Evidence map›Paper›PMID 33499218›Full record

ArticleBiology2021

Long-Term Aspartame Administration Leads to Fibrosis, Inflammasome Activation, and Gluconeogenesis Impairment in the Liver of Mice.

Isabela A Finamor, Caroline A Bressan, Isabel Torres-Cuevas, Sergio Rius-Pérez, Marcelo da Veiga, Maria I Rocha, Maria A Pavanato, Salvador Pérez

Open access · goldAbstract read
In one paragraph

Article in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Isabela A FinamorDepartment of Physiology and Pharmacology, Federal University of Santa Maria, Santa Maria 97105900, Rio Grande do Sul, Brazil.
Caroline A BressanDepartment of Physiology and Pharmacology, Federal University of Santa Maria, Santa Maria 97105900, Rio Grande do Sul, Brazil.
Isabel Torres-CuevasNeonatal Research Group, Health Research Institute La Fe, 46026 Valencia, Spain.ORCID 0000-0002-8098-1106
Sergio Rius-PérezDepartment of Physiology, Faculty of Pharmacy, University of Valencia, 46100 Burjassot, Valencia, Spain.
Marcelo da VeigaDepartment of Morphology, Federal University of Santa Maria, Santa Maria 97105900, Rio Grande do Sul, Brazil.
Maria I RochaDepartment of Morphology, Federal University of Santa Maria, Santa Maria 97105900, Rio Grande do Sul, Brazil.
Maria A PavanatoDepartment of Physiology and Pharmacology, Federal University of Santa Maria, Santa Maria 97105900, Rio Grande do Sul, Brazil.
Salvador PérezDepartment of Physiology, Faculty of Pharmacy, University of Valencia, 46100 Burjassot, Valencia, Spain.ORCID 0000-0003-0766-1744
Universidade Federal de Santa Maria · BRUniversitat de València · ES

Funding

Conselleria d'Educació, Investigació, Cultura i Esport GV/2019/153
6 · The paper itself

Abstract

backgroundAspartame 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.

methodsMice 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.

resultsAspartame caused liver damage and elevated serum transaminase levels. Aspartame also generated liver fibrosis, as evidenced by histology analysis, and pro-fibrotic markers' upregulation, including transforming growth factor β 1, collagen type I alpha 1, and alpha-smooth muscle actin. Furthermore, aspartame reduced nuclear factor erythroid 2-related factor 2 (Nrf2) activation and enzymatic antioxidant activity and increased lipid peroxidation, which triggered NOD-like receptor containing protein 3 (NLRP3) inflammasome activation and p53 induction. Furthermore, aspartame reduced peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) levels, possibly through p53 activation. This PGC-1α deficiency could be responsible for the changes in lipid profile in serum, total lipid accumulation, and gluconeogenesis impairment in liver, evidenced by the gluconeogenic enzymes' downregulation, thus causing hypoglycemia.

conclusionsThis work provides new insights to understand the mechanisms related to the adverse effects of aspartame on liver tissue.

Indexed as

aspartamegluconeogenesishypoglycemiainflammasomelipidlipid peroxidationliver fibrosisNrf2PGC-1α

Identifiers

PMID33499218
PMCPMC7911935
OpenAlexW3124074796

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.