Glucocorticoids, 11β-hydroxysteroid dehydrogenase type 1, and visceral obesity

被引：5
|
作者：
Paulmyer-Lacroix, O
Boullu-Ciocca, S
Oliver, C
Dutour, A
Grino, M
机构：
[1] Univ Mediterranee, Inst Jean Rochei, UFR Med Secteur Nord, Lab Interact Fonctionnelles, F-13916 Marseille 20, France
[2] Hop Nord Marseille, Serv Endocrinol Malad Metab & Nutr, F-13015 Marseille, France
来源：
M S-MEDECINE SCIENCES | 2003年 / 19卷 / 04期
关键词：
D O I：
10.1051/medsci/2003194473
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Glucocorticoids are implicated as a pathophysiological mediator of obesity and its accompanying metabolic and cardiovascular complications. Obese patients exhibit normal circulating cortisol levels, related to increased glucocorticoid production and degradation. However, it has been demonstrated that local production of active cortisol from inactive cortisone driven by 11beta-hydroxysteroid dehydrogenase type 1 is exaggerated in adipose tissue of obese subjects. Such local hypercortisolism may be responsible for increased adipocyte differentiation and enhanced secretion of free fatty acids and other substances involved in the metabolic and cardiovascular complications observed in obesity.
引用
收藏
页码：473 / 476
页数：4
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