食品科学 ›› 2026, Vol. 47 ›› Issue (16): 174-182.doi: 10.7506/spkx1002-6630-20260128-262

• 营养卫生 • 上一篇    下一篇

磷脂酰葡萄糖苷通过PPARγ/TrkB双重调控高脂高糖饮食诱导小鼠糖脂代谢的作用

郭筱晨,刘峻屹,高锐,薛长湖,徐杰,刘炎峻   

  1. (1.中国海洋大学食品科学与工程学院,山东?青岛 266100;2.青岛海洋食品营养与健康创新研究院,山东?青岛 266100)
  • 出版日期:2026-08-25 发布日期:2026-09-03
  • 基金资助:
    “十四五”国家重点研发计划重点专项(2024YFD2401602);山东省泰山学者青年专家项目(tsqn202507093); 中国海洋大学青年交叉创新研究计划项目(2024104);中央高校基本科研业务费项目(862401013170)

Effect of Phosphatidylglucoside on Glucose and Lipid Metabolism in Mice Fed High-Fat and High-Sugar Diet through Dual Regulation of PPARγ and TrkB

GUO Xiaochen, LIU Junyi, GAO Rui, XUE Changhu, XU Jie, LIU Yanjun   

  1. (1. College of Food Science and Engineering, Ocean University of China, Qingdao 266100, China;2. Qingdao Institute of Marine Bioresources for Nutrition & Health Innovation, Qingdao 266100, China)
  • Online:2026-08-25 Published:2026-09-03

摘要: 本实验通过磷脂酶D介导的酶法转化技术制备高纯度的磷脂酰葡萄糖苷(phosphatidylglucoside,PtdGlc),其主要结构为C16:0/18:2-PtdGlc与C18:2/18:2-PtdGlc,并在改善糖脂代谢的作用及其机制上进行系统研究。首先通过过氧化物酶体增殖物激活受体γ2亚型(peroxisome proliferator-activated receptor γ2,PPARγ2)双荧光素酶报告基因技术检测PtdGlc对PPARγ2转录活性的影响,发现PtdGlc具有PPARγ2转录激活作用。此外,以高脂高糖饮食诱导的代谢紊乱小鼠为模型,考察PtdGlc对小鼠糖脂代谢的影响。结果发现PtdGlc可通过激活PPARγ及其下游基因表达(Adpn、Acc1、Ap2)有效降低高脂高糖饮食诱导的小鼠空腹血糖及胰岛素水平,显著改善葡萄糖耐受能力和胰岛素敏感性,且其活性优于磷脂酰胆碱。此外,PtdGlc干预显著降低小鼠体质量,并降低血清中的总甘油三酯与总胆固醇水平。最重要的是,PtdGlc膳食干预可通过上调脑源性神经营养因子/原肌球蛋白受体激酶B信号通路显著抑制小鼠食欲,从而减少能量摄入,规避了传统PPARγ激动剂诱发体质量增加的副作用。本研究结果可为利用PtdGlc开发具有调控糖脂代谢的健康食品提供理论基础。

关键词: 磷脂酰葡萄糖苷;肥胖;糖脂代谢

Abstract: In this study, high-purity phosphatidylglucoside (PtdGlc) was prepared via phospholipase D-mediated enzymatic conversion, and its major structures were identified as C16:0/18:2-PtdGlc and C18:2/18:2-PtdGlc. A systematic investigation was then conducted on the effect of PtdGlc on glycolipid metabolism and the underlying mechanisms. First, the dual-luciferase reporter gene assay was employed to detect the impact of PtdGlc on the transcriptional activity of peroxisome proliferator-activated receptor γ2 (PPARγ2), revealing that PtdGlc transcriptionally activated PPARγ2. In addition, we evaluated the regulatory effect of PtdGlc on glycolipid metabolism disorders induced by a high-fat and high-sugar diet in mice. The results demonstrated that PtdGlc effectively reduced the fasting blood glucose and insulin levels in mice fed a high-fat and high-sugar diet by activating PPARγ and the expression of its downstream genes (Adpn, Acc1, Ap2), thereby significantly improving glucose tolerance and insulin sensitivity, and its activity was superior to that of phosphatidylcholine. Moreover, PtdGlc intervention notably decreased body mass and serum triglyceride and total cholesterol levels in mice. Most importantly, dietary intervention with PtdGlc could significantly suppress the appetite of mice via upregulation of the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) signaling pathway, thereby reducing energy intake and avoiding the side effect of weight gain induced by traditional PPARγ agonists. The findings of this study provide a theoretical basis for the development of PtdGlc-based health foods for regulating glucose and lipid metabolism.

Key words: hosphatidylglucoside; obesity; glucose and lipid metabolism

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