Effects of Consuming Beverages Sweetened with Fructose, Glucose, High-Fructose Corn Syrup, Sucrose, or Aspartame on OGTT-Derived Indices of Insulin Sensitivity in Young Adults

Abstract

(1) Background: Clinical results on the effects of excess sugar consumption on insulin sensitivity are conflicting, possibly due to differences in sugar type and the insulin sensitivity index (ISI) assessed. Therefore, we compared the effects of consuming four different sugars on insulin sensitivity indices derived from oral glucose tolerance tests (OGTT). (2) Methods: Young adults consumed fructose-, glucose-, high-fructose corn syrup (HFCS)-, sucrose-, or aspartame-sweetened beverages (SB) for 2 weeks. Participants underwent OGTT before and at the end of the intervention. Fasting glucose and insulin, Homeostatic Model Assessment-Insulin Resistance (HOMA-IR), glucose and insulin area under the curve, Surrogate Hepatic Insulin Resistance Index, Matsuda ISI, Predicted M ISI, and Stumvoll Index were assessed. Outcomes were analyzed to determine: (1) effects of the five SB; (2) effects of the proportions of fructose and glucose in all SB. (3) Results: Fructose-SB and the fructose component in mixed sugars negatively affected outcomes that assess hepatic insulin sensitivity, while glucose did not. The effects of glucose-SB and the glucose component in mixed sugar on muscle insulin sensitivity were more negative than those of fructose. (4) Conclusion: the effects of consuming sugar-SB on insulin sensitivity varied depending on type of sugar and ISI index because outcomes assessing hepatic insulin sensitivity were negatively affected by fructose, and outcomes assessing muscle insulin sensitivity were more negatively affected by glucose.

Keywords: aspartame; dietary intervention study; fructose; glucose; hepatic insulin sensitivity; high-fructose corn syrup; insulin resistance; insulin sensitivity index; muscle insulin sensitivity; sucrose.

Figure 1

Study protocol.

Figure 2

The group means of the OGTT glucose and insulin profiles at baseline (Week 0) and the end of intervention (Week 2) in participants consuming HFCS- ((A,B) respectively, n = 28), sucrose- ((C,D), n = 24), fructose- ((E,F), n = 28), glucose- ((G,H), n = 28), or aspartame-SB ((I,J), n = 23). * p < 0.05, ** p < 0.01, *** p < 0.001, paired t test.

Figure 3

Δ fasting glucose (A), insulin (B), HOMA−IR (C), and Surrogate Hepatic IRI (D) (Week 2–Week 0) during OGTT in participants consuming beverages sweetened with HFCS−, sucrose−, fructose−, glucose−, or aspartame-sweetened beverages for 2 weeks. ** p < 0.01, *** p < 0.001, effect of beverage, two−factor (beverage, sex) ANCOVA with adjustment for MSRF and outcome at baseline. ⁺ p < 0.05, ⁺⁺ p < 0.01, ⁺⁺⁺⁺ p < 0.0001, LS mean different from zero; groups without shared letters are significantly different, Tukey’s post-test.

Figure 4

Δ 3 h glucose (A) and insulin (B) AUC (Week 2–Week 0) during OGTT in participants consuming beverages sweetened with HFCS-, sucrose-, fructose-, glucose-, or aspartame-sweetened beverages for 2 weeks. ** p < 0.01, effect of beverage, two-factor (beverage, sex) ANCOVA with adjustment for MSRF and outcome at baseline. ⁺ p < 0.05, ⁺⁺ p < 0.01, LS mean different from zero; groups without shared letters are significantly different, Tukey’s post-test.

Figure 5

Absolute ΔMatsuda ISI (A), ΔPredicted M ISI (B), and ΔStumvoll Index (C) after young adults consume beverages sweetened with 25% Ereq HFCS, sucrose, fructose, or glucose; or with aspartame for 2 weeks. A and B: two-factor (beverage, sex) ANCOVA (SAS 9.4) with adjustment for MSRF and outcome at baseline. p = 0.056, * p < 0.05 effect of beverage; ⁺ p < 0.05, ⁺⁺ p < 0.01 LS mean of change different than zero; groups without shared letters are significantly different, Tukey’s post-test. C: Kruskal–Wallis test, * p < 0.05 effect of beverage, ⁺ p < 0.05, ⁺⁺ p < 0.01, Wilcoxon matched-pairs signed rank test of within-group 0 vs. 2 wk. Groups without shared letters are significantly different, Mann–Whitney U test.