ArticleFood chemistry: X2025
Artificially fermented dark loose tea ameliorates metabolic-associated fatty liver disease by activating the PI3K/AKT signalling pathway and regulating gut microbiota dysbiosis.
Article in Food chemistry: X, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
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Who cites it
2 citing papers in PubMed.
- Emodin Exerts Dual Hepatoprotective/Hepatotoxic Effects Dependent on Metabolic Microenvironment via Gut-Liver Axis Crosstalk: A Multi-Omics Study in MAFLD and Normal Mice.International journal of molecular sciences · 2026Article
- Editorial Special issue:Food chemistry: X · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Artificially fermented dark loose tea (AFT) has demonstrated potential lipid-lowering effects. However, the effects, including the dose-dependent effects, of AFT on metabolic-associated fatty liver disease (MAFLD) and their underlying mechanisms remain largely unclear. In vitro, AFT was found to effectively reduce intracellular lipid droplet formation and decrease the levels of total cholesterol and triglycerides. In vivo, AFT significantly prevented body weight gain, ameliorated serum lipid metabolism disorders, and alleviated hepatic steatosis. The ameliorative effect of AFT on MAFLD was associated with the activation of the PI3K/AKT signalling pathway, as indicated by the increased levels of phosphorylated (p)-PI3K/PI3K and p-AKT/AKT and the decreased expression of FOXO-1 and PEPCK at both the gene and protein levels. AFT supplementation regulated gut dysbiosis, especially in terms of reversing HFD-induced reductions in the relative abundances of
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Registered trials
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