Cortisol - Wikipedia Cortisol This article is about the natural hormone. For the medication, see Hydrocortisone. Not to be confused with cortisone, a metabolite from cortisol, with a similar name, genesis, and function. This article 's lead section may not adequately summarize its contents. To comply with Wikipedia 's lead section guidelines, please consider modifying the lead to provide an accessible overview of the article 's key points in such a way that it can stand on its own as a concise version of the article. ( discuss ). ( November 2016 ) Cortisol Names IUPAC name 11β, 17α, 21 - Trihydroxypregn - 4 - ene - 3, 20 - dione Identifiers CAS Number 50 - 23 - 7 3D model ( JSmol ) Interactive image ChEBI CHEBI : 17650 ChemSpider 5551 DrugBank DB00741 ECHA InfoCard 100.000. 019 KEGG D00088 PubChem CID 5754 UNII WI4X0X7BPJ 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 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. When used as a medication, it is known as hydrocortisone. It is produced in humans by the zona fasciculata of the adrenal cortex within the adrenal gland. It is released in response to stress and low blood - glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates. It also decreases bone formation. Contents 1 Health effects 1.1 Metabolic response 1.2 Immune response 2 Other effects 2.1 Metabolism 2.1. 1 Glucose 2.1. 2 Bone and collagen 2.1. 3 Amino acid 2.2 Wound healing 2.3 Electrolyte balance 2.3. 1 Sodium 2.3. 2 Potassium 2.4 Stomach and kidneys 2.5 Memory 2.6 Sleep, stress, and mood 2.7 Effects during pregnancy 3 Synthesis and release 3.1 Normal levels 3.2 Disorders of cortisol production 4 Regulation 4.1 Factors reducing cortisol levels 4.2 Factors increasing cortisol levels 5 Biochemistry 5.1 Biosynthesis 5.2 Metabolism 6 Chemistry 7 Other animals 8 See also 9 References 10 External links Health effects Metabolic response In the early fasting state, cortisol stimulates gluconeogenesis ( the formation of glucose ), and activates antistress and anti-inflammatory pathways. Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose - 1 - phosphate and glucose. This is done through its passive influence on glucagon. Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for epinephrine to have an effect on glycogenolysis. In the late fasting state, the function of cortisol changes slightly and increases glycogenesis. This response allows the liver to take up glucose not being used by the peripheral tissue and turn it into liver glycogen stores to be used if the body moves into the starvation state. Elevated levels of cortisol, if prolonged, can lead to proteolysis ( breakdown of proteins ) and muscle wasting. Several studies have shown that cortisol can have a lipolytic effect ( promote the breakdown of fat ). Under some conditions, however, cortisol may somewhat suppress lipolysis. Immune response Cortisol prevents the release of substances in the body that cause inflammation. It is used to treat conditions resulting from overactivity of the B - cell - mediated antibody response. Examples include inflammatory and rheumatoid diseases, as well as allergies. Low - potency hydrocortisone, available as a nonprescription medicine in some countries, is used to treat skin problems such as rashes and eczema. It inhibits production of interleukin ( IL ) - 12, interferon ( IFN ) - gamma, IFN - alpha, and tumor - necrosis - factor ( TNF ) - alpha by antigen - presenting cells ( APCs ) and T helper ( Th ) 1 cells, but upregulates IL - 4, IL - 10, and IL - 13 by Th2 cells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system ( and resulting increase in cortisol and Th2 shift ) seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response. Cortisol can weaken the activity of the immune system. It prevents proliferation of T - cells by rendering the interleukin - 2 producer T - cells unresponsive to interleukin - 1 ( IL - 1 ), and unable to produce the T - cell growth factor ( IL - 2 ). Cortisol also has a negative - feedback effect on interleukin - 1. Though IL - 1 is useful in combating some diseases, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels ( forcing the secretion of corticotropin - releasing hormone, thus antagonizing IL - 1 ). The suppressor cells are not affected by glucosteroid response - modifying factor, so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes ( reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin ). Rapid administration of corticosterone ( the endogenous type I and type II receptor agonist ) or RU28362 ( a specific type II receptor agonist ) to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are affected by cortisol. Cortisol stimulates many copper enzymes ( often to 50 % of their total potential ), probably to increase copper availability for immune purposes. This includes lysyl oxidase, an enzyme that cross-links collagen, and elastin. Especially valuable for immune response is cortisol 's stimulation of the superoxide dismutase, since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria. Other effects Metabolism Glucose Cortisol counteracts insulin, contributes to hyperglycemia - causing hepatic gluconeogenesis and inhibits the peripheral use of glucose ( insulin resistance ) by decreasing the translocation of glucose transporters ( especially GLUT4 ) to the cell membrane. However, cortisol increases glycogen synthesis ( glycogenesis ) in the liver. The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown. Bone and collagen Cortisol reduces bone formation, favoring long - term development of osteoporosis ( progressive bone disease ). It transports potassium out of cells in exchange for an equal number of sodium ions ( see above ). This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine. Collagen is an important component of connective tissue. It is vital for structural support and is found in muscles, tendons, and joints, as well as throughout the entire body. Cortisol down - regulates the synthesis of collagen. Amino acid Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis. Cortisol ( as opticortinol ) may inversely inhibit IgA precursor cells in the intestines of calves. Cortisol also inhibits IgA in serum, as it does IgM ; however, it is not shown to inhibit IgE. Wound healing Cortisol and the stress response have known deleterious effects on the immune system. High levels of perceived stress and increases in cortisol have been found to lengthen wound - healing time in healthy, male adults. Those who had the lowest levels of cortisol the day following a 4 mm punch biopsy had the fastest healing time. In dental students, wounds from punch biopsies took an average of 40 % longer to heal when performed three days before an examination as opposed to biopsies performed on the same students during summer vacation. This is in line with previous animal studies that show similar detrimental effects on wound healing, notably the primary reports showing that turtles recoil from cortisol. Electrolyte balance Cortisol acts as a diuretic, increasing water diuresis, glomerular filtration rate, and renal plasma flow from the kidneys, as well as increasing sodium retention and potassium excretion. It also increases sodium and water absorption and potassium excretion in the intestines. Sodium Cortisol promotes sodium absorption through the small intestine of mammals. Sodium depletion, however, does not affect cortisol levels so cortisol can not be used to regulate serum sodium. Cortisol 's original purpose may have been sodium transport. This hypothesis is supported by the fact that freshwater fish use cortisol to stimulate sodium inward, while saltwater fish have a cortisol - based system for expelling excess sodium. Potassium A sodium load augments the intense potassium excretion by cortisol. Corticosterone is comparable to cortisol in this case. For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell. This should make pH regulation much easier ( unlike the normal potassium - deficiency situation, in which two sodium ions move in for each three potassium ions that move out -- closer to the deoxycorticosterone effect ). Stomach and kidneys Cortisol stimulates gastric - acid secretion. Cortisol 's only direct effect on the hydrogen - ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme. Memory Cortisol works with epinephrine ( adrenaline ) to create memories of short - term emotional events ; this is the proposed mechanism for storage of flash - bulb memories, and may originate as a means to remember what to avoid in the future. However, long - term exposure to cortisol damages cells in the hippocampus ; this damage results in impaired learning. Furthermore, cortisol inhibits memory retrieval of already stored information. Sleep, stress, and mood Diurnal cycles of cortisol levels are found in humans. In humans, the amount of cortisol present in the blood undergoes diurnal variation ; the level peaks in the early morning ( around 8 am ) and reaches its lowest level at about midnight - 4 am, or three to five hours after the onset of sleep. Information about the light / dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus. This pattern is not present at birth ; estimates of when it begins vary from two weeks to nine months of age. Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, mood disorders such as major depressive disorder, anxiety disorders, psychological stress, and physiological stressors such as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion, or temperature extremes. Cortisol levels may also differ for individuals with autism or Asperger 's syndrome. Also, significant individual variation is seen, although a given person tends to have consistent rhythms. Effects during pregnancy During human pregnancy, increased fetal production of cortisol between weeks 30 and 32 initiates production of fetal lung surfactant to promote maturation of the lungs. In fetal lambs, glucocorticoids ( principally cortisol ) increase after about day 130, with lung surfactant increasing greatly, in response, by about day 135, and although lamb fetal cortisol is mostly of maternal origin during the first 122 days, 88 % or more is of fetal origin by day 136 of gestation. Although the timing of fetal cortisol concentration elevation in sheep may vary somewhat, it averages about 11.8 days before the onset of labor. In several livestock species ( e.g. cattle, sheep, goats, and pigs ), the surge of fetal cortisol