Evidence map›Paper›PMID 29713651›Full record

ArticleJournal of diabetes research2018

Novel Mechanisms Modulating Palmitate-Induced Inflammatory Factors in Hypertrophied 3T3-L1 Adipocytes by AMPK.

Naru Morita, Toshio Hosaka, Atsuko Kitahara, Toshitaka Murashima, Hirohisa Onuma, Yoshikazu Sumitani, Kazuto Takahashi, Toshiaki Tanaka, Takuma Kondo, Hitoshi Ishida

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 14 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

10 authors at 1 institution in 1 country.

Naru MoritaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.ORCID 0000-0003-2942-8441
Toshio HosakaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Atsuko KitaharaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Toshitaka MurashimaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Hirohisa OnumaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Yoshikazu SumitaniThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Kazuto TakahashiThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.ORCID 0000-0002-6887-1481
Toshiaki TanakaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Takuma KondoThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.
Hitoshi IshidaThird Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, Kyorin University School of Medicine, Tokyo, Japan.ORCID 0000-0001-6603-6709
Kyorin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveA growing body of evidence indicates that AMP-activated protein kinase (AMPK) contributes to not only energy metabolic homeostasis but also the inhibition of inflammatory responses. However, the underlying mechanisms remain unclear. To elucidate the role of AMPK, in this study, we observed the effects of AMPK activation on monocyte chemoattractant protein-1 (MCP-1) release in mature 3T3-L1 adipocytes.

methodsWe observed signal transduction pathways regulating MCP-1, which increased in obese adipocytes, in an

resultsPalmitate-preloaded cells exhibited significant increase in MCP-1 release and triglyceride (TG) deposition. Increased MCP-1 release and TG deposition were significantly decreased by an AMPK activator. In addition, the AMPK activator not only markedly diminished MCP-1 secretion but also augmented phosphorylation of nuclear factor-

conclusionsMCP-1 release from hypertrophied adipocytes is suppressed by AMPK activation through the NF-

Indexed as

3T3-L1 CellsAdenylate KinaseAdipocytesAminoimidazole CarboxamideAnimalsChemokine CCL2InflammationMetforminMiceNF-kappa BPalmitic AcidPhosphorylationRibonucleotidesSignal TransductionTriglyceridesAdenylate KinaseAICA ribonucleotideAminoimidazole CarboxamideChemokine CCL2MetforminNF-kappa BPalmitic AcidRibonucleotidesTriglycerides

Identifiers

PMID29713651
PMCPMC5866861
OpenAlexW2790345449

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.