Evidence map›Paper›PMID 29026155›Full record

ArticleScientific reports2017

Trk-fused gene (TFG) regulates pancreatic β cell mass and insulin secretory activity.

Takeshi Yamamotoya, Yusuke Nakatsu, Akifumi Kushiyama, Yasuka Matsunaga, Koji Ueda, Yuki Inoue, Masa-Ki Inoue, Hideyuki Sakoda, Midori Fujishiro, Hiraku Ono and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Cell type-specific gene therapy confers protection against motor neuron disease caused by a TFG variant.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  7. TFG regulates secretory and endosomal sorting pathways in neurons to promote their activity and maintenance.Proceedings of the National Academy of Sciences of the United States of America · 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

13 authors at 6 institutions in 2 countries.

Takeshi YamamotoyaDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Yusuke NakatsuDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Akifumi KushiyamaDivision of Diabetes and Metabolism, The Institute for Adult Diseases, Asahi Life Foundation, Chuo-ku, Tokyo, 103-0002, Japan.ORCID 0000-0003-1385-7487
Yasuka MatsunagaCenter for Translational Research in Infection & Inflammation, School of Medicine, Tulane University, 6823, St. Charles Avenue, New Orleans, LA, 70118, USA.
Koji UedaDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Yuki InoueDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Masa-Ki InoueDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan.
Hideyuki SakodaDivision of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
Midori FujishiroDivision of Diabetes and Metabolic Diseases, Nihon University School of Medicine, Itabashi, Tokyo, 173-8610, Japan.
Hiraku OnoDepartment of Clinical Cell Biology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba City, Chiba, 260-8670, Japan.
Hiroshi KiyonariAnimal Resource Development Unit and Genetic Engineering Team, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe, 650-0047, Japan.
Hisamitsu IshiharaDivision of Diabetes and Metabolic Diseases, Nihon University School of Medicine, Itabashi, Tokyo, 173-8610, Japan.
Tomoichiro AsanoDepartment of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima, 734-8551, Japan. tasano@hiroshima-u.ac.jp.
Hiroshima University · JPNihon University · JPChiba University · JPThe Institute of Medical Science, Asahi Life Foundation · JPTulane University · USUniversity of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Trk-fused gene (TFG) is reportedly involved in the process of COPII-mediated vesicle transport and missense mutations in TFG cause several neurodegenerative diseases including hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P). The high coincidence ratio between HMSN-P and diabetes mellitus suggests TFG to have an important role(s) in glucose homeostasis. To examine this possibility, β-cell specific TFG knockout mice (βTFG KO) were generated. Interestingly, βTFG KO displayed marked glucose intolerance with reduced insulin secretion. Immunohistochemical analysis revealed smaller β-cell masses in βTFG KO than in controls, likely attributable to diminished β-cell proliferation. Consistently, β-cell expansion in response to a high-fat, high-sucrose (HFHS) diet was significantly impaired in βTFG KO. Furthermore, glucose-induced insulin secretion was also markedly impaired in islets isolated from βTFG KO. Electron microscopic observation revealed endoplasmic reticulum (ER) dilatation, suggestive of ER stress, and smaller insulin crystal diameters in β-cells of βTFG KO. Microarray gene expression analysis indicated downregulation of NF-E2 related factor 2 (Nrf2) and its downstream genes in TFG depleted islets. Collectively, TFG in pancreatic β-cells plays a vital role in maintaining both the mass and function of β-cells, and its dysfunction increases the tendency to develop glucose intolerance.

Indexed as

Insulin SecretionAnimalsCell ProliferationDown-RegulationEndoplasmic Reticulum StressGlucoseGlucose IntoleranceHypertrophyInsulinInsulin-Secreting CellsIntegrasesMice, KnockoutNF-E2-Related Factor 2Organ SpecificityProteinsVesicular Transport ProteinsCre recombinaseGlucoseInsulinIntegrasesNfe2l2 protein, mouseNF-E2-Related Factor 2ProteinsTfg protein, mouseVesicular Transport Proteins

Identifiers

PMID29026155
PMCPMC5638802
OpenAlexW2763145856

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.