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11β-Hydroxysteroid dehydrogenase

May 04, 2024

11β-Hydroxysteroid dehydrogenase (HSD-11β or 11β-HSD) enzymes catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa,[1] thus regulating the access of glucocorticoids to the steroid receptors.

The human genome encodes two distinct HSD-11β isozymes (HSD-11β Type 1 and HSD-11β Type 2) on distinct genes. The dehydrogenase activity of a HSD-11β converts a 11beta-hydroxysteroid to the corresponding 11-oxosteroid by reducing NADP+ or NAD+. HSD-11βs are part of the larger class of oxidoreductases and HSD-11β Type 1 has oxidoreductase activity (the reverse of dehydrogenase activity). HSD-11βs participate in c21-steroid hormone metabolism and androgen and estrogen metabolism.

Structural studies edit

Several structures for HSD-11β Type 1 have been solved to date with various mutations and inhibitors. There are no known structures for HSD-11β Type 2.

Function edit

 
Cortisol. Note the OH at the 11 position on ring C. (The other differences between the diagrams are not of consequence.)
 
Cortisone

Cortisol, a glucocorticoid, binds the glucocorticoid receptor. However, because of its molecular similarity to aldosterone it also binds the mineralcorticoid receptor at higher concentrations. Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor; however, there is vastly more cortisol in circulation than aldosterone. To prevent overstimulation of the mineralocorticoid receptor by cortisol, HSD-11βs convert the biologically active cortisol to the inactive cortisone, which can no longer bind the mineralocorticoid receptor.[2] HSD-11βs co-localizes with intracellular adrenal steroid receptors. Licorice, which contains glycyrrhizinic acid and enoxolone, can inhibit HSD-11β and lead to the apparent mineralocorticoid excess syndrome. Cortisol levels consequently rise, and cortisol binding to the mineralocorticoid receptor produces clinical signs and symptoms of hypokalemia, alkalosis and hypertension (i.e., mineralocorticoid excess).

Isozymes edit

In humans, there are two 11β-HSD isozymes:[3][4][5]

Enzyme Gene Cofactor Dependence Expression Reactions catalyzed
HSD-11β Type 1 HSD11B1 NADPH-dependent Highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. Reduces cortisone to cortisol.
HSD-11β Type 2 HSD11B2 NAD+-dependent Expressed in aldosterone-selective tissues, including kidneys, liver, lungs, colon, salivary glands, HSD2 neurons and placenta. Oxidizes cortisol to cortisone.

Clinical Application edit

HSD-11βs are enzymes involved in steroid hormone physiology. HSD-11β Type 1 is found in metabolic tissues targeted by glucocorticoids and converts cortisone to active cortisol.[6] HSD-11β Type 1 acts as a reductase producing active cortisol and the amplification of glucocorticoids. This enzyme is most abundant in the liver but can be found in most tissues in the body. HSD11B- Type 1 amplifies glucocorticoid concentrations in the liver and adipose tissue, glucocorticoid excess induces obesity with other features such as hypertension and diabetes mellitus.[7]

HSD-11β Type 2 is expressed by aldosterone-selective tissues and protects the mineralocorticoid receptor from the activation by cortisol by converting it to cortisone using the enzyme 11-Oxoreductase. HSD-11β Type 2 protects tissues from continuous activation by decreasing local cortisol levels and preventing 11-Oxoreductase from activating.[6] In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension.[8]

Since the main functions of HSD-11βs are for the regulation of glucocorticoids, the two isozymes are linked to various overstimulation or depletion of glucocorticosteroids that result in chemical imbalances in the human body. The effects of the enzyme as it relates to specific body functions and its associated disorders are listed below.

