Evidence map›Paper›PMID 32139602›Full record

ArticleBMJ open diabetes research & care2020

Glucagon receptor antagonist upregulates circulating GLP-1 level by promoting intestinal L-cell proliferation and GLP-1 production in type 2 diabetes.

Shan Lang, Jin Yang, Kun Yang, Liangbiao Gu, Xiaona Cui, Tianjiao Wei, Junling Liu, Yunyi Le, Haining Wang, Rui Wei and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.0field-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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  16. GLP1 Exerts Paracrine Activity in the Intestinal Lumen of Human Colon.International journal of molecular sciences · 2022
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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.

Shan LangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Jin YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Kun YangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Liangbiao GuDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Xiaona CuiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Tianjiao WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Junling LiuDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Yunyi LeDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Haining WangDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
Rui WeiDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China weirui@bjmu.edu.cn tpho66@bjmu.edu.cn.
Tianpei HongDepartment of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China weirui@bjmu.edu.cn tpho66@bjmu.edu.cn.ORCID 0000-0002-5744-5129
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGlucagon receptor (GCGR) blockage improves glycemic control and increases circulating glucagon-like peptide-1 (GLP-1) level in diabetic animals and humans. The elevated GLP-1 has been reported to be involved in the hypoglycemic effect of GCGR blockage. However, the source of this elevation remains to be clarified. RESEARCH DESIGN AND

methodsREMD 2.59, a human GCGR monoclonal antibody (mAb), was administrated for 12 weeks in

resultsTreatment with the GCGR mAb lowered blood glucose level, improved glucose tolerance and elevated plasma GLP-1 level in both

conclusionsThe elevated circulating GLP-1 level by GCGR mAb is mainly due to intestinal L-cell proliferation and GLP-1 production, which may be mediated via GLP-1R/PKA signaling pathways. Therefore, GCGR mAb represents a promising strategy to improve glycemic control and restore the impaired GLP-1 production in T2D.

Indexed as

AnimalsAntibodies, MonoclonalCell ProliferationDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Glucagon-Like Peptide 1IleumL CellsMaleMiceMice, Inbred C57BLProglucagonReceptors, GlucagonSignal TransductionAntibodies, MonoclonalGlucagon-Like Peptide 1ProglucagonReceptors, Glucagonglucagon-like peptide-1 (GLP-1)glucagon receptorintestinal hormonestype 2 diabetes

Identifiers

PMID32139602
PMCPMC7059498
OpenAlexW3009177262

What OpenQuestion holds

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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.