Evidence map›Paper›PMID 25100214›Full record

ArticleNature communications2014

Early-onset metabolic syndrome in mice lacking the intestinal uric acid transporter SLC2A9.

Brian J DeBosch, Oliver Kluth, Hideji Fujiwara, Annette Schürmann, Kelle Moley

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 186 citations in OpenAlex.

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  13. Acta pharmaceutica Sinica. B · 2025
    Article
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  15. Foods (Basel, Switzerland) · 2025
    Article
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45 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

5 authors at 1 institution in 1 country.

Brian J DeBoschBJC Institute of Health, Washington University School of Medicine, 10th Floor 425 S., Euclid Avenue Campus, Box 8064, St Louis, MO 63110, USA.
Oliver KluthDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal 14558, Germany.
Hideji FujiwaraBJC Institute of Health, Washington University School of Medicine, 10th Floor 425 S., Euclid Avenue Campus, Box 8064, St Louis, MO 63110, USA.
Annette SchürmannDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal 14558, Germany.
Kelle MoleyBJC Institute of Health, Washington University School of Medicine, 10th Floor 425 S., Euclid Avenue Campus, Box 8064, St Louis, MO 63110, USA.
German Institute of Human Nutrition · DE

Funding

Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
GLUTS AND GLUCOSE TRANSPORT IN THE MOUSE BLASTOCYSTR01HD040390 · NICHD · WASHINGTON UNIVERSITY · PI MOLEY, KELLE H · 2002 to 2012
$2.6M
NICHD NIH HHS 5K12HD000850-27NICHD NIH HHS K12 HD000850NICHD NIH HHS R01 HD040390NICHD NIH HHS R01HD040390-07NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK052574NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P30DK52574NIDDK NIH HHS P60 DK020579
6 · The paper itself

Abstract

Excess circulating uric acid, a product of hepatic glycolysis and purine metabolism, often accompanies metabolic syndrome. However, whether hyperuricaemia contributes to the development of metabolic syndrome or is merely a by-product of other processes that cause this disorder has not been resolved. In addition, how uric acid is cleared from the circulation is incompletely understood. Here we present a genetic model of spontaneous, early-onset metabolic syndrome in mice lacking the enterocyte urate transporter Glut9 (encoded by the SLC2A9 gene). Glut9-deficient mice develop impaired enterocyte uric acid transport kinetics, hyperuricaemia, hyperuricosuria, spontaneous hypertension, dyslipidaemia and elevated body fat. Allopurinol, a xanthine oxidase inhibitor, can reverse the hypertension and hypercholesterolaemia. These data provide evidence that hyperuricaemia per se could have deleterious metabolic sequelae. Moreover, these findings suggest that enterocytes may regulate whole-body metabolism, and that enterocyte urate metabolism could potentially be targeted to modulate or prevent metabolic syndrome.

Indexed as

AllopurinolAnimalsBody CompositionCalorimetryEchocardiographyEnterocytesGlucose Transport Proteins, FacilitativeHyperuricemiaMetabolic SyndromeMiceMice, Inbred C57BLMice, KnockoutUric AcidXanthine OxidaseAllopurinolGlucose Transport Proteins, FacilitativeSlc2a9 protein, mouseUric AcidXanthine Oxidase

Identifiers

PMID25100214
PMCPMC4348061
OpenAlexW2082748546

What OpenQuestion holds

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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.