Journal
EUROPEAN HEART JOURNAL
Volume 39, Issue 26, Pages 2497-+Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehx518
Keywords
Fructose; Cardiometabolic syndrome; Cardiac hypertrophy; Atherosclerosis; Nonalcoholic fatty liver disease; Diabetes type 2; Fructolysis; Ketohexokinase; Hypertension; Alternative splicing; SF3B1; HIF; Hypoxia
Categories
Funding
- Swiss Heart Foundation
- SNF Sinergia
- NIH [NIDDK DK107667]
Ask authors/readers for more resources
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 Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments.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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available