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Glucocorticoids and 11beta-hydroxysteroid dehydrogenase in adipose tissue Seckl JR; Morton NM; Chapman KE; Walker BRRecent Prog Horm Res 2004[]; 59 (ä): 359-93The highly prevalent metabolic syndrome (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, along with abdominal obesity) resembles Cushing's syndrome. However, in simple obesity, plasma cortisol levels are not elevated. 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), at least in mature adipocytes and hepatocytes, converts inactive circulating 11-keto steroids into active glucocorticoids, amplifying local glucocorticoid action. 11beta-HSD1 is elevated in adipose tissue in obese humans and rodents, suggesting that adipose tissue glucocorticoid excess may explain the conundrum. Indeed, transgenic mice overexpressing 11beta-HSD1 in adipose tissue faithfully replicate the metabolic syndrome. Conversely, 11beta-HSD1(-/-) mice resist the metabolic consequences of stress and high-fat feeding via insulin sensitisation and other advantageous effects in the liver and adipose tissue. Adipose 11beta-HSD1 deficiency contributes to a protective metabolic phenotype, supporting its role as a therapeutic target for the metabolic syndrome.|11-beta-Hydroxysteroid Dehydrogenases/genetics/*metabolism[MESH]|Adipose Tissue/*enzymology[MESH]|Adrenal Glands/physiopathology[MESH]|Animals[MESH]|Glucocorticoids/*physiology[MESH]|Humans[MESH]|Hypothalamus/physiopathology[MESH]|Liver/enzymology[MESH]|Metabolic Syndrome/drug therapy/physiopathology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Mice, Transgenic[MESH]|Obesity/physiopathology[MESH]|Pituitary Gland/physiopathology[MESH] |
