Evidence map›Paper›PMID 33498326›Full record

ArticleCells2021

Role of Chitinase 3-Like 1 Protein in the Pathogenesis of Hepatic Insulin Resistance in Nonalcoholic Fatty Liver Disease.

Songhua Zhang, Aryanna Sousa, Mengqui Lin, Ayako Iwano, Rishubh Jain, Bing Ma, Chang Min Lee, Jin Wook Park, Suchitra Kamle, Rolf Carlson and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 23 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

13 authors at 1 institution in 1 country.

Songhua ZhangLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Aryanna SousaLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.ORCID 0000-0002-9169-476X
Mengqui LinLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Ayako IwanoLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Rishubh JainLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Bing MaDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Chang Min LeeDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Jin Wook ParkDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Suchitra KamleDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Rolf CarlsonLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Ghun Geun LeeDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Jack A EliasDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
Jack R WandsLiver Research Center, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Brown University · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
NIH HHS P01 HL114501
6 · The paper itself

Abstract

A recently discovered human glycoprotein, chitinase 3-like 1 (Chi3L1), may play a role in inflammation, tissue remodeling, and visceral fat accumulation. We hypothesize that Chi3L1 gene expression is important in the development of hepatic insulin resistance characterized by the generation of pAKT, pGSK, and pERK in wild type and Chi3L1 knockout (KO) murine liver following insulin stimulation. The Chi3L1 gene and protein expression was evaluated by Real Time PCR and ELISA; lipid accumulation in hepatocytes was also assessed. To alter Chi3L1 function, three different anti-Chi3L1 monoclonal antibodies (mAbs) were administered in vivo and effects on the insulin signaling cascade and hepatic lipid deposition were determined. Transmission of the hepatic insulin signal was substantially improved following KO of the CHi3L1 gene and there was reduced lipid deposition produced by a HFD. The HFD-fed mice exhibited increased Chi3L1 expression in the liver and there was impaired insulin signal transduction. All three anti-Chi3L1 mAbs partially restored hepatic insulin sensitivity which was associated with reduced lipid accumulation in hepatocytes as well. A KO of the Chi3L1 gene reduced lipid accumulation and improved insulin signaling. Therefore, Chi3L1 gene upregulation may be an important factor in the generation of NAFLD/NASH phenotype.

Indexed as

Insulin ResistanceAnimalsAntibodies, MonoclonalBiopsyChitinase-3-Like Protein 1Diet, High-FatFeeding BehaviorInsulinLiverMiceMice, Inbred C57BLMice, KnockoutNon-alcoholic Fatty Liver DiseaseSignal TransductionAntibodies, MonoclonalChil1 protein, mouseChitinase-3-Like Protein 1Insulinanti-Chi3L1 monoclonal antibodyChi3L1hepatic insulin resistancenonalcoholic steatosis (NASH)

Identifiers

PMID33498326
PMCPMC7909438
OpenAlexW3122998252

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.