Vantyghem M C, Hober C, Racadot A, Lefebvre J
Service d'Endocrinologie et Métabolismes, USN A, CHRU, Lille.
Ann Endocrinol (Paris). 1994;55(6):271-7.
The 11 beta OHSD is an ubiquitous enzyme which inactivates cortisol to cortisone by transforming the hydroxyl group at the 11-carbon to a keto group. Therefore, it confers to mineralocorticoid receptors their selectivity toward their ligand and may constitute an important mechanism of regulation tissue-specific of the access of ligand toward its receptors. More widely the 11 beta OHSD would modulate glucocorticoid activity to their own receptor. There is no possibility to measure directly this enzyme and its deficiency is indirectly evaluated by enhancement of the quotient (THF + alpha THF)/THE after analysis of urinary steroid metabolites. Such enzymatic deficits may be congenital and are observed in childhood where they give an apparent mineralocorticoid excess (AME) syndrome (type 1). Sometimes acquired and reversible, they are due to licorice intoxication, hypothyroidism, chronic alcoholism and may be involved in the genesis of some cases of hypertension.
11β-羟类固醇脱氢酶是一种普遍存在的酶,它通过将11位碳原子上的羟基转化为酮基,使皮质醇失活成为可的松。因此,它赋予盐皮质激素受体对其配体的选择性,并可能构成调节配体与受体结合的组织特异性的重要机制。更广泛地说,11β-羟类固醇脱氢酶会调节糖皮质激素对其自身受体的活性。无法直接测量这种酶,其缺乏通过分析尿类固醇代谢产物后提高(四氢皮质醇+α-四氢皮质醇)/四氢皮质酮的比值来间接评估。这种酶缺乏可能是先天性的,在儿童期观察到,会导致明显的盐皮质激素过多(AME)综合征(1型)。有时是后天获得且可逆的,它们是由甘草中毒、甲状腺功能减退、慢性酒精中毒引起的,可能参与某些高血压病例的发病机制。