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肉桂酸甲酯通过激活 3T3-L1 前脂肪细胞中的 CaMKK2-AMPK 通路抑制脂肪细胞分化。

Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes.

机构信息

Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan, ROC.

出版信息

J Agric Food Chem. 2012 Feb 1;60(4):955-63. doi: 10.1021/jf203981x. Epub 2012 Jan 24.

DOI:10.1021/jf203981x
PMID:22273148
Abstract

Methyl cinnamate, an active component of Zanthoxylum armatum , is a widely used natural flavor compound with antimicrobial and tyrosinase inhibitor activities. However, the underlying bioactivity and molecular mechanisms of methyl cinnamate on adipocyte function and metabolism remain unclear. The aim of this study was to investigate the inhibitory effect of methyl cinnamate on adipogenesis in 3T3-L1 preadipocytes. Methyl cinnamate markedly suppressed triglyceride accumulation associated with down-regulation of adipogenic transcription factor expression, including sterol regulatory element binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer-binding protein α (C/EBPα). Additionally, methyl cinnamate-inhibited PPARγ activity and adipocyte differentiation were partially reversed by the PPARγ agonist troglitazone. Furthermore, methyl cinnamate stimulated Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) and phospho-AMP-activated protein kinase (AMPK) expression during adipogenesis. This study first revealed methyl cinnamate has antiadipogenic activity through mechanisms mediated, in part, by the CaMKK2-AMPK signaling pathway in 3T3-L1 cells.

摘要

甲基肉桂酸是花椒中的一种活性成分,是一种广泛使用的天然香料化合物,具有抗菌和酪氨酸酶抑制剂活性。然而,甲基肉桂酸对脂肪细胞功能和代谢的潜在生物活性和分子机制尚不清楚。本研究旨在探讨甲基肉桂酸对 3T3-L1 前体脂肪细胞脂肪生成的抑制作用。甲基肉桂酸明显抑制了与脂肪生成转录因子表达下调相关的甘油三酯积累,包括固醇调节元件结合蛋白-1(SREBP-1)、过氧化物酶体增殖物激活受体γ(PPARγ)和 CCAAT/增强子结合蛋白α(C/EBPα)。此外,PPARγ激动剂曲格列酮部分逆转了甲基肉桂酸抑制的 PPARγ活性和脂肪细胞分化。此外,甲基肉桂酸在脂肪生成过程中刺激钙/钙调蛋白依赖性蛋白激酶激酶 2(CaMKK2)和磷酸化 AMP 激活蛋白激酶(AMPK)的表达。本研究首次揭示了甲基肉桂酸通过 CaMKK2-AMPK 信号通路在 3T3-L1 细胞中部分介导的机制具有抗脂肪生成活性。

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