Effect of Hyperlipidemia on 11β-hydroxysteroid-dehydrogenase

Hyperlipidemia has a great effect on 11β-hydroxysteroid-dehydrogenase.[9] Glucocorticoid is dependent on Glucocorticoid plasma concentration, cellular glucocorticoid receptor expression and the pre-receptor hormone metabolism that is catalyzed by 11β-HSD.[9] There are two types of 11β-Hydroxysteroid dehydrogenases that control cortisol concentration: HSD-11β Type 1 and HSD-11β Type 2.[9] HSD-11β Type 1 is responsible for converting cortisone to cortisol by acting as an oxo-reductase because it is NADP(H) dependent, while HSD-11β Type 2 inactivates cortisol to cortisone via NAD.[9] 10-d hyperlipidemia increases the HSD-11β Type 1 expression in visceral and subcutaneous adipose tissues.[9] Hyperlipidemia decreases HSD-11β Type 2 expression in the liver and adipose tissue.[9] Hyperlipidemia has a great influence on HSD-11β Type 1 and HSD-11β Type 2.[9] This demonstrates that there is likely a relationship between hyperlipidemia and cortisol metabolism.[9] Cushing's Disease, synonymous with hypercortisolism, involves overwhelming the cortisol-neutralizing ability of 11β-HSD2 with high concentrations of cortisol.[10] This allows cortisol to outcompete aldosterone and bind to mineralocorticoid receptors, resulting in the activation of several pathways that increase blood pressure.[11]

Activity of HSD-11βs in organs edit

HSD-11βs are active in organs and in the adrenal gland.[12] The two isoenzymes take on various duties.[12] During an active state, HSD-11β promotes the increase in glucocorticoids in the hepatocytes and also enhances gluconeogenesis.[12] The type 2 isozyme converts active glucocorticoid hormones to inactive metabolites in target tissues such as kidney, salivary glands, intestines, etc.[12] The activation of the two isozymes of HSD-11β in the kidneys and liver triggers the extra-adrenal formation in alloxan diabetes, which affiliates with the reduction in the synthesis of glucocorticoid hormones in the adrenal glands.[12] The extra-adrenal formation leads to the increased local formation of corticosterone in the liver and has a high activity of reactions with gluconeogenesis.[12] These gluconeogenesis reactions add to the continued metabolic disorders similar to that of diabetes.[12] Thus HSD-11β Type 1 can serve as a potential treatment agents for diabetes, obesity, and metabolic syndrome due to increasing local corticosterone.[12]

Involvement in the brain edit

HSD-11βs are expressed in the central nervous system of aged individuals.[13] It is essential in Hypothalamo-Pituitary-Adrenal Axis function.[13] HSD-11βs also partakes involvement in the decline of conscious intellectual activity due to aging.[13] The enzyme also contributes to central effects are also during the development stages.[13] For instance, the HSD-11βs Type 2shows frequently in fetal tissues such as a newborn's brain and placenta.[13] If there is an absence or decline in HSD-11βs Type 2 in the fetus tissues, there are negative developmental consequences such as anxiety.[13]

HSD-11βs are partly responsible for intracellular metabolism that determine the operation of glucocorticoids within cells.[13] Glucocorticoids impact the brain development and ultimately the function of the central nervous system.[13] So much so, that if there is a surplus or scant amounts of it, the consequences are deformities throughout one's entire life.[13] HSD-11β Type 1 is responsible for activating glucocorticoids while HSD-11β Type 2 is responsible for deactivating them.[13] The consequences for HSD-11β Type 1 activating glucocorticoids is that there is a decline in cognition especially as one ages.[13] Contrarily, the effects of HSD-11β Type 2 occur during development.[13] Some consequences of a high expression HSD-11β Type 2 are anxiety and cardiometabolic disorders, both of which are part of the early age glucocorticoid programming.[13]

Involvement in Preterm Births edit

Infants born underweight are susceptible to having metabolic disease throughout their lives.[14] The presence of glucocorticoids has contributed to the relatively low infant birth weight.[14] A decrease in HSD-11β Type 2 in the placenta can lead to infant restriction in growth, specifically during the first 12 months of an infant's life.[14] The reason for this is because the HSD-11β Type 2 is meant to be expressed in high quantities in the placenta, This is so because the enzymes secure the fetus from exposure to increased levels of glucocorticoids, which are linked to underweight newborns.[14]

