Key result
High-fructose diets elevate blood pressure in animal models via enhanced renal transporters and sympathetic activation.
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We are currently in the midst of an epidemic of metabolic disorders, which may, in part, be explained by excess fructose intake. This theory is supported by epidemiological observations as well as experimental studies in animals and humans. Rising consumption of fructose has been matched with growing rates of hypertension, leading to concern from public health experts. At this stage, the mechanisms underlying fructose-induced hypertension have not been fully characterized and the bulk of our knowledge is derived from animal models. Animal studies have shown that high-fructose diets up-regulate sodium and chloride transporters, resulting in a state of salt overload that increases blood pressure. Excess fructose has also been found to activate vasoconstrictors, inactivate vasodilators, and over-stimulate the sympathetic nervous system. Further work is required to determine the relevance of these findings to humans and to establish the level at which dietary fructose increases the risk of developing hypertension.
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Klein et al. (2015) conducted a review in Fructose-induced hypertension. Excess dietary fructose intake was evaluated on Blood pressure elevation and hypertension. High-fructose diets increase blood pressure in animal models by up-regulating sodium and chloride transporters, activating vasoconstrictors, and over-stimulating the sympathetic nervous system.
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