Evidence map›Paper›PMID 19805130›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Insulin resistance is a cellular antioxidant defense mechanism.

Kyle L Hoehn, Adam B Salmon, Cordula Hohnen-Behrens, Nigel Turner, Andrew J Hoy, Ghassan J Maghzal, Roland Stocker, Holly Van Remmen, Edward W Kraegen, Greg J Cooney and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers.

0numbers the graph read from it
0cells of the map it votes in
271citing papers in PubMed
18.9field-weighted citation impact, top 1% 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

271 citing papers in PubMed, 526 citations in OpenAlex.

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  9. Time- and Region-Specific Effects of Intranasal Insulin on Oxidative Stress Parameters in the Rat Brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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211 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Kyle L HoehnDiabetes and Obesity Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia. klh8st@virginia.edu
Adam B Salmon
Cordula Hohnen-Behrens
Nigel Turner
Andrew J Hoy
Ghassan J Maghzal
Roland Stocker
Holly Van Remmen
Edward W Kraegen
Greg J Cooney
Arlan R Richardson
David E James
Garvan Institute of Medical Research · AUThe University of Texas Health Science Center at San Antonio · USUniversity of Sydney · AU

Funding

TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
AMPK, SIRT1 and mTOR:Mediators of Nutrient ExcessR01DK067509 · NIDDK · BOSTON MEDICAL CENTER · PI RUDERMAN, NEIL B · 2006 to 2014
$2.7M
The Role of c-Cbl in Energy HomeostasisF32DK075249 · NIDDK · GARVAN INSTITUTE OF MEDICAL RESEARCH · PI HOEHN, KYLE LEE · 2006 to 2008
$140k
NIA NIH HHS T32 AG021890NIDDK NIH HHS DK067509NIDDK NIH HHS F32 DK075249NIDDK NIH HHS R01 DK067509PHS HHS R378G26557
6 · The paper itself

Abstract

We know a great deal about the cellular response to starvation via AMPK, but less is known about the reaction to nutrient excess. Insulin resistance may be an appropriate response to nutrient excess, but the cellular sensors that link these parameters remain poorly defined. In the present study we provide evidence that mitochondrial superoxide production is a common feature of many different models of insulin resistance in adipocytes, myotubes, and mice. In particular, insulin resistance was rapidly reversible upon exposure to agents that act as mitochondrial uncouplers, ETC inhibitors, or mitochondrial superoxide dismutase (MnSOD) mimetics. Similar effects were observed with overexpression of mitochondrial MnSOD. Furthermore, acute induction of mitochondrial superoxide production using the complex III antagonist antimycin A caused rapid attenuation of insulin action independently of changes in the canonical PI3K/Akt pathway. These results were validated in vivo in that MnSOD transgenic mice were partially protected against HFD induced insulin resistance and MnSOD+/- mice were glucose intolerant on a standard chow diet. These data place mitochondrial superoxide at the nexus between intracellular metabolism and the control of insulin action potentially defining this as a metabolic sensor of energy excess.

Indexed as

3T3-L1 CellsAdipocytesAnimalsAntimycin AAntioxidantsCell LineInsulin ResistanceMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaModels, BiologicalMuscle Fibers, SkeletalReactive Oxygen SpeciesRecombinant ProteinsAntimycin AAntioxidantsReactive Oxygen SpeciesRecombinant ProteinsSuperoxide DismutaseSuperoxides

Identifiers

PMID19805130
PMCPMC2764908
OpenAlexW2112672163

What OpenQuestion holds

Textmetadata
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.