Evidence map›Paper›PMID 34611611›Full record

ArticleiScience2021

Altered microbiota by a high-fat diet accelerates lethal myeloid hematopoiesis associated with systemic SOCS3 deficiency.

Kaori Cho, Takashi Ushiki, Hajime Ishiguro, Suguru Tamura, Masaya Araki, Tatsuya Suwabe, Takayuki Katagiri, Mari Watanabe, Yoko Fujimoto, Riuko Ohashi and 9 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  9. Anti-Inflammatory Effect of Ethanolic Extract fromMolecules (Basel, Switzerland) · 2023
    Article
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 7 institutions in 2 countries.

Kaori ChoDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Takashi UshikiDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Hajime IshiguroDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Suguru TamuraDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Masaya ArakiDepartment of Endocrinology and Metabolism, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Tatsuya SuwabeDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Takayuki KatagiriDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Mari WatanabeDepartment of Transfusion Medicine, Cell Therapy and Regenerative Medicine, Niigata University Medical and Dental Hospital, 1-754 Asahimachi-dori, Chuo-ku, Niigata, Niigata 951-8520, Japan.
Yoko FujimotoDepartment of Transfusion Medicine, Cell Therapy and Regenerative Medicine, Niigata University Medical and Dental Hospital, 1-754 Asahimachi-dori, Chuo-ku, Niigata, Niigata 951-8520, Japan.
Riuko OhashiHistopathology Core Facility, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Yoichi AjiokaHistopathology Core Facility, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Ippei ShimizuDepartment of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Shujiro OkudaDivision of Bioinformatics, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Niigata 951-8510, Japan.
Masayoshi MasukoDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Yoshimi NakagawaDivision of Complex Biosystem Research, Department of Research and Development, Institute of Natural Medicine, University of Toyama, Toyama, Toyama 930-0194, Japan.
Hideyo HiraiDepartment of Clinical Laboratory Medicine, Kyoto University Hospital, Kyoto, Kyoto 606-8507, Japan.
Warren S AlexanderBlood Cells and Blood Cancer Division, the Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia.
Hitoshi ShimanoDepartment of Endocrinology and Metabolism, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Hirohito SoneDepartment of Hematology, Endocrinology and Metabolism, Faculty of Medicine, Niigata University, Niigata, Niigata 951-8510, Japan.
Niigata University · JPNiigata University Medical and Dental Hospital · JPUniversity of Tsukuba · JPJuntendo University · JPThe University of Melbourne · AUTokyo University of Pharmacy and Life Sciences · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The suppressors of cytokine signaling (SOCS) proteins are negative regulators of cytokine signaling required to prevent excessive cellular responses. In particular, SOCS3 is involved in the regulation of metabolic syndromes, such as obesity and diabetes, by suppressing leptin and insulin signals. SOCS3 also suppresses the inflammatory response associated with metabolic stress, but this specific role remains undefined. Wild-type mice on a high-fat diet (HFD) exhibited only fatty liver, whereas systemic deletion of SOCS3 resulted in excessive myeloid hematopoiesis and hepatic inflammation. In addition, depletion of the gut microbiota resulted in considerable improvement in excess granulopoiesis and splenomegaly, halting the progression of systemic inflammation in SOCS3KO mice on the HFD. This result suggests that intestinal dysbiosis is involved in inflammation associated with SOCS3KO. Although contributing to diet-induced obesity and fatty liver, SOCS3 is nevertheless critical to suppress excess myeloid hematopoiesis and severe systemic inflammation associated with intestinal dysbiosis on HFD.

Indexed as

immunologymicrobiome

Identifiers

PMID34611611
PMCPMC8476681
OpenAlexW3199229216

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.