Fructose metabolism, cardiometabolic risk, and the epidemic of coronary artery disease
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Date
2018-07-07
Publication Type
Review Article
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yes
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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 Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments.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.
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Publication status
published
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Book title
Journal / series
Volume
39 (26)
Pages / Article No.
2497 - 2505
Publisher
Oxford University Press
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Edition / version
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Date collected
Date created
Subject
Fructose; Cardiometabolic syndrome; Cardiac hypertrophy; Atherosclerosis; Nonalcoholic fatty liver disease; Diabetes type 2; Fructolysis; Ketohexokinase; Hypertension; Alternative splicing; SF3B1; HIF; Hypoxia
Organisational unit
03630 - Krek, Wilhelm (ehemalig) / Krek, Wilhelm (former)
Notes
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.