Cai Hongying, Wen Zhiguo, Zhao Lulu, Yu Dali, Meng Kun, Yang Peilong
Institute of Feed Research, Chinese Academy of Agricultural Sciences, Beijing, China.
National Engineering Research Center of Biological Feed, Beijing, China.
Food Nutr Res. 2022 May 9;66. doi: 10.29219/fnr.v66.7974. eCollection 2022.
Obesity has become a global epidemic recognized by the World Health Organization. Probiotics supplementation has been shown to contribute to improve lipid metabolism. However, mechanisms of action of probiotics against obesity are still not clear. FRT4, a probiotic previously isolated from a kind of local yogurt, had good acid and bile salt tolerance and lowered cholesterol .
This study aimed to evaluate the effect of FRT4 on serum and liver lipid profile, liver metabolomics, and gut microbiota in mice fed with a high-fat diet (HFD).
Mice were fed with either normal diet or HFD for 16 weeks and administered 0.2 mL of 1 × 10 or 1 × 10 CFU/mL dosage of FRT4 during the last 8 weeks of the diet. Cecal contents were analyzed by 16S rRNA sequencing. Hepatic gene expression and metabolites were detected by real-time quantitative polymerase chain reaction (PCR) and metabolomics, respectively.
FRT4 intervention significantly reduced the HFD-induced body weight gain, liver weight, fat weight, serum cholesterol, triglyceride, and alanine aminotransferase (ALT) levels in the liver ( 0.05). Liver metabolomics demonstrated that the HFD increased choline, glycerophosphocholine, and phosphorylcholine involved in the glycerophospholipid metabolism pathway. All these changes were reversed by FRT4 treatment, bringing the levels close to those in the control group. Further mechanisms showed that FRT4 favorably regulated gut barrier function and pro-inflammatory biomediators. Furthermore, FRT4 intervention altered the gut microbiota profiles and increased microbial diversity. The relative abundances of , , , , , , and were significantly upregulated. Finally, Spearman's correlation analysis revealed that several specific genera were strongly correlated with glycerophospholipid metabolites ( 0.05).
These findings suggested that FRT4 had beneficial effects against obesity in HFD-induced obese mice and can be used as a potential functional food for the prevention of obesity.
肥胖已成为世界卫生组织认可的一种全球流行病。补充益生菌已被证明有助于改善脂质代谢。然而，益生菌对抗肥胖的作用机制仍不清楚。FRT4是一种先前从一种当地酸奶中分离出的益生菌，具有良好的耐酸和耐胆盐能力，并能降低胆固醇。
本研究旨在评估FRT4对高脂饮食（HFD）喂养小鼠的血清和肝脏脂质谱、肝脏代谢组学以及肠道微生物群的影响。
小鼠分别喂食正常饮食或HFD 16周，并在饮食的最后8周给予0.2 mL 1×10⁸或1×10⁹ CFU/mL剂量的FRT4。通过16S rRNA测序分析盲肠内容物。分别通过实时定量聚合酶链反应（PCR）和代谢组学检测肝脏基因表达和代谢产物。
FRT4干预显著降低了HFD诱导的体重增加、肝脏重量、脂肪重量、血清胆固醇、甘油三酯和肝脏中的丙氨酸氨基转移酶（ALT）水平（P<0.05）。肝脏代谢组学表明，HFD增加了参与甘油磷脂代谢途径的胆碱、甘油磷酸胆碱和磷酸胆碱。FRT4处理逆转了所有这些变化，使这些水平接近对照组。进一步的机制表明，FRT4有利地调节肠道屏障功能和促炎生物介质。此外，FRT4干预改变了肠道微生物群谱并增加了微生物多样性。双歧杆菌属、乳杆菌属、阿克曼菌属、拟杆菌属、瘤胃球菌属、粪杆菌属和普雷沃菌属的相对丰度显著上调。最后，Spearman相关性分析显示，几个特定菌属与甘油磷脂代谢产物密切相关（P<0.05）。
这些发现表明，FRT4对HFD诱导的肥胖小鼠具有抗肥胖有益作用，可作为预防肥胖的潜在功能性食品。
