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

Abstract

Stimulation of oral Type II taste receptor cells with T1R2/ R3 receptors elicits sweet taste and invites to consumption. Intestinal Type II taste receptor cells with T1R2/ R3 receptors facilitate glucose absorption by the glucose transporter type 2 (GLUT2). Type II taste receptor cells contain a calcium channel, CALHM1. Genetic deletion of the CALHM1 channel results in loss of ability to sense and perceive the sweet taste quality. Comparison between mice with CALHM1+/+ (WT) and without CALHM1-/- (KO), respectively, provides the means to examine T1R2/R3 receptors' effect on intake and intestinal absorption via measurements of body weight (BW), blood glucose (BG) and plasma insulin. In this study we confirm our findings that WT mice are heavier, eat more, and have higher mortality than KO mice. 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 level. Glucose gavage increased and prolonged BG and plasma insulin increases more consistently in WT than in KO mice. The effects o fructose gavage was small and did not differ between WT and KO mice. Gavage with the high potency artificial sweetener SC 45647 increased both BG and insulin levels in WT but less than with glucose. This increase was also larger in heavier WT mice than lighter. In KO mice the effects of gavage with water or SC 45647 on BG levels and insulin did not differ significantly. In WT mice there was a difference. These results suggest that inhibition of T1R2/R3 receptors lowers intake and intestinal uptake, which then decreases BG and insulin levels. These findings can be applied to weight control in humans.