Lactobacillus plantarum FRT10 alleviated high-fat diet-induced obesity in mice through regulating the PPARα signal pathway and gut microbiota

Lactobacillus plantarum FRT10 alleviated high-fat diet-induced obesity in mice through regulating the PPARα signal pathway and gut microbiota
复制标题

植物乳杆菌 FRT10 通过调节 PPAR α 信号通路和肠道微生物群缓解高脂饮食诱导的小鼠肥胖

DOI:
10.1007/s00253-020-10620-0
复制
发表时间:
2020-05-14
影响因子:
5
通讯作者:
Yang, Peilong
Yang, Peilong
中科院分区:
工程技术2区
文献类型:
--
作者:
Cai, Hongying;Wen, Zhiguo;Yang, Peilong

文献摘要

被引文献

相似文献

以前的研究表明,益生菌补充有助于减轻肥胖。这项工作是为了评估来自酸面团的植物乳杆菌FRT 10在缓解高脂饮食(HFD)喂养的小鼠中的肥胖症的功效,以及关注肠道微生物群分布调节的潜在机制。昆明种小鼠分别饲喂普通饲料(CT)、高脂饲料(HFD)和含低、高剂量L。plantarum FRT 10培养8周。分析了肝脏的生理生化调节作用。通过高通量16 S核糖体RNA测序分析盲肠内容物。FRT 10补充显著降低体重增加、脂肪重量以及肝脏三酰甘油(TG)和丙氨酸氨基转移酶(ALT)浓度(P < 0.05)。FRT 10显著改善了HFD诱导的肠道生态失调,如通过增加的微生物丰度(包括丁酸球菌属、丁酸单胞菌属、肠单胞菌属、气味杆菌属和Alistipes)以及减少的脱硫弧菌科、罗斯拜瑞氏菌属和毛梭菌属丰度所证明的。乳杆菌、双歧杆菌和阿克曼氏菌在FRT 10干预后显著增加。此外,实时定量PCR显示,FRT 10上调肝脏中过氧化物酶体增殖物激活受体α(PPAR α)和肉毒碱棕榈酰转移酶1 α(CPT 1 α)的mRNA表达水平,下调固醇调节元件结合蛋白1(SREBP-1)和TG合成酶二酰基甘油酰基转移酶1(DGAT 1)的mRNA表达水平。这些结果表明FRT 10对肥胖小鼠具有抗肥胖作用,部分与激活PPAR α/CPT 1 α通路有关。FRT 10可以被认为是用于预防人类和动物中HFD诱导的肥胖的单一益生菌剂。
Previous studies showed that probiotics supplementation contributed to alleviate obesity. This work was to assess the efficacy of Lactobacillus plantarum FRT10 from sour dough in alleviating obesity in mice fed with a high-fat diet (HFD), and the underlying mechanisms focusing on modulation of the gut microbiota profile. Kunming mice were fed with a regular diet (CT), a high-fat diet (HFD), and two HFDs containing low and high doses of L. plantarum FRT10 for 8 weeks. The physiological and biochemical modulations in liver were analyzed. Cecal contents were analyzed by high-throughput 16S ribosomal RNA sequencing. FRT10 supplementation significantly reduced body weight gain, fat weight, and liver triacylglycerols (TGs) and alanine aminotransferase (ALT) concentrations (P < 0.05). FRT10 significantly ameliorated the HFD-induced gut dysbiosis, as evidenced by increased abundance of microbes, including Butyricicoccus, Butyricimonas, Intestinimonas, Odoribacter, and Alistipes, and decreased abundance of Desulfovibrionaceae, Roseburia, and Lachnoclostridium. Lactobacillus, Bifidobacterium, and Akkermansia were markedly increased after FRT10 intervention. In addition, real-time quantitative PCR revealed that FRT10 upregulated the mRNA expression levels of peroxisome proliferator-activated receptor-alpha (PPAR alpha) and carnitine palmitoyltransferase-1 alpha (CPT1 alpha), and downregulated the mRNA expression levels of sterol regulatory element-binding protein 1 (SREBP-1) and TG-synthesizing enzyme diacylglycerol acyltransferase 1 (DGAT1) in liver. These findings suggested that FRT10 had anti-obesity effects in obese mice partly related to the activation of PPAR alpha/CPT1 alpha pathway. FRT10 can be considered a single probiotic agent for preventing HFD-induced obesity in humans and animals.