Evidence map›Paper›PMID 19151107›Full record

ReviewEndocrine reviews2009

Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?

Richard J Johnson, Santos E Perez-Pozo, Yuri Y Sautin, Jacek Manitius, Laura Gabriela Sanchez-Lozada, Daniel I Feig, Mohamed Shafiu, Mark Segal, Richard J Glassock, Michiko Shimada and 2 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed, 6 pooled it
21.8field-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

212 citing papers in PubMed, 6 syntheses or guidelines pooled it, 497 citations in OpenAlex.

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  17. New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026
    Review
  18. Conformational changes in ketohexokinase are conserved across isozymes and species.Acta crystallographica. Section F, Structural biology communications · 2025
    Article
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  20. Article

152 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 4 institutions in 4 countries.

Richard J JohnsonDivision of Nephrology, Hypertension and Transplantation, University of Florida, P.O. Box 100224, Gainesville, Florida 32620-0224, USA. johnsrj@medicine.ufl.edu
Santos E Perez-Pozo
Yuri Y Sautin
Jacek Manitius
Laura Gabriela Sanchez-Lozada
Daniel I Feig
Mohamed Shafiu
Mark Segal
Richard J Glassock
Michiko Shimada
Carlos Roncal
Takahiko Nakagawa
University of Florida · USBaylor College of Medicine · USHospital General Mateu Orfila · ESUniversity of Bydgoszcz · PL

Funding

Role of Uric Acid in Hypertension and Renal DiseaseR01HL068607 · NHLBI · UNIVERSITY OF FLORIDA · PI JOHNSON, RICHARD JOSEPH · 2002 to 2011
$3.5M
GLOMERULAR ENDOTHELIAL CELL &HEMOLYTIC UREMIC SYNDROMER01DK052121 · NIDDK · UNIVERSITY OF WASHINGTON · PI JOHNSON, RICHARD JOSEPH · 1996 to 2009
$3.3M
NHLBI NIH HHS HL-68607NHLBI NIH HHS R01 HL068607NIDDK NIH HHS DK-52121NIDDK NIH HHS R01 DK052121
6 · The paper itself

Abstract

We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there are now extensive experimental and clinical data supporting uric acid in the pathogenesis of metabolic syndrome. Fourth, environmental and genetic considerations provide a potential explanation of why certain groups might be more susceptible to developing diabetes. Finally, we discuss the counterarguments associated with the hypothesis and a potential explanation for these findings. If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace.

Indexed as

AnimalsDiabetes Mellitus, Type 2Dietary SucroseFructoseHumansMetabolic SyndromeSweetening AgentsUric AcidDietary SucroseFructoseSweetening AgentsUric Acid

Identifiers

PMID19151107
PMCPMC2647706
OpenAlexW1973931485

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.