Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice | |
Wang Yuejing; Huang Suling; Feng Ying; Ning Mengmeng; Leng Ying | |
刊名 | Acta Pharmacologica Sinica |
2012 | |
卷号 | 33期号:9页码:1195 |
关键词 | emodin 11β-hydroxysteroid dehydrogenase type 1 adipocyte glucocorticoid type 2 diabetes ob/ob mice |
ISSN号 | 1671-4083 |
英文摘要 | 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-HSD1A activity was evaluated with a scintillation proximity assay. The adipogenesis, glucose uptake, lipolysis and adiponectin secretion were investigated in 3T3-L1 adipocytes treated with emodin 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~(-1)·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 μmol/L, respectively, after 1 and 24 h treatment. In 3T3-L1 adipocytes, emodin (30 μmol/L) suppressed 11-dehydrocorticosterone-induced adipogenesis without affecting corticosterone-induced adipogenesis; emodin (3 μmol/L) reduced 11-dehydrocorticosterone-stimulated lipolysis, but had no effect on corticosterone-induced lipolysis. Moreover, emodin (3 μmol/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. |
语种 | 英语 |
内容类型 | 期刊论文 |
源URL | [http://119.78.100.183/handle/2S10ELR8/293766] |
专题 | 中国科学院上海药物研究所 |
作者单位 | 中国科学院上海药物研究所 |
推荐引用方式 GB/T 7714 | Wang Yuejing,Huang Suling,Feng Ying,et al. Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice[J]. Acta Pharmacologica Sinica,2012,33(9):1195. |
APA | Wang Yuejing,Huang Suling,Feng Ying,Ning Mengmeng,&Leng Ying.(2012).Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice.Acta Pharmacologica Sinica,33(9),1195. |
MLA | Wang Yuejing,et al."Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice".Acta Pharmacologica Sinica 33.9(2012):1195. |
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