Dong Wenchao, Mao Yulin, Xiang Zhenhua, Zhu Jingyu, Wang Haixia, Wang Aiju, Jiang Meifang, Gu Yuming
Department of Traditional Chinese Medicine, Affiliated Hospital of Weifang Medical University, School of Clinical Medicine, Weifang Medical University, Weifang 261042, China.
Weifang Medical University, Weifang 261042, China.
Evid Based Complement Alternat Med. 2022 Aug 8;2022:9727889. doi: 10.1155/2022/9727889. eCollection 2022.
The current study employed the high-fat diet (HFD) induced murine model to assess the relationship between the effect of Jian Pi Tiao Gan Yin (JPTGY) and the alterations of gut microbiota and fecal metabolism. C57BL/6 mice were used to establish an animal model of obesity via HFD induce. Serum biochemical indicators of lipid metabolism were used to evaluate the pharmacodynamics of JPTGY in obese mice. Bacterial communities and metabolites in the feces specimens from the controls, the Group HFD, and the JPTGY-exposed corpulency group were studied by 16s rDNA genetic sequence in combination with liquid chromatography-mass spectrometry (LC-MS) based untargeted fecal metabolomics techniques. Results revealed that JPTGY significantly decreased the levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and elevated high-density lipoprotein cholesterol (HDL-C). Moreover, JPTGY could up-regulate the abundance and diversity of fecal microbiota, which was characterized by the higher phylum of proteobacteria. Consistently, at the genus levels, JPTGY supplementation induced enrichments in , , , , and , which were intimately related to 14 pivotal fecal metabolins in respond to JPTGY therapy were determined. What is more, metabolomics further analyses show that the therapeutic effect of JPTGY for obesity involves linoleic acid (LA) metabolism paths, alpha-linolenic acid (ALA) metabolism paths, glycerophospholipid metabolism paths, arachidonic acid (AA) metabolism paths, and pyrimidine metabolism paths, which implied the potential mechanism of JPTGY in treating obesity. It was concluded that the linking of corpulency phenotypes with intestinal flora and fecal metabolins unveils the latent causal link of JPTGY in the treatment of hyperlipidemia and obesity.
本研究采用高脂饮食（HFD）诱导的小鼠模型，以评估健脾调肝饮（JPTGY）的作用与肠道微生物群及粪便代谢变化之间的关系。通过高脂饮食诱导，利用C57BL/6小鼠建立肥胖动物模型。采用脂质代谢血清生化指标评估JPTGY对肥胖小鼠的药效学作用。运用16s rDNA基因序列结合基于液相色谱 - 质谱联用（LC - MS）的非靶向粪便代谢组学技术，研究对照组、高脂饮食组和JPTGY干预肥胖组粪便标本中的细菌群落和代谢产物。结果显示，JPTGY显著降低了总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL - C）水平，并提高了高密度脂蛋白胆固醇（HDL - C）水平。此外，JPTGY可上调粪便微生物群的丰度和多样性，其特征在于变形菌门的比例较高。同样，在属水平上，补充JPTGY诱导了 、 、 、 和 的富集，确定了与JPTGY治疗相关的14种关键粪便代谢物密切相关。更重要的是，代谢组学进一步分析表明，JPTGY对肥胖的治疗作用涉及亚油酸（LA）代谢途径、α - 亚麻酸（ALA）代谢途径、甘油磷脂代谢途径、花生四烯酸（AA）代谢途径和嘧啶代谢途径，这暗示了JPTGY治疗肥胖的潜在机制。得出结论，肥胖表型与肠道菌群和粪便代谢物的关联揭示了JPTGY在治疗高脂血症和肥胖症中的潜在因果联系。
