Cortisol

Cortisol
Names
	IUPAC name 11β,17α,21-Trihydroxypregn-4-ene-3,20-dione
	Systematic IUPAC name (1R,3aS,3bS,9aR,9bS,11aS)-1,10-Dihydroxy-1-(hydroxyacetyl)-9a,11a-dimethyl-1,2,3,3a,3b,4,5,8,9,9a,9b,10,11,11a-tetradecahydro-7H-cyclopenta[a]phenanthen-7-one
Identifiers
CAS Number	50-23-7;
3D model (JSmol)	Interactive image;
ChEBI	CHEBI:17650;
ChEMBL	ChEMBL389621;
ChemSpider	5551;
DrugBank	DB00741;
ECHA InfoCard	100.000.019
KEGG	D00088;
PubChem CID	5754;
UNII	WI4X0X7BPJ;
CompTox Dashboard (EPA)	DTXSID7020714 ;
	InChI InChI=1S/C21H30O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h9,14-16,18,22,24,26H,3-8,10-11H2,1-2H3/t14-,15-,16-,18+,19-,20-,21-/m0/s1 Key: JYGXADMDTFJGBT-VWUMJDOOSA-N;
	SMILES O=C4\C=C2/[C@]([C@H]1[C@@H](O)C[C@@]3([C@@](O)(C(=O)CO)CC[C@H]3[C@@H]1CC2)C)(C)CC4;
Properties
Chemical formula	C21H30O5
Molar mass	362.460 g/mol
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references

Cortisol is a steroid hormone in the glucocorticoid class of hormones and a stress hormone. When used as medication, it is known as hydrocortisone.

It is produced in many animals, mainly by the zona fasciculata of the adrenal cortex in an adrenal gland.^[1] In other tissues, it is produced in lower quantities.^[2] By a diurnal cycle, cortisol is released and increases in response to stress and a low blood-glucose concentration.^[1] It functions to increase blood sugar through gluconeogenesis, suppress the immune system, and aid in the metabolism of calories.^[3] It also decreases bone formation.^[4] These stated functions are carried out by cortisol binding to glucocorticoid or mineralocorticoid receptors inside a cell, which then bind to DNA to affect gene expression.^[1]^[5]

^ ^a ^b ^c Lightman SL, Birnie MT, Conway-Campbell BL (June 2020). "Dynamics of ACTH and Cortisol Secretion and Implications for Disease". Endocrine Reviews. 41 (3). doi:10.1210/endrev/bnaa002. PMC 7240781. PMID 32060528.
^ Taves MD, Gomez-Sanchez CE, Soma KK (July 2011). "Extra-adrenal glucocorticoids and mineralocorticoids: evidence for local synthesis, regulation, and function". American Journal of Physiology. Endocrinology and Metabolism. 301 (1): E11-24. doi:10.1152/ajpendo.00100.2011. PMC 3275156. PMID 21540450.
^ Hoehn K, Marieb EN (2010). Human Anatomy & Physiology. San Francisco: Benjamin Cummings. ISBN 978-0-321-60261-9.
^ Chyun YS, Kream BE, Raisz LG (February 1984). "Cortisol decreases bone formation by inhibiting periosteal cell proliferation". Endocrinology. 114 (2): 477–80. doi:10.1210/endo-114-2-477. PMID 6690287.
^ DeRijk RH, Schaaf M, de Kloet ER (June 2002). "Glucocorticoid receptor variants: clinical implications". The Journal of Steroid Biochemistry and Molecular Biology. 81 (2): 103–122. doi:10.1016/S0960-0760(02)00062-6. PMID 12137800. S2CID 24650907.

[light-1] Lightman SL, Birnie MT, Conway-Campbell BL (June 2020). "Dynamics of ACTH and Cortisol Secretion and Implications for Disease". Endocrine Reviews. 41 (3). doi:10.1210/endrev/bnaa002. PMC 7240781. PMID 32060528.

[2] Taves MD, Gomez-Sanchez CE, Soma KK (July 2011). "Extra-adrenal glucocorticoids and mineralocorticoids: evidence for local synthesis, regulation, and function". American Journal of Physiology. Endocrinology and Metabolism. 301 (1): E11-24. doi:10.1152/ajpendo.00100.2011. PMC 3275156. PMID 21540450.

[Marieb-3] Hoehn K, Marieb EN (2010). Human Anatomy & Physiology. San Francisco: Benjamin Cummings. ISBN 978-0-321-60261-9.

[pmid6690287-4] Chyun YS, Kream BE, Raisz LG (February 1984). "Cortisol decreases bone formation by inhibiting periosteal cell proliferation". Endocrinology. 114 (2): 477–80. doi:10.1210/endo-114-2-477. PMID 6690287.

[5] DeRijk RH, Schaaf M, de Kloet ER (June 2002). "Glucocorticoid receptor variants: clinical implications". The Journal of Steroid Biochemistry and Molecular Biology. 81 (2): 103–122. doi:10.1016/S0960-0760(02)00062-6. PMID 12137800. S2CID 24650907.

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