Effect of increased physical activity on fructose-induced glycemic response in healthy individuals.

BACKGROUND/OBJECTIVES: The purpose of the current study was to determine whether increased physical activity (PA) altered glycemic control while ingesting an energy-balanced high-fructose diet. SUBJECTS/METHODS: Twenty-two normal-weight men and women (age: 21.2±0.6 years; body mass index: 22.6 ±0.6 kg/m(2)) participated in a randomized, cross-over design study in which they ingested an additional 75 g of fructose for 14 days while either maintaining low PA (FR+inactive) (<4500 steps/day) or high PA (FR+active) (>12,000 steps/day). Before and following the 2-week loading period, a fructose-rich meal challenge was administered and blood was sampled at baseline and for 6 h after the meal and analyzed for glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), c-peptide, glucose and insulin concentrations. RESULTS: Plasma insulin, glucose, c-peptide, GIP and GLP-1 concentrations significantly increased in response to the test meal on all test visits (P<0.05). C-peptide incremental area under the curve (AUC) decreased by 10,208 ±120 pmol/l × min for 6 h from pre to post Fr+active intervention (P=0.02) leading to a decrease in plasma insulin total AUC (pre: 58,470.2±6261.0 pmol/l; post: 49,444.3±3883.0 pmol/l; P=0.04) resulting in a decrease Δpeak[Insulin] (P=0.009). Following the FR+active intervention, GIP total AUC significantly decreased (P=0.005) yet only males had a lower total GLP-1 AUC after both interventions (P=0.049). There were no sex differences in GIP levels. CONCLUSIONS: Increased PA attenuates the deleterious effects on glycemic control caused by a high-fructose diet. These changes in glycemic control with PA are associated with decreases in insulin and GIP concentrations.

Assessment of endothelial function and blood metabolite status following acute ingestion of a fructose-containing beverage.

AIM: Fructose intake has increased concurrent with sugar intake and this increase has been implicated in contributing to the development of metabolic syndrome risk factors. Recent evidence suggests a role for uric acid (UA) as a potential mediator via suppression of nitric oxide (NO) bioavailability. The aim of this study was to explore this hypothesis by measuring changes in UA concentration and systemic NO bioavailability as well as endothelial function in response to acute ingestion of a glucose-fructose beverage. METHODS: Ten young (26.80 +/- 4.80 years), non-obese (body mass index: 25.1 +/- 2.55 kg m(-2); percent body fat: 13.5 +/- 6.9%) male subjects ingested either a glucose (100 g dextrose in 300 mL) or isocaloric glucose-fructose (glucose : fructose; 45 : 55 g in 300 mL) beverage. Blood was sampled pre- and every 15-min post-ingestion per 90 min and assayed for glucose, lactate, fructose, total nitrate/nitrate, UA and blood lipids. Forearm blood flow and pulse-wave velocity were recorded prior to and at 30 and 45 min time intervals post-ingestion, respectively, while heart rate, systolic and diastolic blood pressure were recorded every 15 min. RESULTS: The glucose-fructose ingestion was associated with a significant (P < 0.05) increase in plasma lactate concentration and altered free fatty acid levels when compared with glucose-only ingestion. However, UA was not significantly different (P = 0.08) between conditions (AUC: -1018 +/- 1675 vs. 2171 +/- 1270 micromol L(-1) per 90 min for glucose and glucose-fructose conditions respectively). Consequently, no significant (P < 0.05) difference in endothelial function or systemic NO bioavailability was observed. CONCLUSION: Acute consumption of a fructose-containing beverage was not associated with significantly altered UA concentration, endothelial function or systemic NO bioavailability.