Evidence map›Paper›PMID 21346177›Full record

ArticleDiabetes2011

Hyperuricemia as a mediator of the proinflammatory endocrine imbalance in the adipose tissue in a murine model of the metabolic syndrome.

William Baldwin, Steven McRae, George Marek, David Wymer, Varinderpal Pannu, Chris Baylis, Richard J Johnson, Yuri Y Sautin

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed, 5 pooled it
13.9field-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

230 citing papers in PubMed, 5 syntheses or guidelines pooled it, 441 citations in OpenAlex.

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170 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

8 authors at 1 institution in 1 country.

William BaldwinDepartment of Medicine, University of Florida, Gainesville, Florida, USA.
Steven McRae
George Marek
David Wymer
Varinderpal Pannu
Chris Baylis
Richard J Johnson
Yuri Y Sautin
University of Florida · US

Funding

Role of Uric Acid in Hypertension and Renal DiseaseR01HL068607 · NHLBI · UNIVERSITY OF FLORIDA · PI JOHNSON, RICHARD JOSEPH · 2002 to 2011
$3.5M
NHLBI NIH HHS HL-68607NHLBI NIH HHS R01 HL068607
6 · The paper itself

Abstract

objectiveHyperuricemia is strongly associated with obesity and metabolic syndrome and can predict visceral obesity and insulin resistance. Previously, we showed that soluble uric acid directly stimulated the redox-dependent proinflammatory signaling in adipocytes. In this study we demonstrate the role of hyperuricemia in the production of key adipokines. RESEARCH DESIGN AND

methodsWe used mouse 3T3-L1 adipocytes, human primary adipocytes, and a mouse model of metabolic syndrome and hyperuricemia.

resultsUric acid induced in vitro an increase in the production (mRNA and secreted protein) of monocyte chemotactic protein-1 (MCP-1), an adipokine playing an essential role in inducing the proinflammatory state in adipocytes in obesity. In addition, uric acid caused a decrease in the production of adiponectin, an adipocyte-specific insulin sensitizer and anti-inflammatory agent. Uric acid-induced increase in MCP-1 production was blocked by scavenging superoxide or by inhibiting NADPH oxidase and by stimulating peroxisome-proliferator-activated receptor-γ with rosiglitazone. Downregulation of the adiponectin production was prevented by rosiglitazone but not by antioxidants. In obese mice with metabolic syndrome, we observed hyperuricemia. Lowering uric acid in these mice by inhibiting xanthine oxidoreductase with allopurinol could improve the proinflammatory endocrine imbalance in the adipose tissue by reducing production of MCP-1 and increasing production of adiponectin. In addition, lowering uric acid in obese mice decreased macrophage infiltration in the adipose tissue and reduced insulin resistance.

conclusionsHyperuricemia might be partially responsible for the proinflammatory endocrine imbalance in the adipose tissue, which is an underlying mechanism of the low-grade inflammation and insulin resistance in subjects with the metabolic syndrome.

Indexed as

3T3-L1 CellsAdipocytesAdiponectinAdipose TissueAnimalsCells, CulturedChemokine CCL2HumansHyperuricemiaImmunohistochemistryMetabolic SyndromeMiceMice, ObeseReverse Transcriptase Polymerase Chain ReactionThiobarbituratesUric AcidAdiponectinChemokine CCL2Thiobarbituratesthiobarbituric acidUric Acid

Identifiers

PMID21346177
PMCPMC3064099
OpenAlexW2142436219

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.