Abstracts
Résumé
L’importance des glucocorticoïdes dans le développement et le maintien de l’obésité ainsi que la genèse de ses complications métaboliques et cardio-vasculaires est maintenant bien reconnue. L’existence, chez l’obèse, de concentrations circulantes de cortisol normales a fait envisager la possibilité d’anomalies du métabolisme local des glucocorticoïdes, en particulier dans le tissu adipeux. Un ensemble de données récentes a mis en évidence, dans ce tissu, une surexpression de la 11β-hydroxystéroïde déshydrogénase de type 1, enzyme qui convertit la cortisone (inactive) en cortisol (actif). Cette surexpression engendre un hypercorticisme local. Le développement d’inhibiteurs spécifiques de la 11β-hydroxystéroïde déshydrogénase de type 1 pourrait constituer une nouvelle approche du traitement de l’obésité viscérale et de ses complications.
Summary
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 11β-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.
Appendices
Références
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