late in gestation triggers the onset of parturition by removing the progesterone block of cervical dilation and myometrial contraction. The mechanisms yielding this effect on progesterone differ among species. In the sheep, where progesterone sufficient for maintaining pregnancy is produced by the placenta after about day 70 of gestation, the prepartum fetal cortisol surge induces placental enzymatic conversion of progesterone to estrogen. ( The elevated level of estrogen stimulates prostaglandin secretion and oxytocin receptor development. ) Exposure of fetuses to cortisol during gestation can have a variety of developmental outcomes, including alterations in prenatal and postnatal growth patterns. In marmosets, a species of New World primates, pregnant females have varying levels of cortisol during gestation, both within and between females. Infants born to mothers with high gestational cortisol during the first trimester of pregnancy had lower rates of growth in body mass indices than infants born to mothers with low gestational cortisol ( about 20 % lower ). However, postnatal growth rates in these high - cortisol infants was more rapid than low - cortisol infants later in postnatal periods, and complete catch - up in growth had occurred by 540 days of age. These results suggest that gestational exposure to cortisol in fetuses has important potential fetal programming effects on both pre - and postnatal growth in primates. Synthesis and release Cortisol is produced in the human body by the adrenal gland in the zona fasciculata, the second of three layers comprising the adrenal cortex. The cortex forms the outer `` bark '' of each adrenal gland, situated atop the kidneys. The release of cortisol is controlled by the hypothalamus, a part of the brain. The secretion of corticotropin - releasing hormone by the hypothalamus triggers cells in the neighboring anterior pituitary to secrete another hormone, the adrenocorticotropic hormone ( ACTH ), into the vascular system, through which blood carries it to the adrenal cortex. ACTH stimulates the synthesis of cortisol, glucocorticoids, mineralocorticoids, and dehydroepiandrosterone. Normal levels Normal values indicated in the following tables pertain to humans ( normal levels vary among species ). Measured cortisol levels, and therefore reference ranges, depend on the analytical method used and factors such as age and sex. Test results should, therefore, always be interpreted using the reference range from the laboratory that produced the result. Reference ranges for blood plasma content of free cortisol Time Lower limit Upper limit Unit 09 : 00 am 140 700 nmol / L 5 25 μg / dL Midnight 80 350 nmol / l 2.9 13 μg / dl Using the molecular weight of 362.460 g / mole, the conversion factor from μg / dl to nmol / l is approximately 27.6 ; thus, 10 μg / dl is about 276 nmol / l. Reference ranges for urinalysis of free cortisol Lower limit Upper limit Unit 28 or 30 280 or 490 nmol / 24h 10 or 11 100 or 176 μg / 24 h Disorders of cortisol production Cushing 's syndrome or hypercortisolism : Excessive levels of cortisol in the blood Hypocortisolism : Insufficient levels of cortisol in the blood Disorders of cortisol production, and some consequent conditions, are : Primary hypercortisolism ( Cushing 's syndrome ) Primary hypocortisolism ( Addison 's disease, Nelson 's syndrome ) Secondary hypercortisolism ( pituitary tumor resulting in Cushing 's disease, pseudo-Cushing's syndrome ) Secondary hypocortisolism ( pituitary tumor, Sheehan 's syndrome ) Regulation The primary control of cortisol is the pituitary gland peptide, ACTH, which probably controls cortisol by controlling the movement of calcium into the cortisol - secreting target cells. ACTH is in turn controlled by the hypothalamic peptide corticotropin - releasing hormone ( CRH ), which is under nervous control. CRH acts synergistically with arginine vasopressin, angiotensin II, and epinephrine. ( In swine, which do not produce arginine vasopressin, lysine vasopressin acts synergistically with CRH. ) When activated macrophages start to secrete IL - 1, which synergistically with CRH increases ACTH, T - cells also secrete glucosteroid response modifying factor ( GRMF ), as well as IL - 1 ; both increase the amount of cortisol required to inhibit almost all the immune cells. Immune cells then assume their own regulation, but at a higher cortisol setpoint. The increase in cortisol in diarrheic calves is minimal over healthy calves, however, and falls over time. The cells do not lose all their fight - or - flight override because of interleukin - 1 's synergism with CRH. Cortisol even has a negative feedback effect on interleukin - 1 -- especially useful to treat diseases that force the hypothalamus to secrete too much CRH, such as those caused by endotoxic bacteria. The suppressor immune cells are not affected by GRMF, so the immune cells ' effective setpoint may be even higher than the setpoint for physiological processes. GRMF affects primarily the liver ( rather than the kidneys ) for some physiological processes. High - potassium media ( which stimulates aldosterone secretion in vitro ) also stimulate cortisol secretion from the fasciculata zone of