ArticleFEBS open bio2026
Short-term actions of epigalocatechin-3-gallate in the liver: a mechanistic insight into hypoglycemic and potential toxic effects.
Article in FEBS open bio, 2026. 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
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.
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.
Who cites it
2 citing papers in PubMed.
- Review
- Short-term actions of arsenic trioxide on metabolic fluxes in the isolated perfused rat liver.Naunyn-Schmiedeberg's archives of pharmacology · 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
9 authors.
Funding
Abstract
Epigallocatechin-3-gallate (EGCG), the main catechin in green tea, is associated with antidiabetic and anti-obesity effects, although its acute hepatic actions remain unclear. We investigated short-term effects of EGCG (10-500 μm) using isolated perfused rat livers and complementary assays in mitochondrial, microsomal, and cytosolic fractions. EGCG markedly inhibited gluconeogenesis from lactate (up to 52%), glycerol (33%), and alanine (47%), while it stimulated glycolysis, glycogenolysis, and oleic acid oxidation (+42% total ketone bodies). Oxygen uptake was stimulated under glycogenolytic and fatty acid oxidizing conditions but inhibited under gluconeogenic conditions. Mechanistic analyses revealed EGCG-induced mild mitochondrial uncoupling, inhibition of pyruvate carboxylase and glucose-6-phosphatase (with no effect on fructose-1,6-bisphosphatase) and stimulation of phosphoenolpyruvate carboxykinase. EGCG shifted cytosolic and mitochondrial NADH/NAD
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Registered trials
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.