocrinology, 2019
A. Giannini, A. D. Genazzani, A. Napolitano, M. Caretto, M. Stomati, T. Simoncini, A. R. Genazzani
Menopause represents a peculiar moment of women’s life. After 70 years of age, dehydroepiandrosterone [DHEA(S)] levels are 20% or less of the maximum plasma concentrations [1]. It has been hypothesized that during the aging process, the reduction of 17,20 desmolase activity, the enzyme that rules the biosynthesis of the Δ5-adrenal pathway, may induce modifications in DHEA(S) synthesis [2–6]. Growing evidence in literature support the hypothesis that lower levels of DHEA occurring during aging have been associated with impaired glucose tolerance, insulin resistance, and diabetes [7,8]. Moreover, recent data demonstrated that DHEA administration greatly improves most of menopausal symptoms and endocrine impairments [4,5,9,10] acting on each tissue and organ through an intracrinological effect since this molecule acts as a sort of pre-hormone for the production of active metabolites [11]. DHEA administration is not yet considered a medical treatment though this steroid has been demonstrated to induce specific metabolic effects [4,12,13] and to counteract the age-induced changes at the adrenal gland level as well as to increase anxiolytic substances (allopregnanolone) and some neuropeptides (i.e. β-endorphin).
Long-term effects of combined simvastatin and metformin treatment on the clinical abnormalities and ovulation dysfunction in single young women with polycystic ovary syndrome
Published in Gynecological Endocrinology, 2018
The rapid effect on the abnormal lipid profile and total androgen levels could be explained by the primary direct mode of action of both (1) statins, i.e. immediate and direct competitive inhibition of the rate limiting step of cholesterol synthesis via 3-hydroxy- 3methylglutaryl-coenzyme A reductase [46], and (2) metformin, i.e which directly inhibits androgen production in human ovarian thecal cells, and directly decreased hepatic glucose synthesis, and reduces expression of steroidogenic acute regulatory (StAR) protein and 17-hydroxylase/17,20-desmolase (CYP17) and so decreases testosterone production level, with subsequent higher peripheral insulin sensitivity [47]. This is in contrast to the clinical signs of hyperandrogenism (hirsutism, acne, BMI), and occurrence of spontaneous ovulation which showed cumulative progressive improvement, markedly appears after the first 6 months treatment, and reached peaked values at the end of the 12 months treatment [22,30,48].
Formation of secondary allo-bile acids by novel enzymes from gut Firmicutes
Published in Gut Microbes, 2022
Jae Won Lee, Elise S. Cowley, Patricia G. Wolf, Heidi L. Doden, Tsuyoshi Murai, Kelly Yovani Olivos Caicedo, Lindsey K. Ly, Furong Sun, Hajime Takei, Hiroshi Nittono, Steven L. Daniel, Isaac Cann, H. Rex Gaskins, Karthik Anantharaman, João M. P. Alves, Jason M. Ridlon
We previously reported a cortisol-inducible operon (desABCD) in L. scindens ATCC 35704 encoding steroid-17,20-desmolase (DesAB) and NADH-dependent steroid 20α-hydroxysteroid dehydrogenase (DesC).42 DesC reversibly forms cortisol and 20α-dihydrocortisol,42 and DesAB catalyzes the side-chain cleavage of cortisol yielding 11β-hydroxyandrostenedione (11β-OHAD).43 Because substrates and products in the desmolase pathway have 3-oxo-Δ4-structures analogous to 3-oxo-Δ4-DCA and 3-oxo-Δ4-LCA, we next performed resting cell assays with E. coli strain expressing the BaiP enzyme. LC/MS analysis of reaction products indicates that cortisol and 11β-OHAD were not substrates for BaiP (Figure S2).