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植物乳杆菌 FRT10 通过调节 PPARα 信号通路和肠道微生物群缓解高脂饮食诱导的肥胖。

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

机构信息

Key Laboratory of Feed Biotechnology, Ministry of Agriculture and Rural Affairs, Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing, 100081, China.

National Engineering Research Center of Biological Feed, Beijing, 100081, China.

出版信息

Appl Microbiol Biotechnol. 2020 Jul;104(13):5959-5972. doi: 10.1007/s00253-020-10620-0. Epub 2020 May 14.

DOI:10.1007/s00253-020-10620-0
PMID:32409945
Abstract

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-α (PPARα) and carnitine palmitoyltransferase-1α (CPT1α), 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 PPARα/CPT1α pathway. FRT10 can be considered a single probiotic agent for preventing HFD-induced obesity in humans and animals.

摘要

先前的研究表明,益生菌补充剂有助于缓解肥胖。本工作旨在评估来自酸面团的植物乳杆菌 FRT10 在缓解高脂肪饮食(HFD)喂养的肥胖小鼠中的功效,并关注其调节肠道微生物群谱的潜在机制。昆明小鼠分别用常规饮食(CT)、高脂肪饮食(HFD)和两种含低、高剂量植物乳杆菌 FRT10 的 HFD 喂养 8 周。分析肝脏的生理生化调节。通过高通量 16S 核糖体 RNA 测序分析盲肠内容物。FRT10 补充显著降低了体重增加、脂肪重量和肝三酰基甘油(TGs)和丙氨酸转氨酶(ALT)浓度(P<0.05)。FRT10 显著改善了 HFD 诱导的肠道菌群失调,表现为微生物丰度增加,包括丁酸梭菌、丁酸单胞菌、肠球菌、恶臭杆菌和阿里斯泰普斯菌,脱硫弧菌科、玫瑰杆菌和lachnoclostridium 减少。FRT10 干预后,乳杆菌和双歧杆菌和阿克曼氏菌显著增加。此外,实时定量 PCR 显示 FRT10 上调了过氧化物酶体增殖物激活受体-α(PPARα)和肉碱棕榈酰转移酶-1α(CPT1α)的 mRNA 表达水平,并下调了固醇调节元件结合蛋白 1(SREBP-1)和甘油三酯合成酶二酰基甘油酰基转移酶 1(DGAT1)的 mRNA 表达水平。这些发现表明,FRT10 对肥胖小鼠具有抗肥胖作用,部分与激活 PPARα/CPT1α 途径有关。FRT10 可以被认为是一种单一的益生菌制剂,用于预防人类和动物的 HFD 诱导肥胖。

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