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[Glucocorticoids, 11 beta-hydroxysteroid dehydrogenase type 1, and visceral obesity]
Odile Paulmyer-Lacroix1, Sandrine Boullu-Ciocca, Charles Oliver
1Laboratoire des Interactions fonctionnelles en Neuroendocrinologie, UFR de Médecine secteur Nord, Institut Jean Roche, Université de la Méditerranée, boulevard Pierre Dramard, 13916 Marseille, France.
Abstract:
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 11 beta-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.