canine adrenals -- unlike corticosterone, upon which potassium has no effect. Potassium loading also increases ACTH and cortisol in humans. This is probably the reason why potassium deficiency causes cortisol to decline ( as mentioned ) and causes a decrease in conversion of 11 - deoxycortisol to cortisol. This may also have a role in rheumatoid - arthritis pain ; cell potassium is always low in RA. Ascorbic acid presence, particularly in high doses has also been shown to mediate response to psychological stress and speed the decrease of the levels of circulating cortisol in the body post stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol level after treatment with ascorbic acid. Factors reducing cortisol levels Magnesium supplementation decreases serum cortisol levels after aerobic exercise, but not after resistance training. Omega - 3 fatty acids have a dose - dependent effect in slightly reducing cortisol release influenced by mental stress, suppressing the synthesis of interleukin - 1 and - 6 and enhancing the synthesis of interleukin - 2 ; the former promotes higher CRH release. Omega - 6 fatty acids, though, have an inverse effect on interleukin synthesis. Music therapy can reduce cortisol levels in certain situations. Massage therapy can reduce cortisol. Laughing, and the experience of humor, can lower cortisol levels. Soy - derived phosphatidylserine interacts with cortisol ; the correct dose, however, is unclear. Regular dancing has been shown to lead to significant decreases in salivary cortisol concentrations. Withania somnifera ( ashwagandha ) root extract High - dosage treatment with ascorbic acid ( vitamin C ) has been shown to decrease circulating cortisol levels during and shortly after the treatment period. Factors increasing cortisol levels Viral infections increase cortisol levels through activation of the HPA axis by cytokines. Caffeine may increase cortisol levels. Sleep deprivation Intense ( high VO max ) or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose ; however, cortisol declines to normal levels after eating ( i.e., restoring a neutral energy balance ) The Val / Val variation of the BDNF gene in men and the Val / Met variation in women are associated with increased salivary cortisol in a stressful situation. Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods. Subcutaneous adipose tissue regenerates cortisol from cortisone by the enzyme 11 - beta HSD1. Anorexia nervosa may be associated with increased cortisol levels. The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men. Smelling androstadienone has been found in one study to raise cortisol levels in women, as well as, in other studies, to affect mood ( see androstadienone article for details and citations ). Excessive or problematic drinking has been linked to increased cortisol levels, especially in college students. Biochemistry Biosynthesis Steroidogenesis, showing cortisol at right. Cortisol is synthesized from cholesterol. Synthesis takes place in the zona fasciculata of the adrenal cortex. ( The name cortisol is derived from cortex. ) While the adrenal cortex also produces aldosterone ( in the zona glomerulosa ) and some sex hormones ( in the zona reticularis ), cortisol is its main secretion in humans and several other species. ( However, in cattle, corticosterone levels may approach or exceed cortisol levels. ). The medulla of the adrenal gland lies under the cortex, mainly secreting the catecholamines adrenaline ( epinephrine ) and noradrenaline ( norepinephrine ) under sympathetic stimulation. The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with ACTH ; ACTH production is, in turn, stimulated by CRH, which is released by the hypothalamus. ACTH increases the concentration of cholesterol in the inner mitochondrial membrane, via regulation of the steroidogenic acute regulatory protein. It also stimulates the main rate - limiting step in cortisol synthesis, in which cholesterol is converted to pregnenolone and catalyzed by cytochrome P450SCC ( side - chain cleavage enzyme ). Metabolism Cortisol is metabolized by the 11 - beta hydroxysteroid dehydrogenase system ( 11 - beta HSD ), which consists of two enzymes : 11 - beta HSD1 and 11 - beta HSD2. 11 - beta HSD1 uses the cofactor NADPH to convert biologically inert cortisone to biologically active cortisol 11 - beta HSD2 uses the cofactor NAD+ to convert cortisol to cortisone Overall, the net effect is that 11 - beta HSD1 serves to increase the local concentrations of biologically active cortisol in a given tissue ; 11 - beta HSD2 serves to decrease local concentrations of biologically active cortisol. Cortisol is also metabolized into 5 - alpha tetrahydrocortisol ( 5 - alpha THF ) and 5 - beta tetrahydrocortisol ( 5 - beta THF ), reactions for which 5 - alpha reductase and 5 - beta reductase are the rate - limiting factors, respectively. 