Procyanidin C1, a Component of Cinnamon Extracts, Is a Potential Insulin Sensitizer That Targets Adipocytes

Procyanidin C1, a Component of Cinnamon Extracts, Is a Potential Insulin Sensitizer That Targets Adipocytes
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原花青素 C1 是肉桂提取物的一种成分,是一种针对脂肪细胞的潜在胰岛素增敏剂

DOI:
10.1021/acs.jafc.9b02932
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发表时间:
2019-08-14
影响因子:
6.1
通讯作者:
Wang, He-Yao
Wang, He-Yao
中科院分区:
农林科学1区
文献类型:
--
作者:
Sun, Peng;Li, Kai;Wang, He-Yao

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天然产物是发现新先导化合物的主要来源之一。我们以前报道过肉桂提取物在体内调节脂质组织体积和胰岛素敏感性方面具有很好的效果。然而,其有效成分和潜在机制尚不清楚。在本研究中,我们分析了肉桂的不同成分对3 T3-L1脂肪细胞胰岛素敏感性的调节作用。功能测定显示,肉桂提取物的6种主要成分中,B型原花青素(procyanidin C1)促进3 T3-L1细胞的分化(TG含量:25 μ M剂量组为1.10 +/- 0.09 mM,溶媒组为0.67 +/- 0.02 mM,p < 0.001)并促进胰岛素诱导的葡萄糖摄取(在25 μ M剂量下为8.58 +/-1.43,在载体组中为3.05 +/-1.24,p < 0.001)。机制研究进一步表明,原花青素C1激活AKT-eNOS通路,从而上调葡萄糖摄取,增强成熟脂肪细胞的胰岛素敏感性。总之,我们的研究确定了B型原花青素C1,肉桂提取物的一种成分,刺激前脂肪细胞分化,并通过成熟脂肪细胞中的AKT-eNOS途径作为潜在的胰岛素作用增强剂。
Natural products are one of the main sources for discovering new lead compounds. We previously reported that cinnamon extract has a promising effect in regulating lipid tissue volume and insulin sensitivity in vivo. However, its effective component and the underlying mechanism are not known. In the present study, we analyzed the effect of different components of cinnamon on regulating insulin sensitivity in 3T3-L1 adipocytes. Functional assay revealed that, of the six major components of cinnamon extracts, the B-type procyanidin, procyanidin C1, improves the differentiation of 3T3-L1 cells (TG content: 1.10 +/- 0.09 mM at a dosage of 25 mu M vs 0.67 +/- 0.02 mM in vehicle group, p < 0.001) and promotes insulin-induced glucose uptake (8.58 +/- 1.43 at a dosage of 25 mu M vs 3.05 +/- 1.24 in vehicle group, p < 0.001). Mechanism studies further suggested that procyanidin C1 activates the AKT-eNOS pathway, thus up-regulating glucose uptake and enhancing insulin sensitivity in mature adipocytes. Taken together, our study identified B-type procyanidin C1, a component of cinnamon extract, that stimulates preadipocyte differentiation and acts as a potential insulin action enhancer through the AKT-eNOS pathway in mature adipocytes.