See also edit

References edit

  1. ^ Seckl JR, Walker BR (April 2001). "Minireview: 11beta-hydroxysteroid dehydrogenase type 1- a tissue-specific amplifier of glucocorticoid action". Endocrinology. 142 (4): 1371–6. doi:10.1210/en.142.4.1371. PMID 11250914.
  2. ^ Hall, John E. (2021). Guyton and Hall textbook of medical physiology. Michael E. Hall (14th ed.). Philadelphia, PA: Elsevier. p. 958. ISBN 978-0-323-59712-8. OCLC 1129099861.
  3. ^ Stewart PM, Krozowski ZS (1999). "11 beta-Hydroxysteroid dehydrogenase". Vitamins and Hormones. 57: 249–324. doi:10.1016/S0083-6729(08)60646-9. ISBN 978-0-12-709857-9. PMID 10232052.
  4. ^ Seckl JR (January 1997). "11beta-Hydroxysteroid dehydrogenase in the brain: a novel regulator of glucocorticoid action?". Front Neuroendocrinol. 18 (1): 49–99. doi:10.1006/frne.1996.0143. PMID 9000459. S2CID 46477930.
  5. ^ Anagnostis P, Athyros VG, Tziomalos K, Karagiannis A, Mikhailidis DP (2009). "Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis". The Journal of Clinical Endocrinology and Metabolism. 94 (8): 2692–2701. doi:10.1210/jc.2009-0370. PMID 19470627.
  6. ^ a b Lindsay, Kaitlin. . kaitlinlindsay.com. Archived from the original on 2019-04-22.
  7. ^ Hughes, Katherine A; Webster, Scott P; Walker, Brian R (2008-03-25). "11-Beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitors in Type 2 diabetes mellitus and obesity". Expert Opinion on Investigational Drugs. 17 (4): 481–496. doi:10.1517/13543784.17.4.481. ISSN 1354-3784. PMID 18363514. S2CID 72573025.
  8. ^ "HSD11B2 Gene". www.greencards.org.
  9. ^ a b c d e f g h Sieber-Ruckstuhl, Nadja S.; Zini, Eric; Osto, Melanie; Franchini, Marco; Boretti, Felicitas S.; Meli, Marina L.; Sigrist, Brigitte; Lutz, Thomas A.; Reusch, Claudia E. (November 2010). (PDF). Domestic Animal Endocrinology. 39 (4): 222–230. doi:10.1016/j.domaniend.2010.06.003. ISSN 0739-7240. PMID 20688460. Archived from the original (PDF) on 2018-07-19. Retrieved 2019-12-11.
  10. ^ Cicala, Maria Verena; Mantero, Franco (2010). "Hypertension in Cushing's Syndrome: From Pathogenesis to Treatment". Neuroendocrinology. 92 (Suppl. 1): 44–49. doi:10.1159/000314315. ISSN 0028-3835. PMID 20829617.
  11. ^ Fuller Peter J.; Young Morag J. (2005-12-01). "Mechanisms of Mineralocorticoid Action". Hypertension. 46 (6): 1227–1235. CiteSeerX 10.1.1.319.6620. doi:10.1161/01.HYP.0000193502.77417.17. PMID 16286565. S2CID 14749847.
  12. ^ a b c d e f g h Cherkasova, O. P.; Selyatitskaya, V. G.; Pal'chikova, N. A.; Kuznetsova, N. V. (2014-11-29). "Activity of 11β-Hydroxysteroid Dehydrogenase in the Adrenal Glands, Liver, and Kidneys of Rats with Experimental Diabetes". Bulletin of Experimental Biology and Medicine. 158 (2): 185–187. doi:10.1007/s10517-014-2718-3. ISSN 0007-4888. PMID 25430643. S2CID 24224772.
  13. ^ a b c d e f g h i j k l m Wyrwoll, Caitlin S.; Holmes, Megan C.; Seckl, Jonathan R. (August 2011). "11β-Hydroxysteroid dehydrogenases and the brain: From zero to hero, a decade of progress". Frontiers in Neuroendocrinology. 32 (3): 265–286. doi:10.1016/j.yfrne.2010.12.001. ISSN 0091-3022. PMC 3149101. PMID 21144857.
  14. ^ a b c d Rogers, Samantha L.; Hughes, Beverly A.; Jones, Christopher A.; Freedman, Lauren; Smart, Katherine; Taylor, Norman; Stewart, Paul M.; Shackleton, Cedric H. L.; Krone, Nils P. (May 2014). "Diminished 11β-Hydroxysteroid Dehydrogenase Type 2 Activity Is Associated With Decreased Weight and Weight Gain Across the First Year of Life". The Journal of Clinical Endocrinology & Metabolism. 99 (5): E821–E831. doi:10.1210/jc.2013-3254. hdl:2299/14902. ISSN 0021-972X. PMID 24517145.
  • Agarwal AK, Monder C, Eckstein B, White PC (1989). "Cloning and expression of rat cDNA encoding corticosteroid 11 beta-dehydrogenase". J. Biol. Chem. 264 (32): 18939–43. doi:10.1016/S0021-9258(19)47248-7. PMID 2808402.
  • Bush IE, Hunter SA, Meigs RA (1968). "Metabolism of 11-oxygenated steroids. Metabolism in vitro by preparations of liver". Biochem. J. 107 (2): 239–58. doi:10.1042/bj1070239. PMC 1198650. PMID 4384445.
  • Lakshmi V, Monder C (1988). "Purification and characterization of the corticosteroid 11 beta-dehydrogenase component of the rat liver 11 beta-hydroxysteroid dehydrogenase complex". Endocrinology. 123 (5): 2390–8. doi:10.1210/endo-123-5-2390. PMID 3139396.
  • Phillips DM, Lakshmi V, Monder C (1989). "Corticosteroid 11 beta-dehydrogenase in rat testis". Endocrinology. 125 (1): 209–16. doi:10.1210/endo-125-1-209. PMID 2661206.

