Plain language summary
Non-nutritive sweeteners (NNS) are food additives that provide a sweet taste to food but have few, if any, calories. Currently, seven NNS (sucralose, saccharin, aspartame, acesulfame potassium, neotame, stevia, and Luo han guo extract) are approved by the U.S. Food and Drug Administration and are widely used in thousands of food products. The aim of this study was to analyse whether sucralose ingestion alters the glycaemic and hormonal responses to glucose ingestion in obese subjects who are not regular users of NNS. Seventeen participants who were obese but not insulin resistant participated in the study. They were studied on two separate occasions, 7 days apart, in a crossover design. Sucralose was used as it matches the sweetness of a typical diet soda and also stimulates glucagon-like peptide 1 [a type of peptide hormone] secretion. Results demonstrate that: - the ingestion of sucralose alters the metabolic response to an oral glucose load in obese people who are not regular consumers of NNS. - insulin clearance from plasma was slower after sucralose than after water ingestion. - glucose-induced glucagon [hormone that helps control blood sugar levels] suppression was the same after both sucralose and water ingestion Authors conclude that sucralose is not metabolically inert but has physiologic effects.
Abstract
OBJECTIVE Nonnutritive sweeteners (NNS), such as sucralose, have been reported to have metabolic effects in animal models. However, the relevance of these findings to human subjects is not clear. We evaluated the acute effects of sucralose ingestion on the metabolic response to an oral glucose load in obese subjects. RESEARCH DESIGN AND METHODS Seventeen obese subjects (BMI 42.3 ± 1.6 kg/m(2)) who did not use NNS and were insulin sensitive (based on a homeostasis model assessment of insulin resistance score ≤ 2.6) underwent a 5-h modified oral glucose tolerance test on two separate occasions preceded by consuming either sucralose (experimental condition) or water (control condition) 10 min before the glucose load in a randomized crossover design. Indices of β-cell function, insulin sensitivity (SI), and insulin clearance rates were estimated by using minimal models of glucose, insulin, and C-peptide kinetics. RESULTS Compared with the control condition, sucralose ingestion caused 1) a greater incremental increase in peak plasma glucose concentrations (4.2 ± 0.2 vs. 4.8 ± 0.3 mmol/L; P = 0.03), 2) a 20 ± 8% greater incremental increase in insulin area under the curve (AUC) (P < 0.03), 3) a 22 ± 7% greater peak insulin secretion rate (P < 0.02), 4) a 7 ± 4% decrease in insulin clearance (P = 0.04), and 5) a 23 ± 20% decrease in SI (P = 0.01). There were no significant differences between conditions in active glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, glucagon incremental AUC, or indices of the sensitivity of the β-cell response to glucose. CONCLUSIONS These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS.
Methodological quality
Jadad score
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Not applicable
Allocation concealment
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Not applicable
