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Effect of stress on hepatic 11-hydroxysteroid dehydrogenase activity and its influence on carbohydrate metabolism

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Stress activates the synthesis and secretion of catecholamines and adrenal glucocorticoids, increasing their circulating levels. In vivo, hepatic 11-hydroxysteroid dehydrogenase 1 (HSD1) stimulates the shift of 11-dehydrocorticosterone to corticosterone, enhancing active glucocorticoids at tissue level. We studied the effect of 3 types of stress, 1 induced by bucogastric overload with 200mmol/L HCl causing metabolic acidosis (HCl), the second induced by bucogastric overload with 0.45% NaCl (NaCl), and the third induced by simulated overload (cannula), on the kinetics of hepatic HSD1 of rats and their influence on the activity of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase, glycemia, and glycogen deposition. Compared with unstressed controls, all types of stress significantly increased HSD1 activity (146% cannula, 130% NaCl, and 253% HCl), phosphoenolpyruvate carboxykinase activity (51% cannula, 48% NaCl, and 86% HCl), and glycemia (29% cannula, 30% NaCl, and 41% HCl), but decreased hepatic glycogen (68% cannula, 68% NaCl, and 78% HCl). Owing to these results, we suggest the following events occur when stress is induced: an increase in hepatic HSD1 activity, augmented active glucocorticoid levels, increased gluconeogenesis, and glycemia. Also involved are the multiple events indirectly related to glucocorticoids, which lead to the depletion of hepatic glycogen deposits, thereby contributing to increased glycemia. This new approach shows that stress increments the activity of hepatic HSD1 and suggests that this enzyme could be involved in the development of the Metabolic Syndrome.

Le stress active la synthèse et la sécrétion des catécholamines et des glucocorticoïdes surrénaux en augmentant leux taux circulants. In vivo, la 11-hydroxystéroïde déshydrogénase 1 (HSD1) stimule la conversion de la 11-déshydrocorticostérone en corticostérone, en stimulant les glucorticoïdes actifs au niveau tissulaire. Nous avons examiné l’effet de 3 types de stress, le premier induit par une surcharge bucco-gastrique au moyen de 200mmol/L de HCl provoquant une acidose métabolique (HCl), le second par une surcharge bucco-gastrique avec 0,45 % de NaCl (NaCl) et le troisième par une surcharge stimulée (canule), sur la cinétique de la HSD1hépatique des rats. Nous avons aussi examiné l’influence des trois stress sur l’activité de l’enzyme de la gluconéogenèse, phosphoenolpyruvate carboxykinase (PEPCK), la glycémie et le dépôt de glycogène. Comparativement à ce qui a été observé chez les témoins non stressés, les trois types de stress ont significativement augmenté l’activité HSD1 (canule 146 %, NaCl 130 %, HCl 253 %), l’activité PEPCK (canule 51 %, NaCl 48 %, HCl 86 %) et la glycémie (canule 29 %, NaCl 30 %, HCl 41 %), mais diminué le glycogène hépatique (canule 68 %, NaCl 68 %, HCl 78 %). Nous suggérons les événements suivants : augmentation de l’activité HSD1hépatique, augmentation des taux de glucocorticoïdes actifs, augmentation de la gluconéogenèse et de la glycémie. Nous mettons aussi en cause les multiples événements liés indirectement aux glucocorticoïdes et conduisant à la déplétion des dépôts de glycogène hépatique, contribuant ainsi à l’augmentation de la glycémie. Cette nouvelle approche montre que le stress augmente l’activité de la HSD1hépatique et donne à penser que cette enzyme pourrait jouer un rôle dans le développement du syndrome métabolique.
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Document Type: Research Article

Publication date: 2006-10-01

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