External links edit

May 04, 2024
11β, hydroxysteroid, dehydrogenase, 11β, 11β, enzymes, catalyze, conversion, inert, keto, products, cortisone, active, cortisol, vice, versa, thus, regulating, access, glucocorticoids, steroid, receptors, human, genome, encodes, distinct, 11β, isozymes, 11β, t. 11b Hydroxysteroid dehydrogenase HSD 11b or 11b HSD enzymes catalyze the conversion of inert 11 keto products cortisone to active cortisol or vice versa 1 thus regulating the access of glucocorticoids to the steroid receptors The human genome encodes two distinct HSD 11b isozymes HSD 11b Type 1 and HSD 11b Type 2 on distinct genes The dehydrogenase activity of a HSD 11b converts a 11beta hydroxysteroid to the corresponding 11 oxosteroid by reducing NADP or NAD HSD 11bs are part of the larger class of oxidoreductases and HSD 11b Type 1 has oxidoreductase activity the reverse of dehydrogenase activity HSD 11bs participate in c21 steroid hormone metabolism and androgen and estrogen metabolism Contents 1 Structural studies 2 Function 3 Isozymes 4 Clinical Application 4 1 Activity of HSD 11bs in organs 4 1 1 Involvement in the brain 4 2 Involvement in Preterm Births 5 See also 6 References 7 External linksStructural studies editSeveral structures for HSD 11b Type 1 have been solved to date with various mutations and inhibitors There are no known structures for HSD 11b Type 2 Function edit nbsp Cortisol Note the OH at the 11 position on ring C The other differences between the diagrams are not of consequence nbsp Cortisone Cortisol a glucocorticoid binds the glucocorticoid receptor However because of its molecular similarity to aldosterone it also binds the mineralcorticoid receptor at higher concentrations Both aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor however there is vastly more cortisol in circulation than aldosterone To prevent overstimulation of the mineralocorticoid receptor by cortisol HSD 11bs convert the biologically active cortisol to the inactive cortisone which can no longer bind the mineralocorticoid receptor 2 HSD 11bs co localizes with intracellular adrenal steroid receptors Licorice which contains glycyrrhizinic acid and enoxolone can inhibit HSD 11b and lead to the apparent mineralocorticoid excess syndrome Cortisol levels consequently rise and cortisol binding to the mineralocorticoid receptor produces clinical signs and symptoms of hypokalemia alkalosis and hypertension i e mineralocorticoid excess Isozymes editIn humans there are two 11b HSD isozymes 3 4 5 Enzyme Gene Cofactor Dependence Expression Reactions catalyzed HSD 11b Type 1 HSD11B1 NADPH dependent Highly expressed in key metabolic tissues including liver adipose tissue and the central nervous system Reduces cortisone to cortisol HSD 11b Type 2 HSD11B2 NAD dependent Expressed in aldosterone selective tissues including kidneys liver lungs colon salivary glands HSD2 neurons and placenta Oxidizes cortisol to cortisone Clinical Application editHSD 11bs are enzymes involved in steroid hormone physiology HSD 11b Type 1 is found in metabolic tissues targeted by glucocorticoids and converts cortisone to active cortisol 6 HSD 11b Type 1 acts as a reductase producing active cortisol and the amplification of glucocorticoids This enzyme is most abundant in the liver but can be found in most tissues in the body HSD11B Type 1 amplifies glucocorticoid concentrations in the liver and adipose tissue