Evidence mapPaperPMID 40066121Full record

ArticleIranian journal of pharmaceutical research : IJPR

The Glucagon-Like Peptide-1 (GLP-1) Receptor Agonist Liraglutide Regulates Sirtuin-1-Mediated Neutrophil Extracellular Traps to Improve Diabetes-Induced Bone Metabolism Imbalance.

Shuai Zhong, Liangzhi Huang, Tingting Lin, Yanyan Li, Bin Deng, Dezhi Kong, Zhanlin Liao, Zugui Huang

Abstract read
In one paragraph

Article in Iranian journal of pharmaceutical research : IJPR. 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. Review
  3. Review
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

8 authors.

Shuai ZhongDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Liangzhi HuangDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Tingting LinDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Yanyan LiDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Bin DengDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Dezhi KongDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Zhanlin LiaoDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.
Zugui HuangDepartment of Endocrinology, The Affiliated Nanping First Hospital, Fujian Medical University, Nanping, Fujian, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Diabetes mellitus (DM) is a chronic metabolic disorder that disrupts normal bone remodeling. Objectives: This study aimed to investigate how the glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide (LIR) addresses bone metabolism imbalances induced by type-II diabetes. Methods: Type-II diabetic rat models were established through a single intraperitoneal injection of streptozotocin (STZ). Blood glucose levels were measured using a blood glucose meter, and insulin levels were assessed using an assay kit. Bone formation markers [alkaline phosphatase (ALP), osteocalcin (OCN), and procollagen I N-terminal propeptide (PINP)] and bone resorption markers [tartrate-resistant acid phosphatase (TRACP) and CTX-1] were monitored using assay kits. Bone marrow mesenchymal stem cells (BMSCs) were cultured in vitro under high-fat and high-glucose (HFHS) conditions to mimic diabetic bone metabolism dysregulation. Neutrophil extracellular traps (NETs) formation was examined through immunofluorescent staining and Western blot analysis. Results: Liraglutide was found to reduce STZ-induced NETs formation, as indicated by decreased expression of cit-H3 by 36.90% - 53.57%, myeloperoxidase (MPO) by 55.81% - 65.12%, NE by 53.95% - 65.17%, and PAD4 by 46.81% - 63.83%, alongside increased Sirtuin-1 (SIRT1) expression in femur tissue (70.71% - 91.19%). In vitro, LIR enhanced osteogenesis and inhibited apoptosis, effects that were partially reversed by SIRT1 knockdown. Additionally, SIRT1 knockdown partially restored LIR-induced reductions in oxidative stress, inflammation, and NETs formation. Conclusions: LIR mitigates diabetes-induced bone metabolism imbalance by inhibiting NETs formation through SIRT1 mediation.

Indexed as

Bone MetabolismDiabetes MellitusLiraglutideNeutrophil Extracellular TrapsSIRT1

Identifiers

PMID40066121
PMCPMC11892751

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.