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Stimulation of oral Type II taste cells with T1R2/R3 receptors elicits sweet taste and invites consumption. Intestinal Type II taste cells with T1R2/R3 receptors facilitate glucose absorption. Type II taste receptor cells contain a calcium channel, CALHM1, which if deleted results in loss of ability to sense and perceive the sweet taste quality. Comparison between mice with (+/+; WT) and without (-/-; KO) CALHM1 provides the means to examine T1R2/R3 receptor effects on intake and intestinal absorption via measurements of body weight (BW), blood glucose (BG) and plasma insulin. In this study we confirm our previous findings that WT mice are heavier, eat more, and have higher mortality than KO mice [1]. We report that higher BG and insulin levels accompany higher BW in both WT and KO mice, although, KO mice with the same BW as their WT counterpart have lower BG and insulin levels. Glucose gavage increased and prolonged BG and plasma insulin levels more consistently in WT than KO mice. Fructose exerted little effects on BG or insulin. Gavage with the high potency, non-saccharide sweetener SC 45647 had no effect on BG or insulin of KO mice, but caused some increase of both BG and insulin levels in the WT mice. The effect on insulin and BG by water gavage was negligible compared to that of glucose. These results suggest that inhibition of T1R2/R3 receptors lowers oral intake and intestinal uptake, which then results in lower BG and insulin levels. These findings can be applied to weight control in humans.

Oral and Intestinal Sweet Taste T1R2/R3 Receptors in Mice; Effect on Consumption, Bodyweight, Blood Glucose and Insulin Levels