Sex steroid

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Sex steroids, also known as gonadal steroids, are steroid hormones that interact with vertebrate androgen or estrogen receptors.[1] Their effects are mediated by slow genomic mechanisms through nuclear receptors as well as by fast nongenomic mechanisms through membrane-associated receptors and signaling cascades.[2] The term sex hormone is nearly always synonymous with sex steroid. The non-steroid hormones luteinizing hormone, follicle-stimulating hormone and gonadotropin-releasing hormone are usually not regarded as sex hormones, although they play major sex-related roles.

Production[edit]

Natural sex steroids are made by the gonads (ovaries or testes),[3] by adrenal glands, or by conversion from other sex steroids in other tissue such as liver or fat.[4]

Synthetic sex steroids[edit]

There are also many synthetic sex steroids. Synthetic androgens are often referred to as anabolic steroids. Synthetic estrogens and progestins are used in methods of hormonal contraception. Ethinylestradiol is a semi-synthetic estrogen. Specific compounds that have partial agonist activity for steroid receptors, and therefore act in part like natural steroid hormones, are in use in medical conditions that require treatment with steroid in one cell type, but where systemic effects of the particular steroid in the entire organism are only desirable within certain limits.[5]

Types[edit]

In many contexts, the two main classes of sex steroids are androgens and estrogens, of which the most important human derivatives are testosterone and estradiol, respectively. Other contexts will include progestogens as a third class of sex steroids, distinct from androgens and estrogens. Progesterone is the most important and only naturally-occurring human progestogen. In general, androgens are considered "male sex hormones", since they have masculinizing effects, while estrogens and progestogens are considered "female sex hormones"[6] although all types are present in each sex, albeit at different levels.

Sex steroids include:

See also[edit]

References[edit]

  1. ^ Guerriero, G (April 2009). "Vertebrate sex steroid receptors: evolution, ligands, and neurodistribution.". Annals of the New York Academy of Sciences 1163: 154–68. doi:10.1111/j.1749-6632.2009.04460.x. PMID 19456336. 
  2. ^ Thakur, MK; Paramanik, V (2009). "Role of steroid hormone coregulators in health and disease". Hormone research 71 (4): 194–200. doi:10.1159/000201107. PMID 19258710. 
  3. ^ Brook, CG (1999). "Mechanism of puberty". Hormone research. 51 Suppl 3: 52–4. PMID 10592444. 
  4. ^ Catherine Panter-Brick, Agustín Fuentes. "Glossary". Health, Risk, and Adversity - Volume 2 of Studies of the Biosocial Society. Berghahn Books, 2011. p. 280. 
  5. ^ Copland, JA; Sheffield-Moore, M; Koldzic-Zivanovic, N; Gentry, S; Lamprou, G; Tzortzatou-Stathopoulou, F; Zoumpourlis, V; Urban, RJ; Vlahopoulos, SA (June 2009). "Sex steroid receptors in skeletal differentiation and epithelial neoplasia: is tissue-specific intervention possible?". BioEssays : news and reviews in molecular, cellular and developmental biology 31 (6): 629–41. doi:10.1002/bies.200800138. PMID 19382224. 
  6. ^ ElAttar, TM; Hugoson, A (1974). "Comparative metabolism of female sex steroids in normal and chronically inflamed gingiva of the dog". Journal of periodontal research 9 (5): 284–9. doi:10.1111/j.1600-0765.1974.tb00683.x. PMID 4281823. 

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