Evidence map›Paper›PMID 37852976›Full record

ArticleNature communications2023

Gut insulin action protects from hepatocarcinogenesis in diabetic mice comorbid with nonalcoholic steatohepatitis.

Kotaro Soeda, Takayoshi Sasako, Kenichiro Enooku, Naoto Kubota, Naoki Kobayashi, Yoshiko Matsumoto Ikushima, Motoharu Awazawa, Ryotaro Bouchi, Gotaro Toda, Tomoharu Yamada and 15 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. 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
3.2field-weighted citation impact, top 7% 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, 15 citations in OpenAlex.

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  8. New advances in oral microbiology and tumor research.World journal of clinical oncology · 2025
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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

25 authors at 8 institutions in 1 country.

Kotaro SoedaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0001-9942-5081
Takayoshi SasakoDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0002-7644-309X
Kenichiro EnookuDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Naoto KubotaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Naoki KobayashiDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Yoshiko Matsumoto IkushimaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Motoharu AwazawaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Ryotaro BouchiDiabetes and Metabolism Information Center, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Gotaro TodaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Tomoharu YamadaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Takuma NakatsukaDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-5727-5385
Ryosuke TateishiDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-3021-2517
Miwako KakiuchiGenome Science Division, The University of Tokyo, Tokyo, Japan.
Shogo YamamotoGenome Science Division, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-5564-2567
Kenji TatsunoGenome Science Division, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-3046-3941
Koji AtarashiDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0001-5422-0736
Wataru SudaRIKEN Center for Integrative Medical Sciences, Yokohama City, Kanagawa, Japan.
Kenya HondaDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0001-8937-9835
Hiroyuki AburataniGenome Science Division, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-0438-1544
Toshimasa YamauchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4827-6404
Mitsuhiro FujishiroDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-4074-1140
Tetsuo NodaDepartment of Cell Biology, Cancer Institute, Japanese Foundation of Cancer Research, Tokyo, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, The University of Tokyo, Tokyo, Japan.
Takashi KadowakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kohjiro UekiDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan. uekik@ri.ncgm.go.jp.ORCID http://orcid.org/0000-0003-1523-8102
National Center for Global Health and Medicine · JPThe University of Tokyo · JPUniversity of Tokyo Hospital · JPKeio University · JPJapanese Foundation For Cancer Research · JPJikei University School of Medicine · JPRIKEN Center for Integrative Medical Sciences · JPToranomon Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is known to increase the risk of nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). Here we treat male STAM (STelic Animal Model) mice, which develop diabetes, NASH and HCC associated with dysbiosis upon low-dose streptozotocin and high-fat diet (HFD), with insulin or phlorizin. Although both treatments ameliorate hyperglycemia and NASH, insulin treatment alone lead to suppression of HCC accompanied by improvement of dysbiosis and restoration of antimicrobial peptide production. There are some similarities in changes of microflora from insulin-treated patients comorbid with diabetes and NASH. Insulin treatment, however, fails to suppress HCC in the male STAM mice lacking insulin receptor specifically in intestinal epithelial cells (ieIRKO), which show dysbiosis and impaired gut barrier function. Furthermore, male ieIRKO mice are prone to develop HCC merely on HFD. These data suggest that impaired gut insulin signaling increases the risk of HCC, which can be countered by restoration of insulin action in diabetes.

Indexed as

Carcinoma, HepatocellularDiabetes Mellitus, ExperimentalLiver NeoplasmsNon-alcoholic Fatty Liver DiseaseAnimalsDiet, High-FatDisease Models, AnimalDysbiosisHumansInsulinLiverMaleMiceMice, Inbred C57BLInsulin

Identifiers

PMID37852976
PMCPMC10584811
OpenAlexW4387739308

What Socratic 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 Socratic graph.