Evidence map›Paper›PMID 36331598›Full record

ArticleDiabetologia2023

Pancreatic alpha cell glucagon-liver FGF21 axis regulates beta cell regeneration in a mouse model of type 2 diabetes.

Xiaona Cui, Jin Feng, Tianjiao Wei, Linxi Zhang, Shan Lang, Kun Yang, Jin Yang, Junling Liu, Michael Sterr, Heiko Lickert and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Xiaona CuiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0002-4932-1281
Jin FengDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0001-7265-0051
Tianjiao WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0003-1546-4257
Linxi ZhangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0002-5185-9742
Shan LangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0001-6889-2867
Kun YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0002-7012-4557
Jin YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.ORCID 0000-0001-6004-955X
Junling LiuDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Michael SterrInstitute of Diabetes and Regeneration Research, Helmholtz Center Munich, Neuherberg, Germany.
Heiko LickertInstitute of Diabetes and Regeneration Research, Helmholtz Center Munich, Neuherberg, Germany.ORCID 0000-0002-4597-8825
Rui WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China. weirui@bjmu.edu.cn.ORCID 0000-0002-8838-703X
Tianpei HongDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China. tpho66@bjmu.edu.cn.ORCID 0000-0002-5744-5129
Peking University · CNHelmholtz Zentrum München · DE

Funding

China Postdoctoral Science Foundation 2020M670068National Natural Science Foundation of China 82170875Natural Science Foundation of Beijing Municipality 7212127
6 · The paper itself

Abstract

aims/hypothesisGlucagon receptor (GCGR) antagonism ameliorates hyperglycaemia and promotes beta cell regeneration in mouse models of type 2 diabetes. However, the underlying mechanisms remain unclear. The present study aimed to investigate the mechanism of beta cell regeneration induced by GCGR antagonism in mice.

methodsThe db/db mice and high-fat diet (HFD)+streptozotocin (STZ)-induced mice with type 2 diabetes were treated with antagonistic GCGR monoclonal antibody (mAb), and the metabolic variables and islet cell quantification were evaluated. Plasma cytokine array and liver RNA sequencing data were used to screen possible mediators, including fibroblast growth factor 21 (FGF21). ELISA, quantitative RT-PCR and western blot were applied to verify FGF21 change. Blockage of FGF21 signalling by FGF21-neutralising antibody (nAb) was used to clarify whether FGF21 was involved in the effects of GCGR mAb on the expression of beta cell identity-related genes under plasma-conditional culture and hepatocyte co-culture conditions. FGF21 nAb-treated db/db mice, systemic Fgf21-knockout (Fgf21

resultsGCGR mAb treatment improved blood glucose control, and increased islet number (db/db 1.6±0.1 vs 0.8±0.1 per mm CONCLUSIONS/

interpretationOur findings demonstrate that liver-derived FGF21 is involved in the GCGR antagonism-induced beta cell regeneration in a mouse model of type 2 diabetes.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Glucagon-Secreting CellsAnimalsCytokinesDisease Models, AnimalFibroblast Growth FactorsGlucagonLiverMiceMice, Inbred C57BLReceptors, GlucagonCytokinesfibroblast growth factor 21Fibroblast Growth FactorsGlucagonReceptors, GlucagonAlpha cellBeta cell regenerationFGF21Glucagon receptorLiver

Identifiers

PMID36331598
PMCPMC9892158
OpenAlexW4308183658

What OpenQuestion 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 OpenQuestion graph.