Fructose Intake from Sugar-Sweetened Beverages and Acute Plasma Uric Acid Production

Abstract

Background: Sucrose intake, half of which is fructose, has been increasing over recent decades. Additionally, the introduction of high fructose corn syrup in North America in the 1970s has also led to an increase of fructose in the diet. Fructose has caused much debate in the scientific and wider community. The unregulated metabolic pathway of fructose leads to uric acid and fat production, which contributes to the burden of disease. Studies have linked fructose consumption to obesity, diabetes, gout, hypertension, fatty liver disease and increased visceral fat. Some researchers question the previous research, with the largest concern being around the feasibility of the fructose dose used in the current literature, which is producing the pathological change. Objective: To determine the effects of two commonly consumed single-serve amounts of a sugar-sweetened beverage on acute plasma uric acid concentration in the body within a healthy New Zealand population. Design: Randomised crossover control trial Methods: Forty-two participants were randomised to the control group or the sugar-sweetened beverage intervention. Across two testing days, the control group consumed a 600 ml fructose and a 600 ml glucose beverage, while the intervention group consumed a 355 ml and 600 ml Sprite beverage in random order. Control beverages were matched for fructose content with the 600 ml bottle of Sprite (26.7 g). The 355 ml can of Sprite delivered 15.8 g of fructose. Blood samples were collected at baseline, 30 and 60 minutes and were analysed for plasma uric acid. This study design enabled the assessment of the effect of different doses of fructose and the form of fructose, pure or as a component of sucrose on plasma uric acid response. Results: Both sugar-sweetened beverage volumes significantly raised plasma uric acid levels after 30 and 60 minutes (P<0.05). The fructose control produced the largest rise in plasma uric acid concentration at 60 minutes across all consumed beverages of 26.34 μmol/L (P=0.004). The glucose control significantly decreased plasma uric acid concentration after 60 minutes (P=0.018). IAUC of the plasma uric acid response was measured, with no significant difference in the body’s response between the Sprite beverages (P=0.499) and the Sprite and fructose beverage (P=0.114). However, there was a significant difference in iAUC between the glucose and fructose control (P=<0.001) and the glucose and 600 ml Sprite beverage (P=0.015). Conclusion: Both the 355 ml and 600 ml Sprite exhibited statistically significant rises in plasma uric acid concentration, however, this transient rise in plasma uric acid response was perceived as clinically insignificant. We found no difference in the body’s plasma uric acid response between the pure fructose control and the sucrose sweetened 600 ml Sprite beverage.