Evidence mapPaperPMID 36463128Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Exenatide regulates Th17/Treg balance via PI3K/Akt/FoxO1 pathway in db/db mice.

Qinqin Xu, Xiaoling Zhang, Tao Li, Shiying Shao

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.4field-weighted citation impact, top 3% of its field
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

30 citing papers in PubMed, 45 citations in OpenAlex.

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  20. Fu-Fang-Qi-Di-Hua-Yu-Tang Improves Diabetic Macrovascular Disease via PI3K/AKT Pathway Regulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    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

4 authors at 2 institutions in 1 country.

Qinqin XuDivision of Endocrinology, Tongji Hospital, Huazhong University of Science and Technology, Jiefang Road 1095, Wuhan, 430030, Hubei Province, People's Republic of China.
Xiaoling ZhangDivision of Endocrinology, Tongji Hospital, Huazhong University of Science and Technology, Jiefang Road 1095, Wuhan, 430030, Hubei Province, People's Republic of China.
Tao LiDivision of Ophthalmology, Tongji Hospital, Huazhong University of Science and Technology, Jiefang Road 1095, Wuhan, 430030, Hubei Province, People's Republic of China. dr_litao@163.com.
Shiying ShaoDivision of Endocrinology, Tongji Hospital, Huazhong University of Science and Technology, Jiefang Road 1095, Wuhan, 430030, Hubei Province, People's Republic of China. shaoshiying@hotmail.com.ORCID 0000-0001-7077-5184
National Clinical Research Center for Digestive Diseases · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe T helper 17 (Th17)/T regulatory (Treg) cell imbalance is involved in the course of obesity and type 2 diabetes mellitus (T2DM). In the current study, the exact role of glucagon-like peptide-1 receptor agonist (GLP-1RA) exenatide on regulating the Th17/Treg balance and the underlying molecular mechanisms are investigated in obese diabetic mice model.

methodsMetabolic parameters were monitored in db/db mice treated with/without exenatide during 8-week study period. The frequencies of Th17 and Treg cells from peripheral blood and pancreas in db/db mice were assessed. The phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/Forkhead box O1 (FoxO1) pathway in Th17 and Treg cells from the spleens of male C57BL/6J mice was detected by western blotting. In addition, the expression of glucagon-like peptide-1 receptor (GLP-1R) in peripheral blood mononuclear cells (PBMCs) of male C57BL/6J mice was analyzed.

resultsExenatide treatment improved β-cell function and insulitis in addition to glucose, insulin sensitivity and weight. Increased Th17 and decreased Treg cells in peripheral blood were present as diabetes progressed while exenatide corrected this imbalance. Progressive IL-17 + T cell infiltration of pancreatic islets was alleviated by exenatide intervention. In vitro study showed no significant difference in the level of GLP-1R expression in PBMCs between control and palmitate (PA) groups. In addition, PA could promote Th17 but suppress Treg differentiation along with down-regulating the phosphorylation of PI3K/Akt/FoxO1, which was reversed by exenatide intervention. FoxO1 inhibitor AS1842856 could abrogate all these effects of exenatide against lipid stress.

conclusionsExenatide could restore systemic Th17/Treg balance via regulating FoxO1 pathway with the progression of diabetes in db/db mice. The protection of pancreatic β-cell function may be partially mediated by inhibiting Th17 cell infiltration into pancreatic islets, and the resultant alleviation of islet inflammation.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2AnimalsExenatideForkhead Box Protein O1Glucagon-Like Peptide-1 ReceptorLeukocytes, MononuclearMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktT-Lymphocytes, RegulatoryExenatideForkhead Box Protein O1Foxo1 protein, mouseGlucagon-Like Peptide-1 ReceptorPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktExenatideForkhead box O1T helper 17 cellT regulatory cellType 2 diabetes mellitus

Identifiers

PMID36463128
PMCPMC9719171
OpenAlexW4311197765

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.