Evidence map›Paper›PMID 28426713›Full record

ArticlePloS one2017

Metallothioneins regulate the adipogenic differentiation of 3T3-L1 cells via the insulin signaling pathway.

Yoshito Kadota, Yuriko Toriuchi, Yuka Aki, Yuto Mizuno, Takashige Kawakami, Tomoko Nakaya, Masao Sato, Shinya Suzuki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  6. Mapping the Single-Cell Differentiation Landscape of Osteosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
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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

8 authors at 1 institution in 1 country.

Yoshito KadotaFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.ORCID http://orcid.org/0000-0002-2721-4100
Yuriko ToriuchiFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Yuka AkiFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Yuto MizunoFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Takashige KawakamiFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Tomoko NakayaFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Masao SatoFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Shinya SuzukiFaculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan.
Tokushima Bunri University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Knockout of metallothionein (MT) genes contributes to a heavier body weight in early life and the potential to become obese through the intake of a high fat diet (HFD) in mice. It has thus been suggested that MT genes regulate the formation of adipose tissue, which would become the base for later HFD-induced obesity. We evaluated the fat pads of mice during the lactation stage. The fat mass and adipocyte size of MT1 and MT2 knockout mice were greater than those of wild type mice. Next, we assayed the ability of small interfering RNA (siRNA) to silence MT genes in the 3T3-L1 cell line. The expressions of MT1 and MT2 genes were transiently upregulated during adipocyte differentiation, and the siRNA pretreatment led to the suppression of the expression of both MT mRNAs and proteins. The MT siRNA promoted lipid accumulation in adipocytes and caused proliferation of post-confluent preadipocytes; these effects were suppressed by an inhibitor of phosphatidylinositol 3-kinase (LY294002). In addition, MT siRNA promoted insulin-stimulated phosphorylation of Akt, a downstream kinase of the insulin signaling pathway. Enhanced lipid accumulation in 3T3-L1 cells resulting from MT-gene silencing was inhibited by pretreatment with an antioxidant, N-acetylcysteine, used as a substitute for antioxidant protein MTs. These results suggest that interference in MT expression enhanced the activation of the insulin signaling pathway, resulting in higher lipid accumulation in 3T3-L1 adipocytes.

Indexed as

Signal Transduction3T3-L1 CellsAdipose TissueAnimalsCell DifferentiationCulture MediaInsulinMetallothioneinMiceMice, KnockoutCulture MediaInsulinMetallothionein

Identifiers

PMID28426713
PMCPMC5398611
OpenAlexW2606737908

What OpenQuestion holds

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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.