Evidence map›Paper›PMID 24358263›Full record

ArticlePloS one2013

Transcriptional regulation of an insulin-sensitizing adipokine adipolin/CTRP12 in adipocytes by Krüppel-like factor 15.

Takashi Enomoto, Koji Ohashi, Rei Shibata, Takahiro Kambara, Yusuke Uemura, Daisuke Yuasa, Yoshiyuki Kataoka, Megumi Miyabe, Kazuhiro Matsuo, Yusuke Joki and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Adipocytokines in Cardiovascular and Metabolic Diseases.Journal of atherosclerosis and thrombosis · 2016
    Review
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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

15 authors at 1 institution in 1 country.

Takashi EnomotoDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Koji OhashiDepartment of Molecular Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Rei ShibataDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takahiro KambaraDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yusuke UemuraDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Daisuke YuasaDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yoshiyuki KataokaDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Megumi MiyabeDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kazuhiro MatsuoDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yusuke JokiDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Satoko HayakawaDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Mizuho Hiramatsu-ItoDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masanori ItoDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Toyoaki MuroharaDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Noriyuki OuchiDepartment of Molecular Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obese states characterized by chronic inflammation are closely linked to the development of metabolic dysfunction. We identified adipolin/CTRP12 as an insulin-sensitizing and anti-inflammatory adipokine. Although obese conditions down-regulate adipolin expression, its molecular mechanism is largely unknown. Here we show that the transcriptional regulator Krüppel-like factor (KLF) 15 is involved in the regulation of adipolin expression in adipocytes. White adipose tissue from diet-induced obese (DIO) mice showed decreased expression of KLF9 and KLF15 among several KLFs, which was accompanied by reduced expression of adipolin. In cultured 3T3L1 adipocytes, treatment with TNFα significantly reduced the mRNA levels of KLF9, KLF15 and adipolin. Adenovirus-mediated overexpression of KLF15 but not KLF9 reversed TNFα-induced reduction of adipolin expression in adipocytes. Conversely, gene targeting ablation of KLF15 attenuated adipolin expression in adipocytes. Expression of KLF15 but not KLF9 enhanced the promoter activity of adipolin in HEK293 cells. Pretreatment of 3T3L1 adipocytes with the JNK inhibitor SP600125, but not p38 MAPK inhibitor SB203580 blocked the inhibitory effects of TNFα on adipolin and KLF15 expression. These data suggest that adipose inflammation under conditions of obesity suppresses adipolin expression via JNK-dependent down-regulation of KLF15 in adipocytes.

Indexed as

Gene Expression Regulation3T3-L1 CellsAdipocytesAdipokinesAnimalsDNA-Binding ProteinsHEK293 CellsHumansKruppel-Like Transcription FactorsMiceMice, Inbred C57BLObesityTranscription FactorsTranscription, GeneticTumor Necrosis Factor-alphaAdipokinesC1qtnf12 protein, mouseDNA-Binding ProteinsKlf15 protein, mouseKruppel-Like Transcription FactorsTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID24358263
PMCPMC3865152
OpenAlexW2035424677

What Socratic 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 Socratic graph.