Cancer cell metabolism is characterized by high rates of glucose uptake and anaerobic glycolysis. Sugar consumption has increased dramatically in the industrialized world, with refined fructose intake skyrocketing upwards in the USA over the past 30 years. Fructose provides an alternative carbon source for glycolysis, entering downstream of glucose and bypassing two key rate-limiting steps. Considering that glycolysis is the major pathway which fuels cancer growth, this review will focus on regulation and flux of glucose versus fructose through this pathway, and consider whether epidemiologic and experimental data support a mechanism whereby fructose might potentiate cancer growth in transformed cells.
Fructose intake is associated with increased risk of pancreatic and small intestinal cancers, and possibly others. Fructose promotes flux through the pentose phosphate, which enhances protein synthesis and may indirectly increase tumor growth. Fructose treatment is associated with more aggressive cancer behavior and may promote metastasis.
Whereas glucose favors overall growth kinetics, fructose enhances protein synthesis and appears to promote a more aggressive cancer phenotype. Fructose has become ubiquitous in our food supply, with the highest consumers being teens and young adults. Therefore, understanding the potential health consequences of fructose and its role in chronic disease development is of critical importance.
aDivision of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland, Baltimore, Maryland
bSection of Endocrinology, Diabetes, Nutrition and Weight Management, Department of Medicine, Boston University Medical Center, Boston, Massachusetts, USA
Correspondence to Ava M. Port, MD, 660 W. Redwood Street, Howard Hall Room 567, Baltimore, MD 21201, USA. Tel: +1 410 328 6219; e-mail: firstname.lastname@example.org