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Eur Heart J. 2018 Jul 7;39(26):2497-2505. doi: 10.1093/eurheartj/ehx518.

Fructose metabolism, cardiometabolic risk, and the epidemic of coronary artery disease.

Author information

1
Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Otto-Stern-Weg 7, Zurich, Switzerland.
2
Department of Clinical Pathobiochemistry, Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Dresden, Fetscherstr. 74, Dresden, Germany.
3
Department of Medicine, Cardiovascular Institute and Institute Diabetes Obesity and Metabolism, Perelman School of Medicine, University of Pennsylvania, 11th floor, Civic Blvd, Philadelphia, 19104 PA, USA.

Abstract

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 Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments.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.

PMID:
29020416
PMCID:
PMC6037111
[Available on 2019-07-07]
DOI:
10.1093/eurheartj/ehx518

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