Effect of the artificial sweetener, acesulfame potassium, a sweet taste receptor agonist, on glucose uptake in small intestinal cell lines.

INTRODUCTION

Sweet taste receptors may enhance glucose absorption.

AIM

This study aimed to explore the cell biology of sweet taste receptors on glucose uptake.

HYPOTHESIS

Artificial sweeteners increase glucose uptake via activating sweet taste receptors in the enterocyte to translocate GLUT2 to the apical membrane through the PLC βII pathway.

METHODS

Caco-2, RIE-1, and IEC-6 cells, starved from glucose for 1 h were pre-incubated with 10 mM acesulfame potassium (AceK). Glucose uptake was measured by incubating cells for 1 to 10 min with 0.5-50 mM glucose with or without U-73122, chelerythrine, and cytochalasin B.

RESULTS

In Caco-2 and RIE-1 cells, 10 mM AceK increased glucose uptake by 20-30 % at glucose >25 mM, but not in lesser glucose concentrations (<10 mM), nor at 1 min or 10 min incubations. U-73122 (PLC βII inhibitor) inhibited uptake at glucose >25 mM and for 5 min incubation; chelerythrine and cytochalasin B had similar effects. No effect occurred in IEC-6 cells. Activation of sweet taste receptors had no effect on glucose uptake in low (<25 mM) glucose concentrations but increased uptake at greater concentrations (>25 mM).

CONCLUSIONS

Role of artificial sweeteners on glucose uptake appears to act in part by effects on the enterocyte itself.