The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
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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“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“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]
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“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]
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“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]
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“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]
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“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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Citations
Cites
Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1.
Jang, H.-J., Kokrashvili, Z., Theodorakis, M. J., Carlson, O. D., Kim, B.-J., Zhou, J., Kim, H. H., Xu, X., Chan, S. L., Juhaszova, M., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706890104 · Cited by 995 · cited 4×
“Second, NNS-induced activation of gut sweet taste receptors in isolated duodenal L cells and pancreatic b-cells triggers the secretion of glucagon-like peptide 1 (GLP-1) (4,5) and insulin (6– 9), respectively.”
BackgroundInfluentialT1R3 and gustducin in gut sense sugars to regulate expression of Na + -glucose cotransporter 1
Margolskee, R. F., Dyer, J., Kokrashvili, Z., Salmon, K. S. H., Ilegems, E., Daly, K., Maillet, E. L., Ninomiya, Y., Mosinger, B., & Shirazi-Beechey, S. P. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706678104 · Cited by 882
Effects of arterial versus venous sampling on analysis of glucose kinetics in man
McGuire, E. A., Helderman, J. H., Tobin, J. D., Andres, R., & Berman, M. D. (1976) · Journal of Applied Physiology · doi:10.1152/jappl.1976.41.4.565 · Cited by 704
Ascaso, J. F., Pardo, S., Real, J. T., Lorente, R. I., Priego, A., & Carmena, R. (2003) · Diabetes Care · doi:10.2337/diacare.26.12.3320 · Cited by 490
Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2
Mace, O. J., Affleck, J. A., Patel, N., & Kellett, G. L. (2007) · The Journal of Physiology · doi:10.1113/jphysiol.2007.130906 · Cited by 453
The Use of Areas Under Curves in Diabetes Research
Allison, D. B., Paultre, F., Maggio, C. A., Mezitis, N. H. E., & Pi-Sunyer, X. (1995) · Diabetes Care · doi:10.2337/diacare.18.2.245 · Cited by 398
Oral Glucose Tolerance Test Minimal Model Indexes of β-Cell Function and Insulin Sensitivity
Breda, E., Cavaghan, M. K., Toffolo, G., Polonsky, K. S., & Cobelli, C. (2001) · Diabetes · doi:10.2337/diabetes.50.1.150 · Cited by 320
Nakagawa, Y. S., Nagasawa, M., Yamada, S., Hara, A., Mogami, H., Nikolaev, V. O., Lohse, M. J., Shigemura, N., Ninomiya, Y., & Kojima, I. (2009) · PLoS ONE · doi:10.1371/journal.pone.0005106 · Cited by 308
Nonnutritive Sweeteners: Current Use and Health Perspectives
Gardner, C. D., Wylie‐Rosett, J., Gidding, S. S., Steffen, L. M., Johnson, R. K., Reader, D., & Lichtenstein, A. H. (2012) · Circulation · doi:10.1161/cir.0b013e31825c42ee · Cited by 308
Corkey, B. E. (2011) · Diabetes · doi:10.2337/db11-1483 · Cited by 295
Cited by
Sorted by citations
Srour, B., Fezeu, L. K., Kesse-Guyot, E., Allès, B., Méjean, C., Andrianasolo, R. M., Chazelas, E., Deschasaux, M., Hercberg, S., Galan, P., et al. (2019) · BMJ · doi:10.1136/bmj.l1451 · Cited by 955
Metabolic effects of non-nutritive sweeteners
Pepino, M. Y. (2015) · Physiology & Behavior · doi:10.1016/j.physbeh.2015.06.024 · Cited by 285
Self-citationBauer, P. V., Duca, F. A., Waise, T. M. Z., Rasmussen, B. A., Abraham, M. A., Dranse, H. J., Puri, A., O’Brien, C. A., & Lam, T. K. T. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2017.09.019 · Cited by 265
Non-caloric artificial sweeteners and the microbiome: findings and challenges
Suez, J., Korem, T., Zilberman-Schapira, G., Segal, E., & Elinav, E. (2015) · Gut Microbes · doi:10.1080/19490976.2015.1017700 · Cited by 217
The Association Between Artificial Sweeteners and Obesity
Pearlman, M. Y., Obert, J., & Casey, L. C. (2017) · Current Gastroenterology Reports · doi:10.1007/s11894-017-0602-9 · Cited by 221
Metadata
- 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
- 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 › Endocrinology, Diabetes and Metabolism › 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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