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Non-nutritive sweetener effects may contribute to insulin resistance in consumers with obesity
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NEW ORLEANS — Sucralose, a no-calorie sweetener widely used in beverages, may adversely affect glucose metabolism in consumers with obesity, according to a presenter here.
“There seem to be differential effects of sucralose on glucose metabolism in normal-weight people and in people with obesity, so previous findings in lean subjects cannot be extrapolated to what will be the effects of sucralose in subjects with obesity (and vice versa),” Marta Yanina Pepino De Gruev, PhD, assistant professor in food science and human nutrition at the University of Illinois in Urbana, told Endocrine Today. “Clinicians may find surprising that sucralose is not metabolically inert, as generally thought, at least for people with obesity.”
In a randomized crossover study, Pepino and colleagues conducted 5-hour modified oral glucose tolerance tests on two separate occasions in eight normal-weight adults (mean BMI, 22.9 kg/m2) and seven with obesity (mean BMI 37.9 kg/m2) to determine metabolic effects of sucralose ingestion. All participants had normal insulin response based on Homeostasis Model Assessment of Insulin Resistance (HOMA-IR score, < 2.6) and were not regular users of non-nutritive sweeteners. Ten minutes before each OGTT, participants consumed either water or the amount of sucralose typically found in a single serving of a diet soda, Pepino said during the presentation.
Area under the curve for glucose response was similar in all tests. However, following the sucralose test, area under the curve was increased in the group with obesity by 18% for insulin response and by 12% for C-peptide (P < .02); no differences were seen between the water and sucralose tests in the group with normal weight.
Pepino reported that this finding replicated results from a previous trial conducted by her group “that acute sucralose consumption increases insulin responses to a glucose load in people with obesity, which in the long term may have adverse effects on glucose metabolism.”
“Perhaps we should revise the recommendation of replacing sugar-sweetened beverages with non-caloric sweetened beverages for subjects with obesity who are trying to control their weight,” Pepino told Endocrine Today. “We may benefit from considering sweet-tasting beverages, regardless if sweetened with sugars or non-caloric sweeteners, really as a treat, and move toward the recommendation of replacing such beverages with water.”
Reference:
Pepino Y. T-OR-2024. Presented at: ObesityWeek 2016; Oct. 31-Nov. 4, 2016; New Orleans.
Disclosure: Pepino reports no relevant financial disclosures.
Perspective
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Michael D. Jensen, MD
Pepino and colleagues conducted a prospective cross-over trial comparing glucose and insulin responses with and without sucralose ingestion. They included eight normal-weight and seven obese adults in their studies. Before each oral glucose tolerance test, participants consumed either water or sucralose equivalent to the amount typically found in a single diet soda. They suggested that the glucose responses were similar in all tests and that the greater insulin and C-peptide responses were due to acute insulin resistance; however, in fact, the peak glucose response was greater in those who ingested sucralose. This almost surely accounts for the 18% greater insulin response and 12% greater C-peptide (P < .02) in the group with obesity following sucralose ingestion. It is unclear why sucralose ingestion would increase peak glucose responses to an OGTT; also unclear is whether this would also occur if a mixed meal is consumed. The take home message from my perspective is that insulin secretion is driven by the rate of rise and peak glucose concentrations achieved. Thus, interpreting insulin and C-peptide responses to an OGTT is complex, and extreme care must be taken when attempting to discern insulin resistance and glycemic variation. Although it is possible sucralose may accelerate glucose absorption during an OGTT, it is premature to conclude sucralose has any effect on insulin action.
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