Presenting author: Alexander Nichol

Co-authors: Mihoko Yoshino, Bruce W. Patterson, Samuel Klein, M. Belen Acevedo, and M. Yanina Pepino

Department of Food Science and Human Nutrition

Objective: The theory that sucralose, a non-nutritive sweetener (NNS), is metabolically inert is challenged. As discovered through our previous findings, sucralose, when consumed prior to an oral glucose tolerance test, enhances insulinemic responses in subjects with obesity who are not regular consumers of NNS. Conversely, other studies conducted on lean subjects, which do not control for use of NNS, discovered that sucralose does not alter insulin responses in the presence of carbohydrates. In response to the previous studies, this study will focus on determining if the sucralose effects we found in people with obesity are replicable, generalizable to lean people when controlling for prior history of NNS use, and caused merely by the sensation of sweet taste in the mouth. Design and Methods: Eleven people with obesity (BMI: 37.7 ± 5.5 kg/m^2) and nine lean people (BMI: 22.8 ± 1.0 kg/m^2), all non-diabetic, with a HOMA-IR < 3, and non-regular users of NNS, participated in the study. In a randomized cross-over design, participants were evaluated on three separate days. On each day they either drank water (absolute control condition) or sucralose (experimental condition), or were sham-fed sucralose (taste control condition), 10 minutes prior to a fixed glucose load. Blood samples were taken periodically before and after consumption to measure the fasting and post-treatment concentrations of glucose, insulin, and gastric inhibitory polypeptide (GIP) in the blood. Results: Compared with the absolute control condition, consumption of sucralose caused a 29 ± 10% greater increase in glucose area under the curve (AUC) in both groups (p = 0.02), an 18 ± 8% greater increase in insulin AUC in subjects with obesity, but an 11 ± 7% smaller increase in insulin AUC in lean people (p = 0.03). No significant differences were found between conditions in GIP. Sham feeding sucralose was not statistically different than either condition for either group. Conclusion: Sucralose differentially alters insulinemic responses to a glucose load in subjects with obesity and lean subjects. Sucralose post-ingestive effects, as opposed to merely tasting sucralose, caused the altered glycemic and insulinemic responses observed in both groups.