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Relationship Between High-Fructose Corn Syrup, Uric Acid, and Metabolic Syndrome

McChesney, Monica J. MS, RD, LD

Journal of Pediatric Surgical Nursing: October/December 2016 - Volume 5 - Issue 4 - p 88
doi: 10.1097/JPS.0000000000000115
Pediatric Obesity Column

Monica J. McChesney, MS, RD, LD, Registered Dietitian, Children's of Alabama, Birmingham, AL.

The author declares no conflict of interest.

Correspondence: Monica J. McChesney, MS, RD, LD, Children's of Alabama, 1600 7th Avenue South, Birmingham, AL 35233. E‐mail:

High-fructose corn syrup (HFCS) usage has reached an all-time high with a 2,000% increase in products consumed in a Western diet (Bomback et al., 2010). HFCS is made up of 55% fructose and 45% glucose and is widely used because of its inexpensive cost (Johnson et al., 2009). The increase in HFCS has also paralleled the increase in obesity, metabolic syndrome, and chronic kidney disease (Johnson et al., 2013). Fructose varies from other sugars because of its ability to cause intracellular adenosine triphosphate (ATP) depletion and nucleotide turnover and promote the generation of uric acid. Uric acid is the by-product of purine metabolism made by the enzyme xanthine oxidase and is excreted in the kidneys. Diets high in purine, HFCS, and sucrose can all cause an elevation in uric acid levels within the body (Johnson et al., 2013).

As stated above, fructose metabolism is very different compared with the other sugars. When fructose is metabolized, hepatic adenosine triphosphate is depleted, which causes the promotion of uric acid formation as well as the breakdown of nucleotides. Fructose is absorbed in the intestines and undergoes metabolism primarily in the liver but also in the kidneys and adipocytes. The key enzyme responsible for this is fructokinase. This enzyme uses ATP to phosphorylate fructose to fructose-1-phosphate. Fructokinase is poorly regulated; therefore, the fructose is rapidly phosphorylated and, in the meantime, causes depletion of ATP. This mechanism of action causes the ATP to act like a type of ischemia and can cause transient arrest of protein synthesis, production of inflammatory proteins, endothelial dysfunction, and oxidative stress. Fructose is also highly lipogenic, stimulating triglyceride synthesis and increasing fat deposits in the liver.

Finally, fructose stimulates the production of uric acid. When ATP is consumed, adenosine monophosphate (AMP) accumulates and stimulates ATP deaminase, which then triggers the production of uric acid, which can induce the accumulation of triglycerides. Therefore, the lipogenic characteristics of fructose, in association with the ability to induce ATP depletion and uric acid generation, are largely responsible for HFCS role in inducing metabolic syndrome (Johnson et al., 2013).

Research suggests a proposed relationship between the intake of HFCS and elevated uric acid levels as well as the role elevated uric acid levels play in metabolic syndrome. Excessive fructose consumption via HFCS not only causes an increase in uric acid levels but also can lead to weight gain, an increase in blood pressure, an increase in triglycerides, and the development of insulin resistance. It is imperative to educate healthcare professionals to screen for elevated uric acid levels in their patients. Healthcare professionals should also be educated on how to teach their patients to avoid foods containing HFCS to help lessen or reverse the adverse health outcomes discussed above.

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Bomback A. S., Derebail V. K., Shoham D. A., Anderson C. A., Steffen L. M., Rosamond W. D., & Kshirsagar A. V. (2010). Sugar-sweetened soda consumption, hyperuricemia, and kidney disease. Kidney International, 77, 609–616.
Johnson R. J., Nakagawa T., Sanchez-Lozada L. G., Shafiu M., Sundarum S., Le M., … Lanaspa M. A. (2013). Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes, 62, 3307–3315.
Johnson R. J., Perez-Pozo S. E., Sautin Y. Y., Manitius J., Sanchez-Lozada L. G., Feig D. I., … Nakagawa T. (2009). Hypothesis: Could excessive fructose intake and uric acid cause type 2 diabetes? Endocrine Reviews, 30, 96–116.
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