Evidence map›Paper›PMID 41199094›Full record

ArticleChinese journal of integrative medicine2026

Isoquercitrin Improves Insulin Resistance by Inhibiting PTP1B-Regulated IRS/PI3K/AKT Signaling Pathway.

Si-Yu Liu, Lu-Jing Yu, Sheng-Nan Zhang, Jia-Kui Yue, Guo-Jun Jiang, Si-Hua Lu, Ying-Jia Li, Jun-Yu Meng, Gui-Hong Huang

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Article in Chinese journal of integrative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. International journal of molecular sciences · 2026
    Article
  3. Article
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

9 authors.

Si-Yu LiuDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Lu-Jing YuDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Sheng-Nan ZhangDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Jia-Kui YueDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Guo-Jun JiangDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Si-Hua LuDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Ying-Jia LiDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Jun-Yu MengDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China.
Gui-Hong HuangDepartment of Pharmacy, the Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, 541199, China. Guihonghuang666@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the molecular mechanism by which protein tyrosine phosphatase 1B (PTP1B) enzyme regulates insulin resistance (IR) in diabetes mellitus, and the regulation of isoquercitrin (IS) on PTP1B in vitro and in vivo.

methodsIn vitro, PTP1B overexpression plasmid was constructed and transiently transfected into human hepatocellular liver carcinoma (HepG2) cells. A co-inducer was prepared by mixing a 0.125 mmol/L palmitic acid solution with a 1.0 × 10

resultsIn both in vivo and in vitro experiments, IS significantly improved IR, reduced levels of blood glucose, total cholesterol, triglycerides, and other metabolic indicators in mice, effectively controlled body weight, and restored pancreatic cell morphology (P<0.05 or P<0.01). At the genomic level, IS improved the expressions of related factors in the IRS/PI3K/AKT signaling pathway by regulating the expression of PTP1B (P<0.05 or P<0.01), thereby maintaining the homeostasis of the pathway.

conclusionIS can improve IR by inhibiting the IRS/PI3K/AKT signaling pathway through PTP1B intervention.

Indexed as

Insulin Receptor Substrate ProteinsInsulin ResistancePhosphatidylinositol 3-KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktQuercetinSignal TransductionAnimalsGlucoseHep G2 CellsHumansMaleMiceGlucoseInsulin Receptor Substrate ProteinsisoquercitrinPhosphatidylinositol 3-KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Proto-Oncogene Proteins c-aktPTPN1 protein, humanQuercetinChinese medicineinsulin receptor substrate/phosphatidylinositol-3-kinase/protein kinase B signal pathwayinsulin resistanceisoquercitrinprotein tyrosine phosphatase 1B

Identifiers

What Socratic holds

Textmetadata
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Registered trials

None linked

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 Socratic graph.