Evidence map›Paper›PMID 20699433›Full record

Trial reportDiabetes care2010

Insulin suppresses endotoxin-induced oxidative, nitrosative, and inflammatory stress in humans.

Paresh Dandona, Husam Ghanim, Arindam Bandyopadhyay, Kelly Korzeniewski, Chang Ling Sia, Sandeep Dhindsa, Ajay Chaudhuri

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Diabetes care, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Chicken Primordial Germ Cells Do Not Proliferate in Insulin-Lacking Media.International journal of molecular sciences · 2025
    Article
  7. Article
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  12. Observational
  13. Article
  14. Review
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  18. 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

7 authors at 2 institutions in 1 country.

Paresh DandonaDivision of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo and Kaleida Health, Buffalo, New York, USA. pdandona@kaleidahealth.org
Husam Ghanim
Arindam Bandyopadhyay
Kelly Korzeniewski
Chang Ling Sia
Sandeep Dhindsa
Ajay Chaudhuri
Kaleida Health · USUniversity at Buffalo, State University of New York · US

Funding

Testosterone effects on insulin sensitivity & inflammation in T2DM and obesityR01DK075877 · NIDDK · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI DANDONA, PARESH · 2009 to 2012
$2.3M
Inflammation in obesity: Modulation by Weight LossR01DK069805 · NIDDK · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI DANDONA, PARESH · 2005 to 2009
$1.5M
NIDDK NIH HHS R01 DK069805NIDDK NIH HHS R01-DK-069805NIDDK NIH HHS R01 DK075877NIDDK NIH HHS R01-DK-075877
6 · The paper itself

Abstract

objectiveTo investigate whether insulin reduces the magnitude of oxidative, nitrosative, and inflammatory stress and tissue damage responses induced by endotoxin (lipopolysaccharide [LPS]). RESEARCH DESIGN AND

methodsNine normal subjects were injected intravenously with 2 ng/kg LPS prepared from Escherichia coli. Ten others were infused with insulin (2 units/h) for 6 h in addition to the LPS injection along with 100 ml/h of 5% dextrose to maintain normoglycemia.

resultsLPS injection induced a rapid increase in plasma concentrations of nitric oxide metabolites, nitrite and nitrate (NOM), and thiobarbituric acid-reacting substances (TBARS), an increase in reactive oxygen species (ROS) generation by polymorphonuclear leukocytes (PMNLs), and marked increases in plasma free fatty acids, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), macrophage migration inhibition factor (MIF), C-reactive protein, resistin, visfatin, lipopolysaccharide binding protein (LBP), high mobility group-B1 (HMG-B1), and myoglobin concentrations. The coinfusion of insulin led to a total elimination of the increase in NOM, free fatty acids, and TBARS and a significant reduction in ROS generation by PMNLs and plasma MIF, visfatin, and myoglobin concentrations. Insulin did not affect TNF-α, MCP-1, IL-6, LBP, resistin, and HMG-B1 increases induced by the LPS.

conclusionsInsulin reduces significantly several key mediators of oxidative, nitrosative, and inflammatory stress and tissue damage induced by LPS. These effects of insulin require further investigation for its potential use as anti-inflammatory therapy for endotoxemia.

Indexed as

Acute-Phase ProteinsCarrier ProteinsChemokine CCL2C-Reactive ProteinEndotoxinsHumansInjections, IntravenousInsulinInterleukin-6Lipopolysaccharide-Binding ProteinMacrophage Migration-Inhibitory FactorsMembrane GlycoproteinsMyoglobinNicotinamide PhosphoribosyltransferaseNitratesNitric AcidAcute-Phase ProteinsCarrier ProteinsChemokine CCL2C-Reactive ProteinEndotoxinsInsulinInterleukin-6Lipopolysaccharide-Binding ProteinMacrophage Migration-Inhibitory FactorsMembrane GlycoproteinsMyoglobinNicotinamide PhosphoribosyltransferaseNitratesNitric AcidNitritesReactive Oxygen SpeciesThiobarbituric Acid Reactive Substances

Identifiers

PMID20699433
PMCPMC2963505
OpenAlexW2134525099

What OpenQuestion holds

Textmetadata
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.