Evidence map›Paper›PMID 35789836›Full record

ArticleiScience2022

Pro-α-cell-derived β-cells contribute to β-cell neogenesis induced by antagonistic glucagon receptor antibody in type 2 diabetic mice.

Xiaona Cui, Jin Feng, Tianjiao Wei, Liangbiao Gu, Dandan Wang, Shan Lang, Kun Yang, Jin Yang, Hai Yan, Rui Wei and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 22 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

11 authors at 1 institution in 1 country.

Xiaona CuiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Jin FengDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Tianjiao WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Liangbiao GuDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Dandan WangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Shan LangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Kun YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Jin YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Hai YanREMD Biotherapeutics, Camarillo, CA 93012, USA.
Rui WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Tianpei HongDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The deficiency of pancreatic β-cells is the key pathogenesis of diabetes, while glucagon-secreting α-cells are another player in the development of diabetes. Here, we aimed to investigate the effects of glucagon receptor (GCGR) antagonism on β-cell neogenesis in type 2 diabetic (T2D) mice and explore the origins of the neogenic β-cells. We showed that GCGR monoclonal antibody (mAb) elevated plasma insulin level and increased β-cell mass in T2D mice. By using α-cell lineage-tracing (

Indexed as

Cell biologyCellular physiologyEndocrinologyPhysiology

Identifiers

PMID35789836
PMCPMC9249614
OpenAlexW4281947100

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.