Despite strong indications that increased consumption of added sugars correlates with greater risks of developing cardiometabolic syndrome (CMS) and cardiovascular disease (CVD), independent of the caloric intake, the worldwide sugar consumption remains high. In considering the negative health impact of overconsumption of dietary sugars, increased attention is recently being given to the role of the fructose component of high-sugar foods in driving CMS. The primary organs capable of metabolizing fructose include liver, small intestine, and kidneys. In these organs, fructose metabolism is initiated by ketohexokinase (KHK) isoform C of the central fructose-metabolizing enzyme KHK. Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments. In this review, we highlight recent progress in understanding how fructose metabolism contributes to the development of major systemic pathologies that cooperatively promote CMS and CVD, reference recent insights into microenvironmental control of fructose metabolism under stress conditions and discuss how this understanding is shaping preventive actions and therapeutic approaches.

中文翻译：

---

果糖代谢、心脏代谢风险和冠状动脉疾病的流行

尽管有强有力的迹象表明，添加糖的摄入量增加与患心脏代谢综合征 (CMS) 和心血管疾病 (CVD) 的风险增加相关，而与热量摄入无关，但全球糖摄入量仍然很高。考虑到膳食糖摄入过多对健康的负面影响，最近人们越来越关注高糖食品中的果糖成分在导致 CMS 中的作用。能够代谢果糖的主要器官包括肝脏、小肠和肾脏。在这些器官中，果糖代谢是由中心果糖代谢酶 KHK 的酮己糖激酶 (KHK) 亚型 C 启动的。新数据表明，这种果糖代谢的组织限制可以在缺氧环境中消除。在这篇综述中，我们重点介绍了在理解果糖代谢如何促进协同促进 CMS 和 CVD 的主要系统病理学发展方面的最新进展，参考了对应激条件下果糖代谢微环境控制的最新见解，并讨论了这种理解如何影响预防行动和治疗方法。