Evaluating the effect of fructose and glucose ingestion on arterial stiffness and the renin angiotensin system in healthy humans

Abstract

Sugar, particularly fructose, consumption has increased exponentially and has been shown to adversely affect the kidney and cardiovascular systems. Animal studies suggest a role for the vascular renin angiotensin system (RAS) in response to fructose intake, activation of which is deleterious to cardiovascular outcomes, though the mechanism remains elusive in humans. A randomized, blinded, two-period crossover study will be performed to determine the effect of fructose ingestion on arterial stiffness in 30 healthy, normotensive men and women adults. Subjects will be studied in high-salt balance to ensure maximum RAS suppression. Arterial stiffness, expressed as pulse wave velocity and aortic augmentation index, will be measured by tonometry at baseline and in response to 60min of graded Angiotensin II infusion, an index of RAS activity. Participants will then be randomized to either a 2 week period of daily ingestion of 200g fructose or glucose and will undergo an identical study day to measure arterial stiffness. After a minimum 1 week washout period, subjects will then cross over to the other treatment for the second study period after which time they will undergo a third identical study day. Six subjects have been recruited and three have completed the study to date. Due to the blinded nature of the study, no preliminary data is available. Ingestion of fructose is expected to increase baseline arterial stiffness and result in a blunted arterial stiffness response to Angiotensin II infusion compared to glucose ingestion, implying a more activated RAS. This will suggest that the increased fructose-associated cardiorenal risk may be mediated, in part, by changes in vascular RAS activity.