5 - Beta reductase is also the rate - limiting factor in the conversion of cortisone to tetrahydrocortisone. An alteration in 11 - beta HSD1 has been suggested to play a role in the pathogenesis of obesity, hypertension, and insulin resistance known as metabolic syndrome. An alteration in 11 - beta HSD2 has been implicated in essential hypertension and is known to lead to the syndrome of apparent mineralocorticoid excess ( SAME ). Chemistry Cortisol is a naturally occurring pregnane corticosteroid and is also known as 11β, 17α, 21 - trihydroxypregn - 4 - ene - 3, 20 - dione. Other animals In non-human animals, cortisol is often used as an indicator of stress and can be measured in blood, saliva, urine, hair, and faeces. See also Cortisone, a hormone Membrane glucocorticoid receptor List of corticosteroids References ^ Jump up to : Scott E ( 2011 - 09 - 22 ). `` Cortisol and Stress : How to Stay Healthy ''. About.com. Retrieved 2011 - 11 - 29. Jump up ^ Hoehn K, Marieb EN ( 2010 ). Human Anatomy & Physiology. San Francisco : Benjamin Cummings. 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Retrieved November 24, 2014. ^ Jump up to : Biochemistry Reference Ranges at Good Hope Hospital Retrieved 8 November 2009 ^ Jump up to : Derived from molar values using molar mass of 362 g / mol ^ Jump up to : Converted from μg / 24h, using molar mass of 362.460 g / mol ^ Jump up to : Görges R, Knappe G, Gerl H, Ventz M, Stahl F ( April 1999 ). `` Diagnosis of Cushing 's syndrome : re-evaluation of midnight plasma cortisol vs urinary free cortisol and low - dose dexamethasone suppression test in a large patient group ''. Journal of Endocrinological Investigation. 22 ( 4 ) : 241 -- 9. doi : 10.1007 / bf03343551. PMID 10342356. ^ Jump up to : MedlinePlus Encyclopedia Cortisol -- urine ^ Jump up to : Converted from nmol / 24h, using molar mass of 362.460 g / mol Jump up ^ `` Cushing 's Syndrome ''. National Endocrine and Metabolic Diseases Information Service ( NEMDIS ). July 2008. Retrieved 16 March 2015. These benign, or noncancerous, tumors of the pituitary gland secrete extra ACTH. 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Jump up ^ Robson PJ, Blannin AK, Walsh NP, Castell LM, Gleeson M ( February 1999 ). `` Effects of exercise intensity, duration and recovery on in vitro neutrophil function in male athletes ''. International Journal of Sports Medicine. 20 ( 2 ) : 128 -- 35. doi : 10.1055 / s - 2007 - 971106. PMID 10190775. Jump up ^ Fuqua JS, Rogol AD ( July 2013 ). `` Neuroendocrine alterations in the exercising human : implications for energy homeostasis ''. Metabolism. 62 ( 7 ) : 911 -- 21. doi : 10.1016 / j. metabol. 2013.01. 016. PMID 23415825. Cortisol has wide - ranging effects, including alterations of carbohydrate, protein, and lipid metabolism ; catabolic effects on skin, muscle, connective tissue, and bone ; immunomodulatory effects ; blood pressure and circulatory system regulation ; and effects on mood and central nervous system function. In the short term, activation of the HPA axis in response to stress is adaptive. However, long - term stress promoting chronic exposure of tissues to high cortisol concentrations becomes maladaptive... Exercise, particularly sustained aerobic activity, is a potent stimulus of cortisol secretion. The circulating concentrations of cortisol are directly proportional to the intensity of exercise as measured by oxygen uptake. As is the case for the GH / IGF - 1 and HPG axes, the HPA axis also receives many other inputs, including the light / dark cycle, feeding schedules, immune regulation, and many neurotransmitters that mediate the effects of exercise and physical and psychic stress ( 52 )... The HPA is activated by stress, whether physical ( exercise ) or psychological. Increased cortisol production, along with activation of the sympathetic nervous system, affects whole body metabolism. This is apparently part of the catabolic response of the entire organism, with the purpose of mobilizing metabolic fuels that are subsequently broken down to produce energy and to dampen the threat or perceived threat... Thus, a negative net energy balance leads to activation of the HPA axis and the circulating concomitants of the catabolic state in an attempt to keep core processes functional, realizing that the stress of exercise has no effect on cortisol and circulating metabolic substrates beyond the impact of the exercise energy expenditure on energy availability ( 60 ). Thuma et al. ( 61 ) had already made the important observation that the reported differences in cortisol levels pre - and postexercise depended on whether this difference was measured from a single pretest level or from the physiologic circadian baseline as determined in an independent session in the resting state. By this analytical technique, these investigators showed that increasing energy expenditure led to significant cortisol release. This release was apparent if they subtracted the physiologic circadian baseline from the postexercise value. Jump up ^ Shalev I, Lerer E, Israel S, Uzefovsky F, Gritsenko I, Mankuta D, Ebstein RP, Kaitz M ( April 2009 ). `` BDNF Val66Met polymorphism is associated with HPA axis reactivity to psychological stress characterized by genotype and gender interactions ''. Psychoneuroendocrinology. 34 ( 3 ) : 382 -- 8. doi : 10.1016 / j. psyneuen. 2008.09. 