Human natural glucocorticoid hormone
This article is about the natural hormone. For the medication, see
Hydrocortisone .
Not to be confused with
cortisone , a
metabolite of cortisol, with a similar name, biosynthesis, and function.
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
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard
100.000.019
KEGG
UNII
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
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
C 21 H 30 O 5
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).
Chemical compound
Cortisol is a steroid hormone , in the glucocorticoid class of hormones and a stress hormone . When used as a medication, it is known as hydrocortisone .
It is produced in many animals, mainly by the zona fasciculata of the adrenal cortex in the adrenal gland .[1] It is produced in other tissues in lower quantities.[2] It is released with a diurnal cycle and its release is increased in response to stress and low blood-glucose concentration .[1] It functions to increase blood sugar through gluconeogenesis , to suppress the immune system , and to aid in the metabolism of fat , protein , and carbohydrates .[3] It also decreases bone formation.[4] Many of these functions are carried out by cortisol binding to glucocorticoid or mineralocorticoid receptors inside the cell, which then bind to DNA to impact 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 .