ArticleFrontiers in nutrition2025
Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Bioactive Component Screening and Mechanistic Study of the Anti-Diabetic Activity ofCurrent issues in molecular biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Prolonged hyperglycemia caused by type 2 diabetes mellitus (T2DM) can lead to liver injury and disrupt the community of the gut microbiota that pose significant risks to human health. As a food rich in a variety of active ingredients, Methods: After a one-week acclimation period, 12 mice were randomly selected as the normal group. The remaining 48 mice were employed T2DM model, and then randomly assigned to four groups: the model group, a low-dose ZSE group (ZSE-L, 100 mg/kg/day), a high-dose ZSE group (ZSE-H, 300 mg/kg/day), and a positive control group treated with metformin hydrochloride (MET, 100 mg/kg/day). Results: After a 4-week intervention, the results revealed that ZSE significantly ameliorated fasting blood glucose (FBG), area under the curve of oral glucose tolerance test (AUC of OGTT) and glycated serum protein (GSP) in T2DM mice. Moreover, the high-dose (ZSE-H) treatment increased the relative abundance of beneficial bacteria such as Conclusion: ZSE plays a pivotal role in mitigating hyperglycemia in T2DM mice through the modulation of intestinal microbiota communities.
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Registered trials
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