Evidence map›Paper›PMID 34546489›Full record

ArticleEndocrine2022

Irisin alleviates FFA induced β-cell insulin resistance and inflammatory response through activating PI3K/AKT/FOXO1 signaling pathway.

Shuang Zheng, Ningxin Chen, Xingjian Kang, Yaomin Hu, Sheng Shi

Abstract read
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In one paragraph

Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.5field-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

45 citing papers in PubMed, 63 citations in OpenAlex.

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  19. Lipotoxicity: A New Perspective in Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
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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

5 authors at 4 institutions in 1 country.

Shuang ZhengSchool of Medicine, Shanghai University, Shanghai, 200444, China.
Ningxin ChenDepartment of Endocrinology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Xingjian KangSchool of Stomatology, Wenzhou Medical University, Wenzhou, 325000, China.
Yaomin HuDepartment of Endocrinology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
Sheng ShiDepartment of Orthopedics, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. shisheng273@163.com.
Renji Hospital · CNShanghai University · CNTongji University · CNWenzhou Medical University · CN

Funding

postdoctoral research foundation of china 2019M651588science and technology commission of shanghai municipality 19YF1428600
6 · The paper itself

Abstract

purposeType 2 diabetes mellitus is characterized by insulin resistance and β-cell dysfunction. Elevated free fatty acids-induced lipotoxicity may play a vital role in the pathogenesis of β-cell insulin resistance. Exercise-stimulated myokine irisin has been reported to be closely related to T2DM. However, its function on β-cell insulin signaling and the underlying mechanisms are only partially elucidated as yet.

methodsHigh-fat diet-fed C57BL/6J mice and palmitic acid-treated MIN6 cell models were utilized as lipotoxic models. Factors associated with β-cell insulin signaling transduction and inflammatory responses were assessed in these models. Furthermore, the role of irisin in β-cells and the underlying mechanisms were also explored.

resultsIrisin effectively decreased lipid levels in HFD mice, enhanced glucose-stimulated insulin secretion and nullified the expressions of inflammatory cytokines in vivo and in vitro experiments. Moreover, irisin improved PI3K/AKT insulin signaling pathway and inhibited TLR4/NF-κB inflammatory signaling pathway in both islets of HFD mice and PA-treated MIN6 cells. Mechanistic analysis indicated that FOXO1 might serve as a bridge between the two pathways.

conclusionIrisin alleviates lipotoxicity-induced β-cell insulin resistance and inflammatory response through the activation of PI3K/AKT/FOXO1 signaling pathways and the inhibition of TLR4/NF-κB signaling pathways. Irisin might provide a novel therapeutic strategy for T2DM.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceAnimalsFatty Acids, NonesterifiedForkhead Box Protein O1InsulinMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionFatty Acids, NonesterifiedForkhead Box Protein O1Foxo1 protein, mouseInsulinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktInflammatory responseInsulin resistanceIrisinIslet β-cellLipotoxicity

Identifiers

PMID34546489
OpenAlexW3199157238

What OpenQuestion holds

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Registered trials

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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.