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Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo

Artificial sweeteners are extensively used by the food industry to replace sugar in food and beverages and are widely considered to be a healthy alternative. However, recent data suggest that artificial sweeteners may impact intestinal glucose absorption and that they might lead to glucose intoleran...

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Autores principales: Jacquillet, Grégory, Debnam, Edward S., Unwin, Robert J., Marks, Joanne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046642/
https://www.ncbi.nlm.nih.gov/pubmed/30009546
http://dx.doi.org/10.14814/phy2.13804
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author Jacquillet, Grégory
Debnam, Edward S.
Unwin, Robert J.
Marks, Joanne
author_facet Jacquillet, Grégory
Debnam, Edward S.
Unwin, Robert J.
Marks, Joanne
author_sort Jacquillet, Grégory
collection PubMed
description Artificial sweeteners are extensively used by the food industry to replace sugar in food and beverages and are widely considered to be a healthy alternative. However, recent data suggest that artificial sweeteners may impact intestinal glucose absorption and that they might lead to glucose intolerance. Moreover, chronic consumption of artificial sweeteners has also been linked to detrimental changes in renal function. Using an in vivo approach, our study aimed to determine if short‐term infusion of the artificial sweetener saccharin can alter renal function and renal glucose absorption. We show that saccharin infusion does not induce any major change in GFR or urine flow rate at either the whole kidney or single nephron level, suggesting that any reported change in renal function with artificial sweeteners must depend on chronic consumption. As expected for a nondiabetic animal, glucose excretion was low; however, saccharin infusion caused a small, but significant, decrease in fractional glucose excretion. In contrast to the whole kidney data, our micropuncture results did not show any significant difference in fractional glucose reabsorption in either the proximal or distal tubules, indicating that saccharin does not influence renal glucose handling in vivo under euglycemic conditions. In keeping with this finding, protein levels of the renal glucose transporters SGLT1 and SGLT2 were also unchanged. In addition, saccharin infusion in rats undergoing a glucose tolerance test failed to induce a robust change in renal glucose excretion or renal glucose transporter expression. In conclusion, our results demonstrate that saccharin does not induce acute physiologically relevant changes in renal function or renal glucose handling.
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spelling pubmed-60466422018-07-19 Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo Jacquillet, Grégory Debnam, Edward S. Unwin, Robert J. Marks, Joanne Physiol Rep Original Research Artificial sweeteners are extensively used by the food industry to replace sugar in food and beverages and are widely considered to be a healthy alternative. However, recent data suggest that artificial sweeteners may impact intestinal glucose absorption and that they might lead to glucose intolerance. Moreover, chronic consumption of artificial sweeteners has also been linked to detrimental changes in renal function. Using an in vivo approach, our study aimed to determine if short‐term infusion of the artificial sweetener saccharin can alter renal function and renal glucose absorption. We show that saccharin infusion does not induce any major change in GFR or urine flow rate at either the whole kidney or single nephron level, suggesting that any reported change in renal function with artificial sweeteners must depend on chronic consumption. As expected for a nondiabetic animal, glucose excretion was low; however, saccharin infusion caused a small, but significant, decrease in fractional glucose excretion. In contrast to the whole kidney data, our micropuncture results did not show any significant difference in fractional glucose reabsorption in either the proximal or distal tubules, indicating that saccharin does not influence renal glucose handling in vivo under euglycemic conditions. In keeping with this finding, protein levels of the renal glucose transporters SGLT1 and SGLT2 were also unchanged. In addition, saccharin infusion in rats undergoing a glucose tolerance test failed to induce a robust change in renal glucose excretion or renal glucose transporter expression. In conclusion, our results demonstrate that saccharin does not induce acute physiologically relevant changes in renal function or renal glucose handling. John Wiley and Sons Inc. 2018-07-16 /pmc/articles/PMC6046642/ /pubmed/30009546 http://dx.doi.org/10.14814/phy2.13804 Text en © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Jacquillet, Grégory
Debnam, Edward S.
Unwin, Robert J.
Marks, Joanne
Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title_full Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title_fullStr Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title_full_unstemmed Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title_short Acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
title_sort acute saccharin infusion has no effect on renal glucose handling in normal rats in vivo
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046642/
https://www.ncbi.nlm.nih.gov/pubmed/30009546
http://dx.doi.org/10.14814/phy2.13804
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