emodinan11hydroxysteroiddehydrogenasetype1inhibitorregulatesadipocytefunctioninvitroandexertsantidiabeticeffectinobobmice

	emodinan11hydroxysteroiddehydrogenasetype1inhibitorregulatesadipocytefunctioninvitroandexertsantidiabeticeffectinobobmice
	Wang Yuejing; Huang Suling; Feng Ying; Ning Mengmeng; Leng Ying
刊名	actapharmacologicasinica
	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/2S10ELR8/284981]
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. emodinan11hydroxysteroiddehydrogenasetype1inhibitorregulatesadipocytefunctioninvitroandexertsantidiabeticeffectinobobmice[J]. actapharmacologicasinica,2012,33(9):1195.
APA	Wang Yuejing,Huang Suling,Feng Ying,Ning Mengmeng,&Leng Ying.(2012).emodinan11hydroxysteroiddehydrogenasetype1inhibitorregulatesadipocytefunctioninvitroandexertsantidiabeticeffectinobobmice.actapharmacologicasinica,33(9),1195.
MLA	Wang Yuejing,et al."emodinan11hydroxysteroiddehydrogenasetype1inhibitorregulatesadipocytefunctioninvitroandexertsantidiabeticeffectinobobmice".actapharmacologicasinica 33.9(2012):1195.