期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 583, 期 -, 页码 79-86出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2015.07.007
关键词
Adipocyte; Differentiation; PPAR gamma; AMPK; mTOR
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT and Future Planning [2014R1A2A1A11050776]
- National Research Foundation of Korea [2014R1A2A1A11050776] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Obesity increases the risk of developing many chronic diseases, including type 2 diabetes and certain cancers, and is thereby associated with premature death. The present study was conducted to identify the inhibitory effect of the ascochlorin derivative 4-O-methylascochlorin (MAC) on the differentiation of 3T3-L1 preadipocytes. MAC suppressed the differentiation of 3T3-L1 preadipocytes and inhibited the expression of adipocyte differentiation marker genes, FABP4, PPAR gamma and C/EBP alpha. In addition, we found that the inhibitory effects of MAC on differentiation of 3T3-L1 preadipocytes were caused by suppression of mTORC1 via inhibition of mTOR/p7056K/4E-BP1 phosphorylation and activation of Raptor phosphorylation. MAC also regulated the PPAR gamma expression and the mTORC1 activation by increasing AMPK phosphorylation and inhibiting PI3K/Akt, which suggest that MAC suppresses the differentiation of 3T3-L1 adipocytes by regulating the AMPK- and PI3K-mTOR-PPAR gamma signaling pathways. Furthermore, animal model results showed that the phosphorylation of AMPK was enhanced in the liver of C57BL/6 mice intraperitoneally injected with MAC. These results indicate that MAC could be a therapeutic agent for obesity involving PPAR gamma and AMPK. (C) 2015 Elsevier Inc. All rights reserved.
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