Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice.
With the prevalence of obesity, artificial, non-nutritive sweeteners have been widely used as dietary supplements that provide sweet taste without excessive caloric load. In order to better understand the overall actions of artificial sweeteners, especially when they are chronically used, we investi...
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oai:doaj.org-article:22b5cfc57d0d495a95b116390e6d0f092021-11-18T09:00:49ZLong-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice.1932-620310.1371/journal.pone.0070257https://doaj.org/article/22b5cfc57d0d495a95b116390e6d0f092013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23950916/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203With the prevalence of obesity, artificial, non-nutritive sweeteners have been widely used as dietary supplements that provide sweet taste without excessive caloric load. In order to better understand the overall actions of artificial sweeteners, especially when they are chronically used, we investigated the peripheral and central nervous system effects of protracted exposure to a widely used artificial sweetener, acesulfame K (ACK). We found that extended ACK exposure (40 weeks) in normal C57BL/6J mice demonstrated a moderate and limited influence on metabolic homeostasis, including altering fasting insulin and leptin levels, pancreatic islet size and lipid levels, without affecting insulin sensitivity and bodyweight. Interestingly, impaired cognitive memory functions (evaluated by Morris Water Maze and Novel Objective Preference tests) were found in ACK-treated C57BL/6J mice, while no differences in motor function and anxiety levels were detected. The generation of an ACK-induced neurological phenotype was associated with metabolic dysregulation (glycolysis inhibition and functional ATP depletion) and neurosynaptic abnormalities (dysregulation of TrkB-mediated BDNF and Akt/Erk-mediated cell growth/survival pathway) in hippocampal neurons. Our data suggest that chronic use of ACK could affect cognitive functions, potentially via altering neuro-metabolic functions in male C57BL/6J mice.Wei-na CongRui WangHuan CaiCaitlin M DaimonMorten Scheibye-KnudsenVilhelm A BohrRebecca TurkinWilliam H WoodKevin G BeckerRuin MoaddelStuart MaudsleyBronwen MartinPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e70257 (2013) |
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Medicine R Science Q |
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Medicine R Science Q Wei-na Cong Rui Wang Huan Cai Caitlin M Daimon Morten Scheibye-Knudsen Vilhelm A Bohr Rebecca Turkin William H Wood Kevin G Becker Ruin Moaddel Stuart Maudsley Bronwen Martin Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| description |
With the prevalence of obesity, artificial, non-nutritive sweeteners have been widely used as dietary supplements that provide sweet taste without excessive caloric load. In order to better understand the overall actions of artificial sweeteners, especially when they are chronically used, we investigated the peripheral and central nervous system effects of protracted exposure to a widely used artificial sweetener, acesulfame K (ACK). We found that extended ACK exposure (40 weeks) in normal C57BL/6J mice demonstrated a moderate and limited influence on metabolic homeostasis, including altering fasting insulin and leptin levels, pancreatic islet size and lipid levels, without affecting insulin sensitivity and bodyweight. Interestingly, impaired cognitive memory functions (evaluated by Morris Water Maze and Novel Objective Preference tests) were found in ACK-treated C57BL/6J mice, while no differences in motor function and anxiety levels were detected. The generation of an ACK-induced neurological phenotype was associated with metabolic dysregulation (glycolysis inhibition and functional ATP depletion) and neurosynaptic abnormalities (dysregulation of TrkB-mediated BDNF and Akt/Erk-mediated cell growth/survival pathway) in hippocampal neurons. Our data suggest that chronic use of ACK could affect cognitive functions, potentially via altering neuro-metabolic functions in male C57BL/6J mice. |
| format |
article |
| author |
Wei-na Cong Rui Wang Huan Cai Caitlin M Daimon Morten Scheibye-Knudsen Vilhelm A Bohr Rebecca Turkin William H Wood Kevin G Becker Ruin Moaddel Stuart Maudsley Bronwen Martin |
| author_facet |
Wei-na Cong Rui Wang Huan Cai Caitlin M Daimon Morten Scheibye-Knudsen Vilhelm A Bohr Rebecca Turkin William H Wood Kevin G Becker Ruin Moaddel Stuart Maudsley Bronwen Martin |
| author_sort |
Wei-na Cong |
| title |
Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| title_short |
Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| title_full |
Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| title_fullStr |
Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| title_full_unstemmed |
Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice. |
| title_sort |
long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in c57bl/6j mice. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2013 |
| url |
https://doaj.org/article/22b5cfc57d0d495a95b116390e6d0f09 |
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