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Ashitaba (Angelica keiskei) extract prevents adiposity in high-fat diet-fed C57BL/6 mice

机译:明日叶(Angelica keiskei)提取物可防止高脂饮食喂养的C57BL / 6小鼠肥胖

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摘要

Two main chalcones, 4-hydroxyderricin and xanthoangelol, from Ashitaba, which is a food ingredient and a folk medicine in Asia, have been demonstrated to modulate lipid metabolism in 3T3-L1 and HepG2 cells. In this study, we investigated the effects of Ashitaba extract on adiposity in mice fed a high-fat (HF) diet and its underlying mechanisms based on adipose tissue and hepatic lipid metabolism. C57BL/6 mice were fed a normal or HF diet supplemented with Ashitaba extract (0.01% and 0.1%, w/w) for 16 weeks. Ashitaba extract suppressed the HF diet-induced body weight gain and fat deposition in white adipose tissue, reduced plasma cholesterol, glucose, and insulin levels, increased the adiponectin level, lowered triglyceride and the liver cholesterol content, increased phosphorylation of AMP-activated protein kinase (AMPK) in adipose tissue and liver, inhibited lipogenesis in adipose tissue by down-expression of peroxisome proliferator-activated receptor (PPAR) gamma, CCAAT/enhancer-binding protein alpha and sterol regulatory element-binding protein 1 (SREBP1), inhibited lipogenesis in the liver by down-expression of SREBP1 and its target enzyme fatty acid synthase, and promoted fatty acid oxidation by up-expression of carnitine palmitoyltransferase-1A and PPAR alpha. In conclusion, Ashitaba extract can possibly prevent adiposity through modulating lipid metabolism through phosphorylation of AMPK in adipose tissue and liver.
机译:来自亚洲明日叶的两个主要的查耳酮(4​​-羟基derricin和黄嘌呤醇)已被证明可调节3T3-L1和HepG2细胞中的脂质代谢,这是亚洲的食品成分和民间药。在这项研究中,我们调查了明日叶提取物对高脂(HF)饮食喂养的小鼠肥胖的影响及其基于脂肪组织和肝脂质代谢的潜在机制。给C57BL / 6小鼠喂食补充Ashitaba提取物(0.01%和0.1%,w / w)的普通或HF饮食16周。 Ashitaba提取物抑制了HF饮食引起的体重增加和白色脂肪组织中的脂肪沉积,降低了血浆胆固醇,葡萄糖和胰岛素水平,增加了脂联素水平,降低了甘油三酸酯和肝胆固醇含量,增加了AMP活化蛋白激酶的磷酸化(AMPK)在脂肪组织和肝脏中,通过过氧化物酶体增殖物激活受体(PPAR)γ,CCAAT /增强子结合蛋白α和固醇调节元素结合蛋白1(SREBP1)的下表达抑制脂肪组织中的脂肪生成SREBP1及其靶酶脂肪酸合酶的下调表达在肝脏中的表达,并通过肉碱棕榈酰转移酶-1A和PPARα的上调表达促进脂肪酸氧化。总之,明日叶提取物可能通过调节脂肪组织和肝脏中AMPK的磷酸化来调节脂质代谢,从而预防肥胖。

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