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RESEARCH PRODUCT
Long-Term Aspartame Administration Leads to Fibrosis, Inflammasome Activation, and Gluconeogenesis Impairment in the Liver of Mice
Isabel Torres-cuevasIsabel Torres-cuevasSergio Rius-pérezIsabela FinamorMarcelo Da VeigaMaria Izabel U.m. Da RochaCaroline A. BressanSalvador PérezMaria A. Pavanatosubject
0301 basic medicinemedicine.medical_specialtyPGC-1αInflammationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyArticleaspartameNrf2Lipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationFibrosislipidinflammasomeInternal medicinemedicinelcsh:QH301-705.5liver fibrosisGeneral Immunology and MicrobiologyAspartameInflammasomelipid peroxidationmedicine.diseaseCollagen type I alpha 1030104 developmental biologyEndocrinologyhypoglycemiagluconeogenesischemistrylcsh:Biology (General)030211 gastroenterology & hepatologymedicine.symptomGeneral Agricultural and Biological SciencesOxidative stressmedicine.drugdescription
Background: Aspartame is an artificial sweetener used in foods and beverages worldwide. However, it is linked to oxidative stress, inflammation, and liver damage through mechanisms that are not fully elucidated yet. This work aimed to investigate the effects of long-term administration of aspartame on the oxidative and inflammatory mechanisms associated with liver fibrosis progression in mice. Methods: Mice were divided into two groups with six animals each: control and aspartame. Aspartame (80 mg/kg, via oral) or vehicle was administrated for 12 weeks. Results: Aspartame caused liver damage and elevated serum transaminase levels. Aspartame also generated liver fibrosis, as evidenced by histology analysis, and pro-fibrotic markers&rsquo
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2021-01-22 | Biology |