Evidence map›Paper›PMID 29364977›Full record

ArticlePloS one2018

Identification of microRNA that represses IRS-1 expression in liver.

Kaoru Ono, Motoyuki Igata, Tatsuya Kondo, Sayaka Kitano, Yuki Takaki, Satoko Hanatani, Masaji Sakaguchi, Rieko Goto, Takafumi Senokuchi, Junji Kawashima and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

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  19. Adipocyte-Specific Inhibition ofFrontiers in endocrinology · 2021
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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.

Kaoru OnoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Motoyuki IgataDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Tatsuya KondoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Sayaka KitanoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yuki TakakiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Satoko HanataniDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Masaji SakaguchiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Rieko GotoDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Takafumi SenokuchiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Junji KawashimaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Noboru FurukawaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Hiroyuki MotoshimaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Eiichi ArakiDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-4064-7525
Kumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are short, non-coding RNAs that post-transcriptionally regulate gene expression and have been shown to participate in almost every cellular process. Several miRNAs have recently been implicated in glucose metabolism, but the roles of miRNAs in insulin-resistant conditions, such as obesity or type 2 diabetes, are largely unknown. Herein, we focused on miR-222, the expression of which was increased in the livers of high fat/high sucrose diet-fed mice injected with gold thioglucose (G+HFHSD). Overexpression of miR-222 in primary mouse hepatocytes attenuated Akt phosphorylation induced by insulin, indicating that miR-222 negatively regulates insulin signaling. As per in silico analysis, miR-222 potentially binds to the 3' untranslated region (3' UTR) of the IRS-1 gene, a key insulin signaling molecule. In fact, IRS-1 protein expression was decreased in the livers of G+HFHSD-fed mice. We further confirmed a direct interaction between miR-222 and the 3' UTR of IRS-1 via luciferase assays. Our findings suggest that up-regulation of miR-222 followed by reduction in IRS-1 expression may be a viable mechanism of insulin resistance in the liver.

Indexed as

3' Untranslated RegionsAnimalsGluconeogenesisInsulinInsulin Receptor Substrate ProteinsLiverMaleMiceMice, Inbred C57BLMicroRNAsPhosphorylationProto-Oncogene Proteins c-akt3' Untranslated RegionsInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseMicroRNAsMIRN222 microRNA, mouseProto-Oncogene Proteins c-akt

Identifiers

PMID29364977
PMCPMC5783395
OpenAlexW2789243384

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.