中国药理学报：英文版, 2012, Vol.33 (9), p.1195-1203
2012
Volltextzugriff (PDF)
Details
- Autor(en) / Beteiligte
- Titel
- Emodin, an 11β-hydroxysteroid dehydrogenase type I inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice
- Ist Teil von
- 中国药理学报：英文版, 2012, Vol.33 (9), p.1195-1203
- Erscheinungsjahr
- 2012
- Quelle
- Alma/SFX Local Collection
- Beschreibungen/Notizen
- Aim： Emodin （1,3,8-trihydroxy-6-methylanthraquinone） is a potent and selective inhibitor of 11β-hydroxysteroid dehydrogenase type 1 （11β-HSD1） with the ability to ameliorate metabolic disorders in diet-induced obese mice. In the present study, we investigated the effects of emodin on adipocyte function and the underlying mechanisms in vitro, and its anti-diabetic effects in ob/ob mice. Methods： 3T3-L1 adipocytes were used for in vitro studies. 11β-HSDIA activity was evaluated with a scintillation proximity assay. The adipogenesis, glucose uptake, lipolysis and adiponectin secretion were investigated in 3T3-L1 adipocytes treated with emo- din in the presence of active （corticosterone） or inactive glucocorticoid （11-dehydrocorticosterone）. For in vivo studies, ob/ob mice were administered emodin （25 and 50 mg.kg-l.d 1, ip） for 26 d. On the last day of administration, the serum was collected and the mesenteric and perirenal fat were dissected for analyses. Results： Emodin inhibited the 11β-HSD1 activity in 3T3-L1 adipocytes in concentration- and time-dependent manners （the IC50 values were 7.237 and 4.204 pmol/L, respectively, after I and 24 h treatment. In 3T3-L1 adipocytes, emodin （30 pmol/L） suppressed 11-dehydrocorticosterone-induced adipogenesis without affecting corticosterone-induced adipogenesis; emodin （3 pmol/L） reduced 11-dehydrocorticosterone-stimulated lipolysis, but had no effect on corticosterone-induced lipolysis. Moreover, emodin （3 pmol/L） partly reversed the impaired insulin-stimulated glucose uptake and adiponectin secretion induced by 11-dehydrocorticosterone but not those induced by corticosterone. In ob/ob mice, long-term emodin administration decreased 11β-HSD1 activity in mesenteric adipose tissues, lowered non-fasting and fasting blood glucose levels, and improved glucose tolerance. Conclusion： Emodin improves the inactive glucocorticoid-induced adipose tissue dysfunction by selective inhibition on 11β-HSD1 in adipocyte in vitro and improves glycemic control in ob/ob mice.