Chen Yiqin, Huang Yanxin, Gan Qiaorong, Zhang Wenhui, Sun Han, Zhu Lingling, Wang Wenxiang
Department of Health Inspection and Quarantine, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China.
Department of Nutrition, The 95th Hospital of Putian, Putian, Fujian, China.
J Food Sci. 2024 Dec;89(12):10064-10078. doi: 10.1111/1750-3841.17575. Epub 2024 Dec 5.
In the present study, we succeeded in extracting tea polysaccharide (TPS) from Tieguanyin oolong tea, and the TPS was characterized. TPS is an acidic heteropolysaccharide containing rhamnose, arabinose, galactose, glucose (Glc), xylose, mannose, galacturonic acid, and guluronic acid. We found that TPS supplementation partially reversed the elevated levels of serum alanine aminotransferase, total cholesterol, and low-density lipoprotein cholesterol in high-fat diet (HD)-induced nonalcoholic fatty liver disease (NAFLD) mice (p < 0.05), and hepatic steatosis and impaired Glc tolerance were also ameliorated. After HD intervention, the activity of Adenosine 5'-monophosphate-activated protein kinase (AMPK) and its downstream genes, including Sirtuin 1 (SIRT1), sterol regulatory element-binding protein-1c (SREBP1c), acetyl-coenzyme A carboxylase 1 (ACC1), and adipose triglyceride lipase (ATGL), was significantly inhibited (p < 0.05). TPS can increase the expression of these genes. The hepatoprotective effects of TPS in AMPK-/- mice almost completely disappeared. Moreover, the expression levels of SIRT1, SREBP1c, ACC1, and ATGL did not significantly change after TPS supplementation (p > 0.05). Therefore, our findings suggest that TPS protects the liver from hepatic glucolipid metabolism disorders in HD-induced NAFLD mice by activating AMPK-mediated signaling pathways.
在本研究中,我们成功从铁观音乌龙茶中提取了茶多糖(TPS),并对其进行了表征。TPS是一种酸性杂多糖,含有鼠李糖、阿拉伯糖、半乳糖、葡萄糖(Glc)、木糖、甘露糖、半乳糖醛酸和古洛糖醛酸。我们发现,补充TPS可部分逆转高脂饮食(HD)诱导的非酒精性脂肪性肝病(NAFLD)小鼠血清丙氨酸氨基转移酶、总胆固醇和低密度脂蛋白胆固醇水平的升高(p < 0.05),肝脂肪变性和葡萄糖耐量受损也得到改善。HD干预后,5'-单磷酸腺苷激活蛋白激酶(AMPK)及其下游基因,包括沉默调节蛋白1(SIRT1)、固醇调节元件结合蛋白-1c(SREBP1c)、乙酰辅酶A羧化酶1(ACC1)和脂肪甘油三酯脂肪酶(ATGL)的活性受到显著抑制(p < 0.05)。TPS可增加这些基因的表达。TPS对AMPK基因敲除小鼠的肝脏保护作用几乎完全消失。此外,补充TPS后,SIRT1、SREBP1c、ACC1和ATGL的表达水平没有显著变化(p > 0.05)。因此,我们的研究结果表明,TPS通过激活AMPK介导的信号通路,保护肝脏免受HD诱导的NAFLD小鼠肝糖脂代谢紊乱的影响。