Abstract

Here, we tested the hypothesis that sucralose differentially affects metabolic responses to labeled oral glucose tolerance tests (OGTTs) in participants with normal weight and obesity. Participants (10 with normal weight and 11 with obesity) without diabetes underwent three dual-tracer OGTTs preceded, in a randomized order, by consuming sucralose or water, or by tasting and expectorating sucralose (e.g., sham-fed; sweetness control). Indices of β-cell function and insulin sensitivity (SI) were estimated using oral minimal models of glucose, insulin, and C-peptide kinetics. Compared with water, sucralose ingested (but not sham-fed) resulted in a 30 ± 10% increased glucose area under the curve in both weight groups. In contrast, the insulin response to sucralose ingestion differed depending on the presence of obesity: decreased within 20–40 min of the OGTT in normal-weight participants but increased within 90–120 min in participants with obesity. Sham-fed sucralose similarly decreased insulin concentrations within 60 min of the OGTT in both weight groups. Sucralose ingested (but not sham-fed) increased SI in normal-weight participants by 52 ± 20% but did not affect SI in participants with obesity. Sucralose did not affect glucose rates of appearance or β-cell function in either weight group. Our data underscore a physiological role for taste perception in postprandial glucose responses, suggesting sweeteners should be consumed in moderation.

Highlights

  • A high-calorie diet with excess sugar intake increases the risk of developing obesity, cardiovascular disease, and type 2 diabetes [1]

  • We recently found that the ingestion of sucralose before an oral glucose tolerance test (OGTT)

  • There were no significant differences in age, sex, or fasting plasma glucose concentrations between weight groups (Table 1)

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Summary

Introduction

A high-calorie diet with excess sugar intake increases the risk of developing obesity, cardiovascular disease, and type 2 diabetes [1]. Even though LCSs have a negligible calorie content, data from animal models and human cell lines suggest that they are metabolically active, presumably by interaction with sweet taste receptors [4,5,6,7,8,9,10,11,12]. The sweet taste receptor T1R2 + T1R3 is a heterodimer that detects sugars and LCSs and is expressed in many tissues beyond the mouth, including the intestine and the pancreas [4].

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