Evidence map›Paper›PMID 18487450›Full record

ArticleDiabetes2008

Impact of oxidative stress and peroxisome proliferator-activated receptor gamma coactivator-1alpha in hepatic insulin resistance.

Naoki Kumashiro, Yoshifumi Tamura, Toyoyoshi Uchida, Takeshi Ogihara, Yoshio Fujitani, Takahisa Hirose, Hideki Mochizuki, Ryuzo Kawamori, Hirotaka Watada

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
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  6. DPP4 Activity, Hyperinsulinemia, and Atherosclerosis.The Journal of clinical endocrinology and metabolism · 2021
    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

9 authors at 1 institution in 1 country.

Naoki KumashiroDepartment of Medicine, Metabolism, and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan.
Yoshifumi Tamura
Toyoyoshi Uchida
Takeshi Ogihara
Yoshio Fujitani
Takahisa Hirose
Hideki Mochizuki
Ryuzo Kawamori
Hirotaka Watada
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecent studies identified accumulation of reactive oxygen species (ROS) as a common pathway causing insulin resistance. However, whether and how the reduction of ROS levels improves insulin resistance remains to be elucidated. The present study was designed to define this mechanism. RESEARCH DESIGN AND

methodsWe investigated the effect of overexpression of superoxide dismutase (SOD)1 in liver of obese diabetic model (db/db) mice by adenoviral injection.

resultsdb/db mice had high ROS levels in liver. Overexpression of SOD1 in liver of db/db mice reduced hepatic ROS and blood glucose level. These changes were accompanied by improvement in insulin resistance and reduction of hepatic gene expression of phosphoenol-pyruvate carboxykinase and peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha), which is the main regulator of gluconeogenic genes. The inhibition of hepatic insulin resistance was accompanied by attenuation of phosphorylation of cAMP-responsive element-binding protein (CREB), which is a main regulator of PGC-1alpha expression, and attenuation of Jun NH(2)-terminal kinase (JNK) phosphorylation. Simultaneously, overexpression of SOD1 in db/db mice enhanced the inactivation of forkhead box class O1, another regulator of PGC-1alpha expression, without the changes of insulin-induced Akt phosphorylation in liver. In hepatocyte cell lines, ROS induced phosphorylation of JNK and CREB, and the latter, together with PGC-1alpha expression, was inhibited by a JNK inhibitor.

conclusionsOur results indicate that the reduction of ROS is a potential therapeutic target of liver insulin resistance, at least partly by the reduced expression of PGC-1alpha.

Indexed as

AdenoviridaeAnimalsBlotting, WesternCell Line, TumorFemaleForkhead Box Protein O1Forkhead Transcription FactorsGenetic VectorsGlucose IntoleranceHumansImmunoprecipitationInsulinInsulin ResistanceLiverMiceOxidative StressForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseInsulinperoxisome-proliferator-activated receptor-gamma coactivator-1Reactive Oxygen SpeciesSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Transcription Factors

Identifiers

PMID18487450
PMCPMC2494675
OpenAlexW2122815043

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.