Consumption of glucose syrup enhances glucose tolerance in mice

There is debate about the metabolic impact of sugar-sweetened beverages. Here, we tested the hypothesis that ad lib consumption of glucose (Gluc) or high-fructose (HiFruc) syrups improves glucose tolerance in mice. We provided C57BL/6 mice with a control (chow and water) or experimental (chow, water and sugar solution) diet across two consecutive 28-day exposure periods, and monitored changes in body composition, glucose tolerance, cephalic-phase insulin release (CPIR) and insulin sensitivity. The sugar solutions contained 11% concentrations of Gluc or HiFruc syrup; these syrups were derived from either corn starch or cellulose. In Experiment 1, con-sumption of the Gluc diets reliably enhanced glucose tolerance, while consumption of the HiFruc diets did not. Mice on the Gluc diets exhibited higher CPIR (relative to baseline) by the end of exposure period 1, whereas mice on the control and HiFruc diets did not do so until the end of exposure period 2. Mice on the Gluc diets also exhibited higher insulin sensitivity than control mice at the end of exposure period 2, while mice on the HiFruc diets did not. In Experiment 2, we repeated the previous experiment, but limited testing to the corn-based Gluc and HiFruc syrups. We found, once again, that consumption of the Gluc (but not the HiFruc) diet enhanced glucose tolerance, in part by increasing CPIR and insulin sensitivity. These results show that mice can adapt metabolically to high glucose diets, and that this adaptation process involves upregulating at least two com-ponents of the insulin response system.

Automated summary

This study examined the effects of ad lib consumption of glucose and high-fructose syrups on glucose tolerance in mice. The results showed that glucose consumption improved glucose tolerance, while high-fructose consumption did not. Glucose consumption also increased cephalic-phase insulin release and insulin sensitivity. These findings suggest that mice can adapt metabolically to high glucose diets by upregulating components of the insulin response system.