017. PMID 18990498. Jump up ^ Smith JL, Gropper SA, Groff JL ( 2009 ). Advanced nutrition and humanmetabolism. Belmont, CA : Wadsworth Cengage Learning. p. 247. ISBN 0 - 495 - 11657 - 2. Jump up ^ Stimson RH, Andersson J, Andrew R, Redhead DN, Karpe F, Hayes PC, Olsson T, Walker BR ( January 2009 ). `` Cortisol release from adipose tissue by 11beta - hydroxysteroid dehydrogenase type 1 in humans ''. 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Cortisol MS Spectrum Cortisol ( serum / plasma ) at Lab Tests Online Cortisol : analyte monograph -- The Association for Clinical Biochemistry and Laboratory Medicine Hormones Endocrine glands Hypothalamic - pituitary Hypothalamus GnRH TRH Dopamine CRH GHRH Somatostatin ( GHIH ) MCH Posterior pituitary Oxytocin Vasopressin Anterior pituitary FSH LH TSH Prolactin POMC CLIP ACTH MSH Endorphins Lipotropin GH Adrenal axis Adrenal cortex aldosterone cortisol cortisone DHEA DHEA - S androstenedione Adrenal medulla epinephrine norepinephrine Thyroid Thyroid hormone Calcitonin Thyroid axis Parathyroid PTH Gonadal axis Testis testosterone AMH inhibin Ovary estradiol progesterone activin and inhibin relaxin Placenta hCG HPL estrogen progesterone Pancreas glucagon insulin amylin somatostatin pancreatic polypeptide Pineal gland melatonin N, N - dimethyltryptamine 5 - methoxy - N, N - dimethyltryptamine Other Thymus Thymosins Thymosin α1 Beta thymosins Thymopoietin Thymulin Digestive system Stomach gastrin ghrelin Duodenum CCK Incretins GIP GLP - 1 secretin motilin VIP Ileum enteroglucagon peptide YY Liver / other Insulin - like growth factor IGF - 1 IGF - 2 Adipose tissue leptin adiponectin resistin Skeleton Osteocalcin Kidney renin EPO calcitriol prostaglandin Heart Natriuretic peptide ANP BNP Endogenous steroids Precursors Cholesterol 22R - Hydroxycholesterol 20α, 22R - Dihydroxycholesterol Pregnenolone 11β - Hydroxypregnenolone 17α - Hydroxypregnenolone 21 - Hydroxypregnenolone 17α, 21 - Dihydroxypregnenolone 11β, 17α, 21 - Trihydroxypregnenolone Corticosteroids Glucocorticoids 3α, 5α - Tetrahydrocorticosterone 5α - Dihydrocorticosterone 11 - Deoxycorticosterone 11 - Deoxycortisol 11 - Ketoprogesterone 21 - Deoxycortisol 21 - Deoxycortisone Corticosterone Cortisol Cortisone 17α - Hydroxypregnenolone 17α - Hydroxyprogesterone Pregnenolone Progesterone Mineralocorticoids 5α - Dihydroaldosterone 11 - Dehydrocorticosterone ( 11 - oxocorticosterone, 17 - deoxycortisone ) 11 - Deoxycortisol 11 - Deoxycorticosterone 11β - Hydroxyprogesterone ( 21 - deoxycorticosterone ) 18 - Hydroxy - 11 - deoxycorticosterone 18 - Hydroxycorticosterone 18 - Hydroxyprogesterone Aldosterone Corticosterone Cortisol Sex steroids Androgens 11 - Ketodihydrotestosterone 11 - Ketotestosterone 7β - Hydroxyepiandrosterone 11β - Hydroxyandrostenedione Adrenosterone ( 11 - ketoandrostenedione ) Androstenediol Androstenedione Androsterone Dehydroandrosterone DHEA DHEA sulfate Dihydrotestosterone Epiandrosterone Epitestosterone 16α - Hydroxyandrostenedione 16α - Hydroxy - DHEA 16α - Hydroxy - DHEA sulfate Testosterone Metabolites : 3α - Androstanediol 3α - Androstanediol glucuronide 3β - Androstanediol 3α, 5β - Androstanediol 3β, 5β - Androstanediol 5β - Androstanedione 5β - Dihydrotestosterone Androstanetriols Androstenediol sulfate Androsterone glucuronide Androsterone sulfate Dihydrotestosterone glucuronide Dihydrotestosterone sulfate Etiocholanolone Etiocholanolone glucuronide Epietiocholanolone Testosterone glucuronide Testosterone sulfate Estrogens Estranes : Estetrol Estradiol Estrone Estriol 16β - Epiestriol ( 16β - hydroxyestradiol ) 17α - Epiestriol ( 16α - hydroxy - 17α - estradiol ) 16β, 17α - Epiestriol ( 16β - hydroxy - 17α - estradiol ) 2 - Hydroxyestradiol 2 - Hydroxyestriol 2 - Hydroxyestrone 4 - Hydroxyestradiol 4 - Hydroxyestriol 4 - Hydroxyestrone 4 - Methoxyestradiol 16α - Hydroxyestrone Others : 27 - Hydroxycholesterol 3α - Androstanediol 3β - Androstanediol 4 - Androstenedione 5 - Androstenediol DHEA DHEA sulfate 7 - Keto - DHEA 7α - Hydroxy - DHEA 16α - Hydroxy - DHEA Metabolites : 2 - Methoxyestradiol 2 - Methoxyestrone 4 - Methoxyestrone Estradiol glucuronide Estradiol sulfate Estrone glucuronide Estrone sulfate Estriol glucuronide Estriol sulfate Lipoidal estradiol ( e.g., estradiol stearate, estradiol palmitate ) Progestogens Progesterone 16α - Hydroxyprogesterone 17α - Hydroxyprogesterone 20α - Dihydroprogesterone 5α - Dihydroprogesterone 11 - Deoxycorticosterone 5α - DHDOC Metabolites : Allopregnanediol Pregnanediol Pregnanediol glucuronide Pregnanetriol Neurosteroids Cholestanes : 24S - Hydroxycholesterol Cholesterol Pregnanes : 3α - Dihydroprogesterone 3β - Dihydroprogesterone 5α - Dihydrocorticosterone 5α - Dihydroprogesterone 5β - Dihydroprogesterone Allopregnanolone Corticosterone DHC DHDOC 11 - Deoxycorticosterone Epipregnanolone Isopregnanolone Pregnanolone Pregnenolone Pregnenolone sulfate Progesterone THB THDOC Androstanes : 3α - Androstanediol 3α - Androstenol 7 - Keto - DHEA 7α - Hydroxy - DHEA 7β - Hydroxy - DHEA 7α - Hydroxyepiandrosterone 7β - Hydroxyepiandrosterone Androsterone DHEA DHEA sulfate Etiocholanolone Pheromones : 3α - Androstenol 3β - Androstenol Androstadienol Androstadienone Androstenone Androsterone Estratetraenol Others Vitamin D: 7 - Dehydrocholesterol Calcidiol / Calcifediol Calcitriol Cholecalciferol Others : 7α - Hydroxycholesterol 11α - Hydroxyprogesterone 11β - Hydroxyprogesterone