glucocorticoid excess induces obesity with other features such as hypertension and diabetes mellitus 7 HSD 11b Type 2 is expressed by aldosterone selective tissues and protects the mineralocorticoid receptor from the activation by cortisol by converting it to cortisone using the enzyme 11 Oxoreductase HSD 11b Type 2 protects tissues from continuous activation by decreasing local cortisol levels and preventing 11 Oxoreductase from activating 6 In tissues that do not express the mineralocorticoid receptor such as the placenta and testis it protects cells from the growth inhibiting and or pro apoptotic effects of cortisol particularly during embryonic development Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension 8 Since the main functions of HSD 11bs are for the regulation of glucocorticoids the two isozymes are linked to various overstimulation or depletion of glucocorticosteroids that result in chemical imbalances in the human body The effects of the enzyme as it relates to specific body functions and its associated disorders are listed below Effect of Hyperlipidemia on 11b hydroxysteroid dehydrogenaseHyperlipidemia has a great effect on 11b hydroxysteroid dehydrogenase 9 Glucocorticoid is dependent on Glucocorticoid plasma concentration cellular glucocorticoid receptor expression and the pre receptor hormone metabolism that is catalyzed by 11b HSD 9 There are two types of 11b Hydroxysteroid dehydrogenases that control cortisol concentration HSD 11b Type 1 and HSD 11b Type 2 9 HSD 11b Type 1 is responsible for converting cortisone to cortisol by acting as an oxo reductase because it is NADP H dependent while HSD 11b Type 2 inactivates cortisol to cortisone via NAD 9 10 d hyperlipidemia increases the HSD 11b Type 1 expression in visceral and subcutaneous adipose tissues 9 Hyperlipidemia decreases HSD 11b Type 2 expression in the liver and adipose tissue 9 Hyperlipidemia has a great influence on HSD 11b Type 1 and HSD 11b Type 2 9 This demonstrates that there is likely a relationship between hyperlipidemia and cortisol metabolism 9 Cushing s Disease synonymous with hypercortisolism involves overwhelming the cortisol neutralizing ability of 11b HSD2 with high concentrations of cortisol 10 This allows cortisol to outcompete aldosterone and bind to mineralocorticoid receptors resulting in the activation of several pathways that increase blood pressure 11 Activity of HSD 11bs in organs edit HSD 11bs are active in organs and in the adrenal gland 12 The two isoenzymes take on various duties 12 During an active state HSD 11b promotes the increase in glucocorticoids in the hepatocytes and also enhances gluconeogenesis 12 The type 2 isozyme converts active glucocorticoid hormones to inactive metabolites in target tissues such as kidney salivary glands intestines etc 12 The activation of the two isozymes of HSD 11b in the kidneys and liver triggers the extra adrenal formation in alloxan diabetes which affiliates with the reduction in the synthesis of glucocorticoid hormones in the adrenal glands 12 The extra adrenal formation leads to the increased local formation of corticosterone in the liver and has a high activity of reactions with gluconeogenesis 12 These gluconeogenesis reactions add to the continued metabolic disorders similar to that of diabetes 12 Thus HSD 11b Type 1 can serve as a potential treatment agents for diabetes obesity and metabolic syndrome