Sucralose affects glycemic and hormonal responses to an oral glucose load
Open accessAbstract
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.
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During an OGTT, glucagon may increase in some time periods while C-peptide (and insulin) is not decreasing, indicating that in those periods the relationship between insulin action and glucagon variations is lost.
“Indeed, such curves suggest that during an OGTT glucagon may increase in some time periods, though slightly, whereas C-peptide (as well as insulin) is not decreasing as one would expect, thus indicating that in those periods the relationship between insulin action and glucagon variations is lost.”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
The Results section reports insulin and C-peptide peaks and glucagon responses during the oral glucose test. It does not state that glucagon rose during periods when insulin and C-peptide were not falling, or that their relationship was lost. The latter is an interpretation of the curves, not a finding reported in the text of our copy. (LLM, conf=0.77)
Experimental — accuracy not yet measuredInsulin secretion values, as assessed in study (31), were similarly not related to glucagon.
“surprisingly, insulin secretion values, as assessed in study (31) were similarly not related to glucagon.”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
The Results report higher insulin responses after sucralose while glucagon responses were similar to those after water. The Conclusions say this makes glucagon unlikely to explain the differences between conditions, but the paper does not establish that insulin secretion values are generally unrelated to glucagon. (LLM, conf=0.84)
Experimental — accuracy not yet measuredModel validation on mean experimental data reported by Pepino et al. (31) provided the best fit shown in Figure 2 and the parameter estimates with related CIs reported in Table 1.
“Model validation on mean experimental data reported by Pepino et al. (31) provided the best fit shown in Figure 2 and the parameter estimates (with related CIs) reported in Table 1 .”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
On reference mean experimental data by Pepino et al. (31), estimated KGLUCA was 0.005 min-1 (95% CI -0.002-0.013).
“KGLUCA | 0.005 | -0.002–0.013”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
On reference mean experimental data by Pepino et al. (31), estimated KΔCPREM was 0.155 min-1 (95% CI 0.119-0.191).
“KΔCPREM | 0.155 | 0.119–0.191”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
In linear regression analysis over the average data of the analyzed population in study (31), C-peptide time samples were significantly inversely related to those of glucagon, whereas those of insulin (as well as those of glucose) were not.
“in linear regression analysis over the average data of the analyzed population in study (31), we verified that C-peptide time samples were significantly inversely related to those of glucagon, whereas those of insulin (as well as those of glucose) were not.”
From Mathematical Model of Glucagon Kinetics for the Assessment of Insulin-Mediated Glucagon Inhibition During an Oral Glucose Tolerance Test (2021) · cites this paper as [31]
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- Authors
- Pepino, M. Y., Tiemann, C. D., Patterson, B. W., Wice, B. M., & Klein, S.
- Affiliations
- Washington University in St. Louis (US)
- Center for Human Nutrition, Washington University School of Medicine, St. Louis, Missouri
- Corresponding author
- Klein, Samuel
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2013-08-13
- Volume
- 36
- Issue
- 9
- Pages
- 2530-2535
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- PMC
- PMC3747933
- OpenAlex
- W2111548886
- Cited by
- 253
- References
- 34
- Citations by year
- 2026: 19 · 2025: 17 · 2024: 23 · 2023: 17 · 2022: 16 · 2021: 15 · 2020: 36 · 2019: 17 · 2018: 26 · 2017: 25 · 2016: 17 · 2015: 12 · 2014: 6 · 2013: 6 · 2012: 1
- FWCI
- 12.63
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes Care (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (KL2TR000450, UL1TR000448, DK56341, TR000448)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK37948, DK56341, DK088126, R01DK088126, R01DK037948, P30DK056341, P30DK020579)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- sucralose, artificial sweeteners, oral glucose tolerance, glycemic response, insulin secretion, insulin sensitivity, insulin clearance, beta-cell function, obesity, glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, glucagon, insulin resistance
- MeSH terms
- Adult, Blood Glucose, Female, Glucose Tolerance Test, Humans, Insulin, Male, Obesity, Sucrose, Cross-Over Studies
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