Targeting the pre-receptor metabolism of cortisol as a novel therapy in obesity and diabetes

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@article{775fdd5e8b44460a8bcbadb73de5e41a,
title = "Targeting the pre-receptor metabolism of cortisol as a novel therapy in obesity and diabetes",
abstract = "Due to its impact upon health and the economy, the mechanisms that contribute to the pathogenesis of obesity and the metabolic syndrome are under intense scrutiny. In addition to understanding the pathogenesis of disease it is important to design and trial novel therapies. Patients with cortisol excess. Cushing's syndrome, have a phenotype similar to that of the metabolic syndrome and as a result there is much interest the manipulation of glucocorticoid (GC) action as a therapeutic strategy. Intracellular GC levels are regulated by 11 beta-hydroxysteriod dehydrogenase (11 beta-HSD1) which converts inactive cortisone to cortisol, thereby increasing local GC action. There is an abundance of data implicating 11 beta-HSD1 in the pathogenesis of obesity, type 2 diabetes and the metabolic syndrome and 11 beta-HSD1 is an attractive therapeutic target. Selective 11 beta-HSD1 inhibitors, which do not act upon 11 beta-HSD2 (which inactivates cortisol to cortisone) are in development. So far studies have primarily been carried out in rodents, with results showing improvements in metabolic profile. Data are now beginning to emerge from human studies and the results are promising. (c) 2010 Elsevier Ltd. All rights reserved.",
keywords = "Obesity, 11 beta-Hydroxysteroid dehydrogenase, Glucocorticoids, Diabetes",
author = "Laura Gathercole and Paul Stewart",
year = "2010",
month = oct
day = "1",
doi = "10.1016/j.jsbmb.2010.03.060",
language = "English",
volume = "122",
pages = "21--27",
journal = "The Journal of Steroid Biochemistry and Molecular Biology",
issn = "0960-0760",
publisher = "Elsevier",
number = "1-3",

}

RIS

TY - JOUR

T1 - Targeting the pre-receptor metabolism of cortisol as a novel therapy in obesity and diabetes

AU - Gathercole, Laura

AU - Stewart, Paul

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Due to its impact upon health and the economy, the mechanisms that contribute to the pathogenesis of obesity and the metabolic syndrome are under intense scrutiny. In addition to understanding the pathogenesis of disease it is important to design and trial novel therapies. Patients with cortisol excess. Cushing's syndrome, have a phenotype similar to that of the metabolic syndrome and as a result there is much interest the manipulation of glucocorticoid (GC) action as a therapeutic strategy. Intracellular GC levels are regulated by 11 beta-hydroxysteriod dehydrogenase (11 beta-HSD1) which converts inactive cortisone to cortisol, thereby increasing local GC action. There is an abundance of data implicating 11 beta-HSD1 in the pathogenesis of obesity, type 2 diabetes and the metabolic syndrome and 11 beta-HSD1 is an attractive therapeutic target. Selective 11 beta-HSD1 inhibitors, which do not act upon 11 beta-HSD2 (which inactivates cortisol to cortisone) are in development. So far studies have primarily been carried out in rodents, with results showing improvements in metabolic profile. Data are now beginning to emerge from human studies and the results are promising. (c) 2010 Elsevier Ltd. All rights reserved.

AB - Due to its impact upon health and the economy, the mechanisms that contribute to the pathogenesis of obesity and the metabolic syndrome are under intense scrutiny. In addition to understanding the pathogenesis of disease it is important to design and trial novel therapies. Patients with cortisol excess. Cushing's syndrome, have a phenotype similar to that of the metabolic syndrome and as a result there is much interest the manipulation of glucocorticoid (GC) action as a therapeutic strategy. Intracellular GC levels are regulated by 11 beta-hydroxysteriod dehydrogenase (11 beta-HSD1) which converts inactive cortisone to cortisol, thereby increasing local GC action. There is an abundance of data implicating 11 beta-HSD1 in the pathogenesis of obesity, type 2 diabetes and the metabolic syndrome and 11 beta-HSD1 is an attractive therapeutic target. Selective 11 beta-HSD1 inhibitors, which do not act upon 11 beta-HSD2 (which inactivates cortisol to cortisone) are in development. So far studies have primarily been carried out in rodents, with results showing improvements in metabolic profile. Data are now beginning to emerge from human studies and the results are promising. (c) 2010 Elsevier Ltd. All rights reserved.

KW - Obesity

KW - 11 beta-Hydroxysteroid dehydrogenase

KW - Glucocorticoids

KW - Diabetes

U2 - 10.1016/j.jsbmb.2010.03.060

DO - 10.1016/j.jsbmb.2010.03.060

M3 - Review article

C2 - 20347978

VL - 122

SP - 21

EP - 27

JO - The Journal of Steroid Biochemistry and Molecular Biology

JF - The Journal of Steroid Biochemistry and Molecular Biology

SN - 0960-0760

IS - 1-3

ER -