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Tea Polysaccharide Ameliorates High-Fat Diet-Induced Renal Tubular Ectopic Lipid Deposition via Regulating the Dynamic Balance of Lipogenesis and Lipolysis

文献类型： 外文期刊

作者： Kuang, Dan-Dan 1 ; Li, Xue-Ying 1 ; Qian, Xin-Ping 1 ; Zhang, Ting 1 ; Deng, Yuan-Yuan 3 ; Li, Qiang-Ming 1 ; Luo, Jian-Ping 1 ; Zha, Xue-Qiang 1 ;

作者机构： 1.Hefei Univ Technol, Minist Educ, Engn Res Ctr Bioproc Minist Educ, Sch Food & Biol Engn, Hefei 230009, Peoples R China

2.Hefei Univ Technol, Sch Food & Biol Engn, Hefei 230009, Peoples R China

3.Guangdong Acad Agr Sci, Sericultural & Agrifood Res Inst, Guangzhou 510610, Peoples R China

关键词： tea; polysaccharide; renal tubular ELD; lipogenesis and lipolysis

期刊名称：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY （ 影响因子：6.1； 五年影响因子：6.3 ）

ISSN： 0021-8561

年卷期： 2024 年 72 卷 22 期

页码：

收录情况： SCI

摘要： Renal tubular ectopic lipid deposition (ELD) plays a significant role in the development of chronic kidney disease, posing a great threat to human health. The present work aimed to explore the intervention effect and potential molecular mechanism of a purified tea polysaccharide (TPS3A) on renal tubular ELD. The results demonstrated that TPS3A effectively improved kidney function and slowed the progression of tubulointerstitial fibrosis in high-fat-diet (HFD)-exposed ApoE(-/-) mice. Additionally, TPS3A notably suppressed lipogenesis and enhanced lipolysis, as shown by the downregulation of lipogenesis markers (SREBP-1 and FAS) and the upregulation of lipolysis markers (HSL and ATGL), thereby reducing renal tubular ELD in HFD-fed ApoE(-/-) mice and palmitic-acid-stimulated HK-2 cells. The AMPK-SIRT1-FoxO1 axis is a core signal pathway in regulating lipid deposition. Consistently, TPS3A significantly increased the levels of phosphorylated-AMPK, SIRT1, and deacetylation of Ac-FoxO1. However, these effects of TPS3A on lipogenesis and lipolysis were abolished by AMPK siRNA, SIRT1 siRNA, and FoxO1 inhibitor, resulting in exacerbated lipid deposition. Taken together, TPS3A shows promise in ameliorating renal tubular ELD by inhibiting lipogenesis and promoting lipolysis through the AMPK-SIRT1-FoxO1 signaling pathway.

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