长期过量摄入果糖激活大鼠内源性嘌呤的原始生物合成和代谢途径。

IF 4.2 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
Qiuxia Yu, Wenwen Tan, Xingdong Ma, Lieqiang Xu, Guoshu Lin, Juanjuan Cheng, Qingfeng Xie, Yuhong Liu, Yucui Li, Yanfang Xian, Zhixiu Lin, Jiannan Chen, Ziren Su, Xiaobo Yang, Jianhui Xie
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引用次数: 0

摘要

果糖是一种广泛使用的营养物质,作为各种食品和饮料的甜味剂。越来越多的证据表明,膳食果糖与高尿酸血症(HUA)等代谢性疾病密切相关。然而,果糖摄入的作用和代谢命运仍然难以理解。目前的工作作出了开创性的努力,以揭示长期果糖过量摄入和HUA发病率之间的潜在机制联系。给予大鼠高果糖(30%)不含饮料17周。结果表明,长期高果糖摄入显著增加了尿酸、肌酐和尿素水平。此外,高尿酸血症大鼠观察到高果糖引起的轻度肾脏改变。高果糖摄入并没有激活酮己糖激酶,而是激活了戊糖磷酸途径(PPP),从而产生丰富的5-磷酸核糖和焦磷酸磷酸核糖。激活新嘌呤生物合成(DNPB)产生嘌呤,加速嘌呤循环。高果糖摄入显著提高了DNPB核心酶的表达,改变了嘌呤酶体的形成和形成区域。此外,黄嘌呤氧化酶(XOD)的上调促进了嘌呤代谢,导致单磷酸肌苷、肌苷、次黄嘌呤和黄嘌呤水平升高。此外,靶向代谢组分析还表明,果糖代谢引发了ATP消耗和NAD+和NADH激增的生物能改变。因此,长期摄入高果糖导致了HUA,这与PPP、DNPB和XOD同时介导的内源性嘌呤原始生物合成和代谢途径的激活密切相关,并伴有生物能的改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Prolonged Fructose Overconsumption Activates Original Biosynthetic and Metabolic Pathways of Endogenous Purine in Rats

Prolonged Fructose Overconsumption Activates Original Biosynthetic and Metabolic Pathways of Endogenous Purine in Rats

Fructose is a nutrient used widely and indiscriminately as a sweetener in various types of foods and beverages. Accumulating evidence suggests that dietary fructose has a close relationship with metabolic diseases like hyperuricemia (HUA). However, the role and metabolic fate of fructose intake remain elusively obscure. The present work made a pioneering endeavor to unravel the potential mechanistic link between prolonged fructose overconsumption and the incidence of HUA. High-fructose (30%) free drinking was provided to rats for 17 weeks. Results indicated that long-term high-fructose intake remarkably increased the levels of uric acid, creatinine, and urea. Besides, mild renal alteration induced by high fructose was observed in the hyperuricemic rats. Instead of activating ketohexokinase, high-fructose intake activated the pentose phosphate pathway (PPP) to produce abundant ribose 5-phosphate and phosphoribosyl pyrophosphate. The de novo purine biosynthesis (DNPB) was activated to produce purines and accelerate the purine cycle. High-fructose intake significantly enhanced the expression of core enzymes of DNPB and changed the purinosome formation and forming areas. Furthermore, up-regulation of xanthine oxidase (XOD) promoted the purine metabolism, resulting in increased levels of inosine monophosphate, inosine, hypoxanthine, and xanthine. Besides, the targeted metabolome analysis also showed that fructose metabolism triggered bioenergetic alteration with the consumption of ATP and a surge in NAD+ and NADH. Hence, chronic ingestion of high-fructose contributed to HUA, which was intimately associated with activation of original biosynthetic and metabolic pathways of endogenous purine simultaneously mediated by PPP, DNPB, and XOD and accompanied by bioenergetic alteration.

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来源期刊
Molecular Nutrition & Food Research
Molecular Nutrition & Food Research 工程技术-食品科技
CiteScore
8.70
自引率
1.90%
发文量
250
审稿时长
1.7 months
期刊介绍: Molecular Nutrition & Food Research is a primary research journal devoted to health, safety and all aspects of molecular nutrition such as nutritional biochemistry, nutrigenomics and metabolomics aiming to link the information arising from related disciplines: Bioactivity: Nutritional and medical effects of food constituents including bioavailability and kinetics. Immunology: Understanding the interactions of food and the immune system. Microbiology: Food spoilage, food pathogens, chemical and physical approaches of fermented foods and novel microbial processes. Chemistry: Isolation and analysis of bioactive food ingredients while considering environmental aspects.
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