欢迎访问《茶叶科学》,今天是

茶叶科学 ›› 2024, Vol. 44 ›› Issue (1): 119-132.doi: 10.13305/j.cnki.jts.2024.01.008

• 研究报告 • 上一篇    下一篇

EGCG对高脂饮食GK大鼠白色脂肪米色化的诱导作用与机制研究

万丽玮, 曾鸿哲, 彭丽媛, 文帅, 刘昌伟, 鲍肃都, 安勤, 黄建安*, 刘仲华*   

  1. 湖南农业大学茶学教育部重点实验室,国家植物功能成分利用工程技术研究中心,植物功能成分利用省部共建协同创新中心,农业农村部园艺作物基因资源评价利用重点实验室,湖南 长沙 410128
  • 收稿日期:2023-10-11 修回日期:2023-11-11 出版日期:2024-02-25 发布日期:2024-03-13
  • 通讯作者: *Jian7513@hunau.edu.cn;larkin-liu@163.com
  • 作者简介:万丽玮,女,硕士研究生,主要从事茶叶功能成分利用与深加工研究。
  • 基金资助:
    国家茶叶产业技术体系(CARS-19)、茶叶功能成分优异资源高效利用技术研究(湘财农指[2021]0015号)

Inductive Effect and Mechanism of EGCG on Beiging of White Adipose Tissue in High-fat Diet-fed GK Rats

WAN Liwei, ZENG Hongzhe, PENG Liyuan, WEN Shuai, LIU Changwei, BAO Sudu, AN Qin, HUANG Jian'an*, LIU Zhonghua*   

  1. Key Lab of Education Ministry of Hunan Agricultural University for Tea Science, National Research Center of Engineering and Technology for Utilization of Botanical Functional Ingredients, Co-Innovation Center of Education Ministry for Utilization of Botanical Functional Ingredients, Key Laboratory for Evaluation and Utilization of Gene Resources of Horticultural Crops, Ministry of Agriculture and Rural Affairs of China, Changsha 410128, China
  • Received:2023-10-11 Revised:2023-11-11 Online:2024-02-25 Published:2024-03-13

摘要: 脂肪组织类型与人体代谢密切相关,通过饮食或营养干预将白色脂肪细胞转变为产热的米色脂肪细胞是一种减少脂肪积蓄、调节代谢的安全策略。目前关于白色脂肪组织米色化作用的研究多聚焦于肥胖群体,为探究EGCG对非肥胖代谢紊乱群体的内脏白色脂肪组织米色化的诱导作用及相关机制,采用非肥胖型自发性2型糖尿病模型Goto-Kakizaki(GK)大鼠,给予每日高脂饮食,并进行40 mg·kg-1和80 mg·kg-1 EGCG灌胃干预,检测GK大鼠的体质量、摄食量、脂肪组织细胞形态及米色化相关基因表达水平、UCP1蛋白表达水平,并进行转录组测序。结果表明,80 mg·kg-1 EGCG灌胃干预对GK大鼠摄食量和体质量无明显影响,但能够促使脂肪细胞呈现向多房型脂肪细胞转变趋势,并显著上调米色化相关的PpargPpargc1aUcp1基因表达水平和UCP1蛋白表达水平,具有诱导高脂饮食GK大鼠内脏附睾白色脂肪组织米色化的作用,且表现出调节脂质代谢的潜力。结合转录组分析结果表明,EGCG对高脂饮食GK大鼠白色脂肪组织米色化的诱导作用机制可能与PPAR信号通路、PI3K/Akt信号通路和MAPK信号通路有关。

关键词: EGCG, 非肥胖型, GK大鼠, 白色脂肪组织, 米色化

Abstract: The types of adipose tissue are closely related to human metabolism. Transforming white adipocytes into thermogenic beige adipocytes through dietary or nutritional interventions is a safe strategy to reduce fat accumulation and regulate metabolism. Currently, research on the role of white adipose tissue beiging has mainly focused on obese populations. To explore the effect of EGCG on promoting the beiging of white adipose tissue in non-obese individuals with metabolic disorders and its related mechanisms, this study used non-obese, spontaneously diabetic type 2 GK rats. These rats were fed a high-fat diet and received 40 mg·kg-1 and 80 mg·kg-1 EGCG daily by gavage. In this study, we assessed body weight, food intake, cellular morphology of adipose tissue, gene expression levels associated with beiging, and protein expression levels of UCP1 in GK rats. Additionally, transcriptome sequencing was also performed on epididymal white adipose tissue. The results show that gavage intervention with 80 mg·kg-1 EGCG has no significant effect on the food intake and body weight of GK rats. It induced a trend of beiging in adipocytes towards a multilocular phenotype transformation, characterized by a decrease in cell size and an increase in cell number. Moreover, it significantly upregulated the expression levels of beiging-related genes Pparg, Ppargc1a, Ucp1 and the protein expression level of UCP1.This demonstrates the inducing effect of EGCG on the beiging of visceral epididymal white adipose tissue in high-fat diet-fed GK rats, indicating its potential in the regulation of lipid metabolism. Combined with transcriptome analysis, the results suggest that the induction mechanism of EGCG on the beiging of white adipose tissue in high-fat diet-fed GK rats may be associated with the PPAR signaling pathway, PI3K/Akt, and MAPK signaling pathway.

Key words: EGCG, non-obesetype, Goto-Kakizaki rats, white adipose tissue, beiging

中图分类号: