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

Goran B Hellekant, Teresa Rose-Hellekant

Research output: Contribution to journalArticle

Abstract

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.
Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalJournal of Obesity and Weight-loss Medication
Volume2
Issue number2
StatePublished - Aug 28 2016

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