MDG-1, an Ophiopogon polysaccharide, restrains process of non-alcoholic fatty liver disease via modulating the gut-liver axis

MDG-1, an Ophiopogon polysaccharide, restrains process of non-alcoholic fatty liver disease via modulating the gut-liver axis
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MDG-1,一种麦冬多糖,通过调节肠肝轴抑制非酒精性脂肪肝疾病的进程

DOI:
10.1016/j.ijbiomac.2019.09.007
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发表时间:
2019
影响因子:
8.2
通讯作者:
Wang Yuan
Wang Yuan
中科院分区:
化学1区
文献类型:
--
作者:
Wang Xu;Shi Linlin;Wang Xinping;Feng Yi;Wang Yuan

文献摘要

被引文献

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MDG-1是从麦冬根中提取的β-D-果聚糖多糖,对高脂饮食(HFD)诱导的肥胖小鼠具有预防肥胖和高脂血症的作用。有趣的是,MDG-1,作为一种菊糖型果聚糖,吸收不良,其可能的机制对脂质紊乱仍不清楚。本研究旨在探讨MDG-1对NAFLD模型的治疗作用,并从肠-肝轴的角度阐明其作用机制,特别是对肠道菌群、短链脂肪酸(SCFAs)和肝脏脂质代谢的影响。本研究将C57 BL/6 J雄性小鼠经高脂饲料喂养2个月后,随机分为高脂饲料组和MDG-1不同剂量组。结果显示,MDG-1可显著抑制体重增加,改善脂质蓄积、肝损伤和大泡性脂肪变性。MDG-1可以恢复肠道微生物群平衡,增加有益细菌的相对丰度,特别是产生SCFAs的细菌。MDG-1被肠道菌群降解利用后,可增加乙酸和戊酸的含量,从而调节炎症反应和肝脏脂质代谢。具体而言,MDG-1增强肝脏磷酸化腺苷激活蛋白激酶的表达,伴随着调节肝脏脂肪生成和脂肪细胞分化,从而抑制NAFLD的进展。本研究为高脂血症及脂代谢综合征的治疗提供了新的思路。
MDG-1, a β-D-fructan polysaccharide extracted from the roots ofOphiopogon japonicus, had preventive effect against obesity and hyperlipidemia in high-fat diet (HFD)-induced obesity mice. Interestingly, MDG-1, as an inulin-type fructan, is poorly absorbed and its possible mechanism against lipid disturbance remained unclear. The present study aimed to investigate the benefits of MDG-1 treatment on NAFLD model and elucidate mechanism from the perspective of gut-liver axis, especially about gut microbiota, short chain fatty acids (SCFAs) and hepatic lipid metabolism. In this study, after two months HFD feeding, C57BL/6J male mice were randomly divided into HFD group and various MDG-1 dose group. Results showed that MDG-1 markedly blocked weight gain, and ameliorated lipid accumulation, liver damage and macrovesicular steatosis. MDG-1 could restore gut microbiota balance and increase relative abundance of beneficial bacteria, especially SCFAs-producing bacteria. After degradation and utilization by the gut microbiota, MDG-1 could increase the contents of acetic acid and valeric acid, thus regulating inflammatory responses and hepatic lipid metabolism. Specifically, MDG-1 enhanced expression of hepatic phosphorylation of adenosine monophosphate-activated protein kinase, accompanying by regulating hepatic adipogenesis and adipocyte differentiation, thereby inhibiting progress of NAFLD. Our findings may provide new ways in the treatment of hyperlipidemia and lipid-related metabolic syndrome.