Abstract
BackgroundProspective studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking. Therefore we investigated the relative effects of 10 wks of fructose or glucose consumption on plasma uric acid and RBP-4 concentrations, as well as liver enzyme (AST, ALT, and GGT) activities in men and women.MethodsAs part of a parallel arm study, older (age 40–72), overweight and obese male and female subjects (BMI 25–35 kg/m2) consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 wks. Fasting and 24-h blood collections were performed at baseline and following 10 wks of intervention and plasma concentrations of uric acid, RBP-4 and liver enzyme activities were measured.ResultsConsumption of fructose, but not glucose, led to significant increases of 24-h uric acid profiles (P < 0.0001) and RBP-4 concentrations (P = 0.012), as well as plasma GGT activity (P = 0.04). Fasting plasma uric acid concentrations increased in both groups; however, the response was significantly greater in subjects consuming fructose (P = 0.002 for effect of sugar). Within the fructose group male subjects exhibited larger increases of RBP-4 levels than women (P = 0.024).ConclusionsThese findings suggest that consumption of fructose at 25% of energy requirements for 10 wks, compared with isocaloric consumption of glucose, may contribute to the development of components of the metabolic syndrome by increasing circulating uric acid, GGT activity, suggesting alteration of hepatic function, and the production of RBP-4.
Highlights
Prospective studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking
Fasting uric acid and 24-h circulating uric acid profiles At 10 wks of intervention fasting plasma uric acid concentrations were significantly increased from baseline in subjects consuming both fructose- and glucosesweetened beverages, but the effect was significantly greater in those consuming fructose-sweetened beverages (P = 0.002 for effect of sugar) (Table 2). 24-h serum uric acid profiles were increased significantly from baseline in subjects consuming fructose but not in those consuming glucose (P < 0.0001 for effect of sugar) (Table 2) (Figure 1)
Plasma gamma-glutamyl transferase (GGT), Aspartate aminotransferase (AST), and Alanine aminotransferase (ALT) Activities Plasma GGT activity was significantly elevated compared with baseline values following 10 wks of fructose consumption but decreased significantly in subjects consuming glucose(P < 0.0001 for effect of sugar) (Table 2)
Summary
Prospective studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking. An increase in the consumption of sweeteners containing fructose has occurred in parallel with the increasing prevalence of overweight and obesity over the past three decades [2], suggesting that increased consumption of fructose may contribute to the current epidemic of obesity-related metabolic disorders [2,3] including increased incidence of the metabolic syndrome [4,5]. Consumption of fructose, but not glucose led to increased hepatic de novo lipogenesis (DNL), and promoted accumulation of intra-abdominal fat, the development of a more atherogenic lipid profile, and reduced insulin sensitivity in overweight/obese adults [6]. We have hypothesized that the increased rate of DNL following consumption of fructose leads to an accumulation of hepatic lipid, which promotes dyslipidemia and decreased insulin sensitivity [7]
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