Cholesterol sulfate Glucocorticoid receptor modulators GR Agonists Cortisol - like and related ( 16 - unsubstituted ) : 3α, 5α - Tetrahydrocorticosterone 5α - Dihydrocorticosterone 9α - Fluorocortisone ( alfluorone ) 11 - Dehydrocorticosterone ( 11 - oxocorticosterone, 17 - deoxycortisone ) 11 - Dehydrocorticosterone acetate 11 - Deoxycorticosterone ( desoxycortone, deoxycortone, desoxycorticosterone ) Desoxycortone esters 11 - Deoxycortisol ( cortodoxone, cortexolone ) Cortifen ( cortiphen, kortifen ) Cortodoxone acetate 21 - Deoxycortisol Δ - Prednisolone Δ - Prednisolone 21 - acetate Amebucort Chloroprednisone Chloroprednisone acetate Cloprednol Cloprednol acetate Corticosterone Corticosterone acetate Corticosterone benzoate Cortisol ( hydrocortisone ) Benzodrocortisone ( hydrocortisone benzoate ) Hydrocortamate ( hydrocortisone diethylaminoacetate ) Hydrocortisone esters Cortisone Cortisone acetate Deprodone Deprodone propionate Dichlorisone Dichlorisone acetate Dichlorisone diacetate Difluprednate Endrisone ( endrysone ) Etiprednol Etiprednol dicloacetate ( etiprednol dichloroacetate ) Fludrocortisone ( fludrocortone ) Fludrocortisone acetate Fluorometholone Fluorometholone acetate Fluperolone Fluperolone acetate Fluprednisolone Fluprednisolone esters Halopredone Halopredone acetate ( halopredone diacetate ) Isoflupredone ( 9α - fluoroprednisolone ) Isoflupredone acetate Loteprednol Loteprednol etabonate Mazipredone ( depersolone ) Medrysone Methylprednisolone Methylprednisolone esters Prebediolone Prebediolone acetate Prednisolone Prednazate Prednazoline Prednicarbate ( prednisolone ethylcarbonate propionate ) Prednimustine Prednisolamate ( prednisolone diethylaminoacetate ) Prednisolone esters Prednisone Prednisone esters Pregnenolone Pregnenolone acetate Pregnenolone succinate ( pregnenolone hemisuccinate ) Resocortol Tipredane Tixocortol Butixocort ( tixocortol butyrate ) Butixocort propionate Tixocortol pivalate Methasones and related ( 16 - substituted ) : 16α - Methyl - 11 - oxoprednisolone Alclometasone Alclometasone dipropionate Amelometasone Beclometasone ( beclomethasone ) Beclometasone esters Betamethasone ( betametasone ) Betamethasone esters Cortobenzolone ( betamethasone salicylate ) Ciclometasone ( ciclomethasone, cyclomethasone ) Clobetasol Clobetasol propionate Clobetasone Clobetasone butyrate Clocortolone Clocortolone esters Cloticasone Cloticasone propionate Cormetasone ( cormethasone ) Cormetasone acetate Descinolone Desoximetasone ( desoxymethasone ) Dexamethasone ( dexametasone ) Dexamethasone esters Diflorasone Diflorasone diacetate Diflucortolone Diflucortolone pivalate Diflucortolone valerate Dimesone Dimesone acetate Doxibetasol ( doxybetasol ) Fluclorolone Flumetasone ( flumethasone ) Flumetasone acetate Flumetasone pivalate Fluocinolone Fluocortin Fluocortin butyl ( fluocortin butylate ) Fluocortolone Fluocortolone esters Fluprednidene ( fluprednylidene ) Fluprednidene acetate Fluticasone Fluticasone furoate Fluticasone propionate Halocortolone Halometasone Icometasone Icometasone enbutate ( icometasone butyrate acetate ) Isoprednidene Locicortolone ( locicortone ) Locicortolone dicibate ( locicortone dicibate ) Meclorisone Meclorisone dibutyrate Meprednisone ( methylprednisone ) Meprednisone acetate Meprednisone hydrogen succinate ( methylprednisone hemisuccinate ) Mometasone Mometasone furoate Paramethasone Paramethasone acetate Paramethasone disodium phosphate Paramethasone phosphate Prednylidene Prednylidene diethylaminoacetate Rimexolone Ticabesone Ticabesone propionate Timobesone Timobesone acetate Triamcinolone Triamcinolone diacetate Ulobetasol ( halobetasol ) Ulobetasol propionate Vamorolone Cyclic ketals ( 16, 17 - cyclized ) : Acrocinonide ( triamcinolone acroleinide ) Amcinafal ( triamcinolone pentanonide ) Amcinafide ( triamcinolone acetophenide ) Amcinonide ( triamcinolone acetate cyclopentanonide ) Budesonide Ciclesonide Cicortonide Deflazacort ( azacort ) Descinolone acetonide Desonide ( hydroxyprednisolone acetonide ) Desonide disodium phosphate Desonide pivalate Dexbudesonide Drocinonide Drocinonide phosphate Fluazacort Fluclorolone acetonide ( flucloronide ) Fludroxycortide ( flurandrenolone, flurandrenolide ) Flumoxonide Flunisolide Flunisolide acetate Fluocinolone acetonide Ciprocinonide ( fluocinolone acetonide cyclopropylcarboxylate ) Fluocinonide ( fluocinolide, fluocinolone acetonide acetate ) Procinonide ( fluocinolone acetonide propionate ) Formocortal Halcinonide Itrocinonide Rofleponide Rofleponide palmitate Tralonide Triamcinolone acetonide Flupamesone ( triamcinolone acetonide metembonate ) Triamcinolone acetonide esters Triamcinolone aminobenzal benzamidoisobutyrate ( TBI - PAB ) Triclonide Others / atypical ( other expanded steroid ring systems, homosteroids, and non-pregnane steroids ) : Cortisuzol Cortivazol Domoprednate Naflocort Nicocortonide Nicocortonide acetate Nivacortol ( nivazol ) Oxisopred RU - 28362 Non-corticosteroids with some glucocorticoid activity : 15β - Hydroxycyproterone acetate 17α - Hydroxyprogesterone Chlormadinone acetate Cyproterone Cyproterone acetate Delmadinone acetate Desogestrel Flugestone Flugestone acetate ( flurogestone acetate ) Fluoxymesterone Gestodene Medrogestone Medroxyprogesterone acetate Megestrol acetate Metribolone Norgestomet Osaterone acetate Progesterone Promegestone Quingestrone Segesterone acetate ( nestorone ) Tetrahydrogestrinone Nonsteroidal glucocorticoids : AZD - 5423 GSK - 9027 Mixed ( SEGRMs ) Dagrocorat Fosdagrocorat Mapracorat Antagonists 7α - Hydroxy - DHEA 17α - Methylprogesterone Aglepristone Asoprisnil Asoprisnil ecamate C108297 C113176 CORT - 108297 Cyproterone acetate Guggulsterone Ketoconazole Lilopristone LLY - 2707 Metapristone ( RU - 42633 ) Miconazole Mifepristone ( RU - 486 ) Onapristone ORG - 34116 ORG - 34517 ( SCH - 900636 ) ORG - 34850 Pregnenolone 16α - carbonitrile Relacorilant ( CORT - 125134 ) RTI 3021 -- 012 RTI 3021 -- 022 Telapristone Tibolone Toripristone Ulipristal acetate Others Antisense oligonucleotides : IONIS - GCCR ( ISIS - 426115 ) See also Receptor / signaling modulators Glucocorticoids and antiglucocorticoids Mineralocorticoid receptor modulators List of corticosteroids Mineralocorticoid receptor modulators MR Agonists 11 - Dehydrocorticosterone ( 11 - oxocorticosterone, 17 - deoxycortisone ) 11 - Dehydrocorticosterone acetate 11 - Deoxycorticosterone ( desoxycortone, deoxycortone, desoxycorticosterone ) Desoxycortone esters 11 - Deoxycortisol ( cortodoxone, cortexolone ) Cortifen ( cortiphen, kortifen ) Cortodoxone acetate 11β - Hydroxyprogesterone 16α, 18 - Dihydroxy - 11 - deoxycorticosterone 17α - Hydroxyaldosterone 18 - Hydroxy - 11 - deoxycorticosterone 19 - Norprogesterone Aldosterone Corticosterone Corticosterone acetate Corticosterone benzoate Cortisol ( hydrocortisone ) Benzodrocortisone ( hydrocortisone benzoate ) Hydrocortamate ( hydrocortisone diethylaminoacetate ) Hydrocortisone esters Cortisone Cortisone acetate Fludrocortisone ( fludrocortone ) Fludrocortisone acetate Mometasone Mometasone furoate Prednisolone Prednazate Prednazoline Prednicarbate ( prednisolone ethylcarbonate propionate ) Prednimustine Prednisolamate ( prednisolone diethylaminoacetate ) Prednisolone esters Prednisone Prednisone esters Antagonists Steroidal : 6β - Hydroxy - 7α - thiomethylspironolactone 7α - Thiomethylspironolactone ( SC - 26519 ) 7α - Thioprogesterone ( SC - 8365 ) 7α - Thiospironolactone ( SC - 24813 ) 16α - Hydroxyprogesterone 17α - Hydroxyprogesterone 18 - Deoxyaldosterone Canrenoate potassium ( potassium canrenoate ) Canrenoic acid ( canrenoate ) Canrenone ( canrenoate y - lactone ) Dicirenone Dimethisterone Drospirenone Dydrogesterone Eplerenone Gestodene Guggulsterone Medrogestone Mespirenone Mexrenoate potassium Mexrenoic acid ( mexrenoate ) Mexrenone Oxprenoic acid ( oxprenoate ) Oxprenoate potassium ( RU - 28318 ) Pregnenolone Progesterone Prorenoate potassium Prorenoic acid ( prorenoate ) Prorenone RO - 14 - 9012 RU - 26752 SC - 5233 ( spirolactone ) SC - 8109 SC - 11927 ( CS - 1 ) SC - 19886 SC - 27169 Spirorenone Spironolactone Spiroxasone Tibolone Trimegestone ZK - 91587 ZK - 97894 Nonsteroidal : Amlodipine Apararenone Benidipine BR - 4628 Esaxerenone Felodipine Finerenone Nifedipine Nimodipine Nitrendipine PF - 03882845 SM - 368229 See also Receptor / signaling modulators Mineralocorticoids and antimineralocorticoids Glucocorticoid receptor modulators List of corticosteroids LCCN : sh85063384 GND : 4160902 - 5 Retrieved from `` https://en.wikipedia.org/w/index.php?title=Cortisol&oldid=821809039 '' Categories : Anxiety Glucocorticoids Otologicals Pregnanes Stress Hidden categories : All articles lacking reliable references Articles lacking reliable references from November 2012 CS1 German - language sources ( de ) CS1 maint : Uses editors parameter CS1 maint : Multiple names : authors list Wikipedia introduction cleanup from November 2016 All pages needing cleanup Articles covered by WikiProject Wikify from November 2016 All articles covered by WikiProject Wikify Use dmy dates from December 2017 Use American English from December 2017 All Wikipedia articles written in American English Articles without InChI source ECHA InfoCard ID from Wikidata Articles containing unverified chemical infoboxes Wikipedia articles needing clarification from March 2015 All articles with unsourced statements Articles with unsourced statements from March 2015 Wikipedia articles with LCCN identifiers Wikipedia articles with GND identifiers Talk Contents About Wikipedia تۆرکجه বাংলা Български Català Čeština Deutsch Ελληνικά Español Esperanto Euskara فارسی Français Gaeilge Galego 한국어 Հայերեն Hrvatski Bahasa Indonesia Italiano עברית Basa Jawa Latviešu Lietuvių Magyar Македонски Nederlands 日本 語 Norsk Occitan Polski Português Română Русский Scots Simple English Slovenčina Slovenščina کوردی Српски / srpski Srpskohrvatski / српскохрватски Suomi Svenska தமிழ் Türkçe Українська Tiếng Việt 中文 Edit links This page was last edited on 22 January 2018, at 19 : 29. 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Question: where does cortisol come from in the body
Answer: the zona fasciculata of the adrenal cortex within the adrenal gland; zona fasciculata of the adrenal cortex within the adrenal gland; the zona fasciculata of the adrenal cortex within the adrenal gland; the zona fasciculata of the adrenal cortex within the adrenal gland