Acute metabolic and endocrine responses induced by glucose and fructose in healthy young subjects: A double-blinded, randomized, crossover trial

A rise in fructose consumption has been implicated in the etiology of obesity, diabetes and cardiovascular disease. Serum uric acid (UA) elevates after fructose ingestion, increasing the risk of cardiovascular disease. However, the impact of fructose ingestion on nitric oxide (NO) has not yet been confirmed. The aim of this study was to investigate the postprandial metabolic and endocrine responses following an acute ingestion of fructose and glucose in healthy subjects.

This was a double-blinded, randomized, crossover postprandial trial. Eighteen healthy young subjects (9 males and 9 females) with a mean age of 23.6 ± 2.3 years and mean BMI of 20.2 ± 1.5 kg/m² completed the experiment that was conducted in Hangzhou, China. Volunteers were randomized to two groups (A and B): after an 8-h overnight fast, volunteers either ingested 300 mL of 25% glucose (group A) or fructose (group B) solution at 0830 within 5 min. After a one-week washout period, volunteers were crossed over to receive the alternate test solution. Blood pressure was measured at 0 h, 1 h, 2 h and 3 h and venous blood was drawn at 0 h, 0.5 h, 1 h, 2 h and 3 h after ingestion of the test solution.

Eighteen subjects completed the study. Serum NO level tended to be lower at 1 h (59.40 ± 3.10 μmol/L and 68.1 ± 3.40 μmol/L, respectively, p ≤ 0.05) and 2 h (62.70 ± 3.10 μmol/L and 70.10 ± 3.50 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC (area under curve) of NO was significantly lower after fructose ingestion than after glucose (p ≤ 0.05). UA level was higher at 1 h (512.17 ± 17.74 μmol/L and 372.11 ± 17.41 μmol/L, respectively, p ≤ 0.01) and 2 h (440.22 ± 16.07 μmol/L and 357.39 ± 14.80 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of UA was significantly higher after fructose ingestion than after glucose (p ≤ 0.01). Correlation analyses revealed that NO was negatively associated with UA at T_0.5h (r = -0.62, p ≤ 0.01), T_1.0h (r = -0.69, p ≤ 0.001), T_2.0h (r = -0.86, p ≤ 0.001) and T_3.0h (r = -0.85, p ≤ 0.001) after fructose ingestion. SBP (systolic blood pressure) tended to be higher at 1 h (125.33 ± 1.95 mmHg and 112.06 ± 1.77 mmHg, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of SBP was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). The 3 h-AUC of TG, TC, HDL-C and LDL-C showed no differences between fructose and glucose. LDH (lactate dehydrogenase) level was higher at 1 h (195.00 ± 5.6 U/L and 177.67 ± 6.8 U/L, respectively, p ≤ 0.05) and 2 h (197.01 ± 6.32 U/L and 185.50 ± 7.37 U/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of LDH was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). AR was significantly higher at 1 h (19.86 ± 0.52 ng/mg Hb and 16.98 ± 0.29 ng/mg Hb, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of AR (p ≤ 0.05) was significantly higher after fructose ingestion than after glucose (p ≤ 0.05).

Ingestion of a 75 g fructose load led to acute but unfavorable changes in certain metabolic and endocrine responses including increased serum concentrations and 3 h-AUC of UA, AR and LDH, increased SBP, and decreased endothelial NO production when compared with the same amount of ingested glucose.