due to increasing local corticosterone 12 Involvement in the brain edit HSD 11bs are expressed in the central nervous system of aged individuals 13 It is essential in Hypothalamo Pituitary Adrenal Axis function 13 HSD 11bs also partakes involvement in the decline of conscious intellectual activity due to aging 13 The enzyme also contributes to central effects are also during the development stages 13 For instance the HSD 11bs Type 2shows frequently in fetal tissues such as a newborn s brain and placenta 13 If there is an absence or decline in HSD 11bs Type 2 in the fetus tissues there are negative developmental consequences such as anxiety 13 HSD 11bs are partly responsible for intracellular metabolism that determine the operation of glucocorticoids within cells 13 Glucocorticoids impact the brain development and ultimately the function of the central nervous system 13 So much so that if there is a surplus or scant amounts of it the consequences are deformities throughout one s entire life 13 HSD 11b Type 1 is responsible for activating glucocorticoids while HSD 11b Type 2 is responsible for deactivating them 13 The consequences for HSD 11b Type 1 activating glucocorticoids is that there is a decline in cognition especially as one ages 13 Contrarily the effects of HSD 11b Type 2 occur during development 13 Some consequences of a high expression HSD 11b Type 2 are anxiety and cardiometabolic disorders both of which are part of the early age glucocorticoid programming 13 Involvement in Preterm Births edit Infants born underweight are susceptible to having metabolic disease throughout their lives 14 The presence of glucocorticoids has contributed to the relatively low infant birth weight 14 A decrease in HSD 11b Type 2 in the placenta can lead to infant restriction in growth specifically during the first 12 months of an infant s life 14 The reason for this is because the HSD 11b Type 2 is meant to be expressed in high quantities in the placenta This is so because the enzymes secure the fetus from exposure to increased levels of glucocorticoids which are linked to underweight newborns 14 See also editSteroidogenic enzyme 11b Hydroxysteroid dehydrogenase type 1 11b Hydroxysteroid dehydrogenase type 2 Cortisone reductase deficiencyReferences edit Seckl JR Walker BR April 2001 Minireview 11beta hydroxysteroid dehydrogenase type 1 a tissue specific amplifier of glucocorticoid action Endocrinology 142 4 1371 6 doi 10 1210 en 142 4 1371 PMID 11250914 Hall John E 2021 Guyton and Hall textbook of medical physiology Michael E Hall 14th ed Philadelphia PA Elsevier p 958 ISBN 978 0 323 59712 8 OCLC 1129099861 Stewart PM Krozowski ZS 1999 11 beta Hydroxysteroid dehydrogenase Vitamins and Hormones 57 249 324 doi 10 1016 S0083 6729 08 60646 9 ISBN 978 0 12 709857 9 PMID 10232052 Seckl JR January 1997 11beta Hydroxysteroid dehydrogenase in the brain a novel regulator of glucocorticoid action Front Neuroendocrinol 18 1 49 99 doi 10 1006 frne 1996 0143 PMID 9000459 S2CID 46477930 Anagnostis P Athyros VG Tziomalos K Karagiannis A Mikhailidis DP 2009 Clinical review The pathogenetic role of cortisol in the metabolic syndrome a hypothesis The Journal of Clinical Endocrinology and Metabolism 94 8 2692 2701 doi 10 1210 jc 2009 0370 PMID 19470627 a b Lindsay Kaitlin Kaitlin Lindsay Medical amp Scientific Illustration kaitlinlindsay com Archived from the original on 2019 04 22 Hughes Katherine A Webster Scott P Walker Brian R 2008 03 25 11 Beta hydroxysteroid dehydrogenase type 1 11b HSD1 inhibitors in Type 2 diabetes mellitus and obesity Expert Opinion on Investigational Drugs 17 4 481 496 doi 10 1517 13543784 17 4 481 ISSN 1354 3784 PMID 18363514 S2CID 72573025 HSD11B2 Gene www greencards org a b c d e f g h Sieber Ruckstuhl Nadja S Zini Eric Osto Melanie Franchini Marco Boretti Felicitas S Meli Marina L Sigrist Brigitte Lutz Thomas A Reusch Claudia E November 2010 Effect of hyperlipidemia on 11b hydroxysteroid dehydrogenase glucocorticoid receptor and leptin expression in insulin sensitive tissues of cats PDF Domestic Animal Endocrinology 39 4 222 230 doi 10 1016 j domaniend 2010 06 003 ISSN 0739 7240 PMID 20688460 Archived from the original PDF on 2018 07 19 Retrieved 2019 12 11 Cicala Maria Verena Mantero Franco 2010 Hypertension in Cushing s Syndrome From Pathogenesis to Treatment Neuroendocrinology 92 Suppl 1 44 49 doi 10 1159 000314315 ISSN 0028 3835 PMID 20829617 Fuller Peter J Young Morag J 2005 12 01 Mechanisms of Mineralocorticoid Action Hypertension 46 6 1227 1235 CiteSeerX 10 1 1 319 6620 doi 10 1161 01 HYP 0000193502 77417 17 PMID 16286565 S2CID 14749847 a b c d e f g h Cherkasova O P Selyatitskaya V G Pal chikova N A Kuznetsova N V 2014 11 29 Activity of 11b Hydroxysteroid Dehydrogenase in the Adrenal Glands Liver and Kidneys of Rats with Experimental Diabetes Bulletin of Experimental Biology and Medicine 158 2 185 187 doi 10 1007 s10517 014 2718 3 ISSN 0007 4888 PMID 25430643 S2CID 24224772 a b c d e f g h i j k l m Wyrwoll Caitlin S Holmes Megan C Seckl Jonathan R August 2011 11b Hydroxysteroid dehydrogenases and the brain From zero to hero a decade of progress Frontiers in Neuroendocrinology 32 3 265 286 doi 10 1016 j yfrne 2010 12 001 ISSN 0091 3022 PMC 3149101 PMID 21144857 a b c d Rogers Samantha L Hughes Beverly A Jones Christopher A Freedman Lauren Smart Katherine Taylor Norman Stewart Paul M Shackleton Cedric H L Krone Nils P May 2014 Diminished 11b Hydroxysteroid Dehydrogenase Type 2 Activity Is Associated With Decreased Weight and Weight Gain Across the First Year of Life The Journal of Clinical Endocrinology amp Metabolism 99 5 E821 E831 doi 10 1210 jc 2013 3254 hdl 2299 14902 ISSN 0021 972X PMID 24517145 Agarwal AK Monder C Eckstein B White PC 1989 Cloning and expression of rat cDNA encoding corticosteroid 11 beta dehydrogenase J Biol Chem 264 32 18939 43 doi 10 1016 S0021 9258 19 47248 7 PMID 2808402 Bush IE Hunter SA Meigs RA 1968 Metabolism of 11 oxygenated steroids Metabolism in vitro by preparations of liver Biochem J 107 2 239 58 doi 10 1042 bj1070239 PMC 1198650 PMID 4384445 Lakshmi V Monder C 1988 Purification and characterization of the corticosteroid 11 beta dehydrogenase component of the rat liver 11 beta hydroxysteroid dehydrogenase complex Endocrinology 123 5 2390 8 doi 10 1210 endo 123 5 2390 PMID 3139396 Phillips DM Lakshmi V Monder C 1989 Corticosteroid 11 beta dehydrogenase in rat testis Endocrinology 125 1 209 16 doi 10 1210 endo 125 1 209 PMID 2661206 External links edit11 beta Hydroxysteroid Dehydrogenases at the U S National Library of Medicine Medical Subject Headings MeSH Portal nbsp Biology Retrieved from https en wikipedia org w index php title 11b Hydroxysteroid dehydrogenase amp oldid 1214424098, wikipedia, wiki, book, books, library,

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