Evidence map›Paper›PMID 30369082›Full record

ArticleJournal of diabetes investigation2019

Nicotinic alpha-7 acetylcholine receptor deficiency exacerbates hepatic inflammation and fibrosis in a mouse model of non-alcoholic steatohepatitis.

Kumi Kimura, Yuka Inaba, Hitoshi Watanabe, Toshiya Matsukawa, Michihiro Matsumoto, Hiroshi Inoue

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  10. [Activation ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

6 authors at 2 institutions in 1 country.

Kumi KimuraMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.
Yuka InabaMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.ORCID http://orcid.org/0000-0001-9757-9669
Hitoshi WatanabeMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.
Toshiya MatsukawaDepartment of Molecular Metabolic Regulation, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Michihiro MatsumotoDepartment of Molecular Metabolic Regulation, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Hiroshi InoueMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Japan.
Kanazawa University · JPNational Center for Global Health and Medicine · JP

Funding

Japan Society for the Promotion of Science 15H05678Japan Society for the Promotion of Science 16K01815Japan Society for the Promotion of Science 17H05499Naito FoundationTakeda Science FoundationUehara Memorial Foundation
6 · The paper itself

Abstract

AIMS/

introductionNon-alcoholic steatohepatitis (NASH), which occurs in association with insulin resistance and hepatic fat accumulation, is characterized by chronic liver injury and fibrosis. NASH onset and progression is closely related to hepatic inflammation, which is partly regulated by the vagus nerve through the α7 nicotinic acetylcholine receptor (α7nAchR). Hepatic α7nAchR action is impeded in obesity and insulin resistance. In the present study, using α7nAchR knockout (α7KO) mice, we elucidated the effect of α7nAchR deficiency on NASH-related inflammation and fibrosis. MATERIALS AND

methodsα7KO mice were fed an atherogenic high-fat diet (AD) for 32 weeks or methionine/choline-deficient diet (MCD) for 6 weeks, both of which induce NASH. Mice were then examined for the degree of NASH-related inflammation and fibrosis by hepatic gene expression analysis and Sirius red histological staining.

resultsHepatic triglyceride accumulation and elevated plasma transaminase levels were observed in both AD and MCD mice, but the plasma transaminase level increase was higher in α7KO mice than in control mice. α7KO mice fed an AD showed significant upregulation of the Col1a1 gene encoding alpha-1 type I collagen, which is involved in liver fibrosis, and the Ccl2 gene encoding C-C motif chemokine ligand 2, a pro-inflammatory chemokine; α7KO mice fed an MCD had significant upregulation of the Col1a1 gene and the Tnf gene, an inflammatory cytokine. Histological analysis showed that AD and MCD exacerbated liver fibrosis in α7KO mice.

conclusionsThe results of this study suggest that α7nAchR deficiency exacerbates hepatic inflammation and fibrosis in a diet-induced mouse model of NASH.

Indexed as

Disease Models, AnimalAnimalsCholine DeficiencyCollagen Type ICollagen Type I, alpha 1 ChainCytokinesDiet, High-FatInflammationLiver CirrhosisMaleMethionineMiceMice, Inbred C57BLMice, KnockoutNon-alcoholic Fatty Liver DiseaseReceptors, NicotinicCollagen Type ICollagen Type I, alpha 1 ChainCytokinesMethionineReceptors, NicotinicFibrosisInflammationNon-alcoholic steatohepatitis

Identifiers

PMID30369082
PMCPMC6497582
OpenAlexW2898375925

What OpenQuestion holds

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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.