Evidence map›Paper›PMID 29208957›Full record

ArticleNature communications2017

Neuronal signals regulate obesity induced β-cell proliferation by FoxM1 dependent mechanism.

Junpei Yamamoto, Junta Imai, Tomohito Izumi, Hironori Takahashi, Yohei Kawana, Kei Takahashi, Shinjiro Kodama, Keizo Kaneko, Junhong Gao, Kenji Uno and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.7field-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

51 citing papers in PubMed, 81 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

19 authors at 6 institutions in 2 countries.

Junpei YamamotoDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Junta ImaiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan. imai@med.tohoku.ac.jp.
Tomohito IzumiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Hironori TakahashiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yohei KawanaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kei TakahashiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Shinjiro KodamaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Keizo KanekoDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Junhong GaoDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kenji UnoDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Shojiro SawadaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Tomoichiro AsanoDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, Hiroshima, 734-8553, Japan.
Vladimir V KalinichenkoDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Etsuo A SusakiDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Makoto KanzakiTohoku University Graduate School of Biomedical Engineering, Sendai, 980-8579, Japan.ORCID http://orcid.org/0000-0002-6884-2955
Hiroki R UedaDepartment of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Yasushi IshigakiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Tetsuya YamadaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Hideki KatagiriDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Tohoku University · JPCincinnati Children's Hospital Medical Center · USHiroshima University · JPIwate Medical University · JPJapan Science and Technology Agency · JPQuantitative BioSciences · US

Funding

Fox Transcription Factors in Development of Pulmonary CapillariesR01HL084151 · NHLBI · UNIVERSITY OF CHICAGO · PI KALINICHENKO, VLADIMIR · 2006 to 2018
$4.9M
Transcriptional regulation of goblet cell metaplasiaR01HL123490 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI KALINICHENKO, VLADIMIR · 2014 to 2017
$1.6M
NHLBI NIH HHS R01 HL084151NHLBI NIH HHS R01 HL123490
6 · The paper itself

Abstract

Under insulin-resistant conditions such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. A liver-brain-pancreas neuronal relay plays an important role in this process. Here, we show the molecular mechanism underlying this compensatory β-cell proliferation. We identify FoxM1 activation in islets from neuronal relay-stimulated mice. Blockade of this relay, including vagotomy, inhibits obesity-induced activation of the β-cell FoxM1 pathway and suppresses β-cell expansion. Inducible β-cell-specific FoxM1 deficiency also blocks compensatory β-cell proliferation. In isolated islets, carbachol and PACAP/VIP synergistically promote β-cell proliferation through a FoxM1-dependent mechanism. These findings indicate that vagal nerves that release several neurotransmitters may allow simultaneous activation of multiple pathways in β-cells selectively, thereby efficiently promoting β-cell proliferation and maintaining glucose homeostasis during obesity development. This neuronal signal-mediated mechanism holds potential for developing novel approaches to regenerating pancreatic β-cells.

Indexed as

Cell ProliferationInsulin ResistanceAnimalsBlood GlucoseBrainCarbacholCholinergic AgonistsForkhead Box Protein M1Gastrointestinal AgentsInsulin-Secreting CellsIslets of LangerhansLiverMiceNeuronsNeurotransmitter AgentsObesityBlood GlucoseCarbacholCholinergic AgonistsForkhead Box Protein M1Foxm1 protein, mouseGastrointestinal AgentsNeurotransmitter AgentsPituitary Adenylate Cyclase-Activating PolypeptideVasoactive Intestinal Peptide

Identifiers

PMID29208957
PMCPMC5717276
OpenAlexW2769266397

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.