Unveiling the sweet culprit: Excessive fructose intake leading to kidney injury through hypoxanthine accumulation
文献类型： 外文期刊
作者： Ai, Gaoxiang 1 ; Tan, Wenwen 3 ; Huang, Ziwei 3 ; Xu, Lieqing 4 ; Yu, Qiuxia 5 ; Wu, Xiaoyan 3 ; Xie, Jianhui 6 ; Su, Ziren 3 ; Chen, Jiannan 3 ; Chen, Xiaolian 1 ; Dou, Yaoxing 8 ;
作者机构： 1.Jiangxi Acad Agr Sci, Inst Anim Husb & Vet Sci, Nanchang 330200, Peoples R China
2.Jiangxi Prov Key Lab Anim Green & Hlth Breeding, Nanchang 330200, Peoples R China
3.Guangzhou Univ Chinese Med, Sch Pharmaceut Sci, Guangzhou 510006, Peoples R China
4.Jiangxi Agr Univ, Coll Biosci & Bioengn, Nanchang 330045, Peoples R China
5.Guangzhou Univ Chinese Med, Affiliated Hosp 2, Guangzhou 510120, Peoples R China
6.Guangzhou Univ Chinese Med, Affiliated Hosp 2, State Key Lab Tradit Chinese Med Syndrome, State Key Lab Dampness Syndrome Chinese Med, Guangzhou, Peoples R China
7.Guangdong Prov Key Lab Clin Res Tradit Chinese Med, Guangzhou 510120, Peoples R China
8.Guangdong Med Univ, Sch Ocean & Trop Med, Zhanjiang 524023, Peoples R China
9.Guangdong Med Univ, Marine Biomed Res Inst Guangdong Zhanjiang, Zhanjiang 524023, Peoples R China
关键词： Fructose; Hypoxanthine; Kidney injury; Keap1-Nrf2 signaling pathway; NLRP3 inflammasome
期刊名称：JOURNAL OF FUNCTIONAL FOODS （ 影响因子：4.0； 五年影响因子：4.9 ）
ISSN： 1756-4646
年卷期： 2025 年 131 卷
页码：
收录情况： SCI
摘要： Fructose, a frequent-using sweeter, has been widely used in the food and beverage industry. Notably, prolonged consumption of fructose-rich diets has been recognized as a culprit causing kidney injury. However, it remains elusively obscure whether excessive fructose intake resulted in hypoxanthine (HX) accumulation and further induced kidney injury. Therefore, the present work made a pioneering endeavor to unravel the potential material basis of fructose-induced kidney injury and further probed its underlying pathogenic mechanism. Results indicated that long-term high-fructose intake contributed to HX accumulation, which subsequently triggered inflammation and oxidative damage. Moreover, further mechanistic investigations suggested that accumulated HX inhibited nuclear factor-erythroid-2-related factor 2 (Nrf2) nuclear translocation and consequently down-regulated expressions of downstream antioxidant proteins. Additionally, it effectively promoted NOD-like receptor 3 (NLRP3) inflammasome activation. Altogether, these findings suggested that excessive fructose consumption facilitated HX accumulation, which further aggravated kidney injury, at least in part, via modulating the Keap1-Nrf2/NLRP3 signaling axis.
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