Schnackenberg Christine G
GlaxoSmithKline Pharmaceuticals, Department of Cardiac Biology, UW2510, Box 1539, 709 Swedeland Road, King of Prussia, PA 19406, USA.
Curr Opin Investig Drugs. 2008 Mar;9(3):295-300.
The metabolic syndrome is a constellation of interrelated metabolic risk factors that appear to promote the development of diabetes and cardiovascular disease. These risk factors include abdominal obesity, insulin resistance, hypertension and dyslipidemia. 11beta-Hydroxysteroid dehydrogenase (11beta-HSD) catalyzes the interconversion of glucocorticoids through the activity of two isozymes: type 1 (11beta-HSD1) and type 2 (11beta-HSD2). 11beta-HSD1 converts inactive glucocorticoid to the active form, whereas 11beta-HSD2 converts active glucocorticoid to the inactive form. It is well established that reduced 11beta-HSD2 activity causes hypertension and electrolyte abnormalities. More recently, the pathophysiological role of 11beta-HSD1 has been explored and studies suggest that increased 11beta-HSD1 activity within target tissues may promote insulin resistance, obesity, hypertension and dyslipidemia. This review will discuss the evidence that inhibition of 11beta-HSD1 may be therapeutic in the treatment of the metabolic syndrome.
代谢综合征是一组相互关联的代谢风险因素,似乎会促进糖尿病和心血管疾病的发展。这些风险因素包括腹部肥胖、胰岛素抵抗、高血压和血脂异常。11β-羟基类固醇脱氢酶(11β-HSD)通过两种同工酶的活性催化糖皮质激素的相互转化:1型(11β-HSD1)和2型(11β-HSD2)。11β-HSD1将无活性的糖皮质激素转化为活性形式,而11β-HSD2将活性糖皮质激素转化为无活性形式。众所周知,11β-HSD2活性降低会导致高血压和电解质异常。最近,人们对11β-HSD1的病理生理作用进行了探索,研究表明,靶组织内11β-HSD1活性增加可能会促进胰岛素抵抗、肥胖、高血压和血脂异常。本综述将讨论抑制11β-HSD1可能对代谢综合征具有治疗作用的证据。