Department of Agricultural Biotechnology and Center for Agricultural Biomaterials, ‡WCU Biomodulation Major, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University , Seoul 151-921, Republic of Korea.
J Agric Food Chem. 2014 May 14;62(19):4306-12. doi: 10.1021/jf405088f. Epub 2014 May 5.
In the present study, we aimed to investigate the antiobesity effect of CAPE in vivo, and the mechanism by which CAPE regulates body weight in vitro. To confirm the antiobesity effect of CAPE in vivo, mice were fed with a high fat diet (HFD) with different concentrations of CAPE for 5 weeks. CAPE significantly reduced body weight gain and epididymal fat mass in obese mice fed a HFD. In accordance with in vivo results, Oil red O staining results showed that CAPE significantly suppressed MDI-induced adipogenesis of 3T3-L1 preadipocytes. FACS analysis results showed that CAPE delayed MDI-stimulated cell cycle progression, thereby contributing to inhibit mitotic clonal expansion (MCE), which is a prerequisite step for adipogenesis. Also, CAPE regulated the expression of cyclin D1 and the phosphorylation of ERK and Akt, which are upstream of cyclin D1. These results suggest that CAPE exerts an antiobesity effect in vivo, presumably through inhibiting adipogenesis at an early stage of adipogenesis.
在本研究中，我们旨在研究 CAPE 的体内抗肥胖作用，以及 CAPE 体外调节体重的机制。为了证实 CAPE 的体内抗肥胖作用，我们用不同浓度的 CAPE 喂养高脂饮食（HFD）的小鼠 5 周。CAPE 显著减少了肥胖小鼠的体重增加和附睾脂肪量。与体内结果一致，油红 O 染色结果表明，CAPE 显著抑制了 MDI 诱导的 3T3-L1 前脂肪细胞的脂肪生成。FACS 分析结果表明，CAPE 延迟了 MDI 刺激的细胞周期进程，从而有助于抑制有丝分裂克隆扩增（MCE），这是脂肪生成的前提步骤。此外，CAPE 调节 cyclin D1 的表达以及 cyclin D1 上游的 ERK 和 Akt 的磷酸化。这些结果表明，CAPE 体内发挥抗肥胖作用，可能是通过在脂肪生成的早期阶段抑制脂肪生成。
