ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2026
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Methods: The chemical constituents of Yuzhu were characterized by UHPLC-Q-TOF-MS/MS. Network pharmacology integrated with GEO dataset analysis was employed to identify potential active compounds, therapeutic targets, and signaling pathways. Molecular docking was performed to evaluate compound-target interactions. A high-fat diet (HFD)-induced obese mouse model and a TNF-α-induced 3T3-L1 adipocyte inflammation model were used for experimental validation. Metabolic parameters, inflammatory cytokines, and TLR4/NLRP3 pathway-related molecules were assessed by biochemical assays, RT-qPCR, Western blot, immunohistochemistry, ELISA, and TUNEL staining. Results: A total of 127 chemical constituents were identified from Yuzhu, of which 67 met the screening criteria for potential bioactivity. Network pharmacology analysis identified 23 overlapping targets and highlighted corchorifatty acid F, 9,10-dihydroxy-12Z-octadecenoic acid, N-trans-feruloyloctopamine, and diosgenin glucoside (DG) as core active components. TLR4 and CCL2 were identified as hub targets, with significant enrichment in the NOD-like receptor signaling pathway. Molecular docking demonstrated favorable binding affinities of the core compounds to TLR4 and NLRP3, with DG exhibiting the strongest binding activity. In vivo, Yuzhu significantly reduced body weight gain, hyperglycemia, dyslipidemia, glucose intolerance, and IR in HFD-fed mice, while suppressing adipose tissue inflammation. Mechanistically, Yuzhu inhibited the expression of TLR4, MyD88, NLRP3, IL-1β, TNF-α, p-p65, p-STAT3, and cleaved caspase-1. In vitro, DG alleviated TNF-α-induced inflammatory responses and apoptosis in adipocytes, whereas recombinant HMGB1 partially reversed these protective effects. Conclusion: Yuzhu may alleviate obesity-associated IR through multi-component and multi-target regulation of the TLR4/NLRP3 signaling pathway. DG may represent a key bioactive constituent responsible for these protective effects. These findings provide mechanistic insights and experimental evidence supporting the potential application of Yuzhu in the management of metabolic disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.