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首页> 外文期刊>The Journal of Nutritional Biochemistry >Daidzein and the daidzein metabolite, equol, enhance adipocyte differentiation and PPAR gamma transcriptional activity.
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Daidzein and the daidzein metabolite, equol, enhance adipocyte differentiation and PPAR gamma transcriptional activity.

机译：黄豆苷元和黄豆苷元代谢物雌马酚增强脂肪细胞分化和PPARγ转录活性。

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摘要

Dietary soy isoflavones have been shown to favorably alter the metabolic phenotypes associated with Type 2 diabetes. However, the identification of direct targets and the underlying molecular mechanisms by which soy isoflaovones exert antidiabetic effects remain elusive. Since the insulin-sensitizing effects of thiazolidinediones, antidiabetic drugs, are mediated through activation of peroxisome proliferators-activated receptor gamma (PPAR gamma), we examined the effects of daidzein and the daidzein metabolite, equol, on adipocyte differentiation and PPAR gamma activation. In 3T3-L1 cells, daidzein enhanced adipocyte differentiation and PPAR gamma expression in a dose-dependent manner. Daidzein also dose-dependently increased insulin-stimulated glucose uptake and the relative abundance of insulin-responsive glucose transporter 4 (GLUT4) and insulin receptor substrate 1 (IRS-1) mRNA. In C3H10T1/2 cells, both daidzein and equol at 1 mumol/L and higher significantly increased adipocyte differentiation and insulin-stimulated glucose uptake. Furthermore, daidzein and equol up-regulated PPAR gamma-mediated transcriptional activity, and daidzein restored the PPAR gamma antagonist-induced inhibition of aP2 and GLUT4 mRNA levels. Our results indicate that daidzein enhances insulin-stimulated glucose uptake in adipocytes by increasing the expression of GLUT4 and IRS-1 via the activation of PPAR gamma. These data further support the recent findings that favorable effects of dietary soy isoflavones may be attributable to daidzein and its metabolite equol.
机译：膳食大豆异黄酮已被证明可以很好地改变与2型糖尿病相关的代谢表型。但是，直接靶标的识别以及大豆异黄酮类化合物发挥抗糖尿病作用的潜在分子机制仍然难以捉摸。由于噻唑烷二酮类抗糖尿病药的胰岛素敏感性作用是通过过氧化物酶体增殖物激活的受体γ（PPARγ）的激活介导的，因此我们检查了大豆苷元和大豆苷元代谢物雌马酚对脂肪细胞分化和PPARγ活化的影响。在3T3-L1细胞中，黄豆苷元以剂量依赖性方式增强脂肪细胞分化和PPARγ表达。大豆苷元还剂量依赖性地增加胰岛素刺激的葡萄糖摄取以及胰岛素应答性葡萄糖转运蛋白4（GLUT4）和胰岛素受体底物1（IRS-1）mRNA的相对丰度。在C3H10T1 / 2细胞中，黄豆苷元和雌马酚的浓度均在1μmol/ L或更高时，显着增加了脂肪细胞的分化和胰岛素刺激的葡萄糖摄取。此外，黄豆苷元和雌马酚上调了PPARγ介导的转录活性，而黄豆苷元则恢复了PPARγ拮抗剂诱导的对aP2和GLUT4 mRNA水平的抑制。我们的结果表明，黄豆苷元通过激活PPARγ来增加GLUT4和IRS-1的表达，从而增强胰岛素刺激的脂肪细胞葡萄糖摄取。这些数据进一步支持了最近的发现，即饮食大豆异黄酮的有利作用可能归因于大豆苷元及其代谢物雌马酚。

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