Evidence map›Paper›PMID 23303409›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Synergistic effect of uricase blockade plus physiological amounts of fructose-glucose on glomerular hypertension and oxidative stress in rats.

Edilia Tapia, Magdalena Cristóbal, Fernando E García-Arroyo, Virgilia Soto, Fabiola Monroy-Sánchez, Ursino Pacheco, Miguel A Lanaspa, Carlos A Roncal-Jiménez, David Cruz-Robles, Takuji Ishimoto and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The fructose survival hypothesis for obesity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  5. Review
  6. Review
  7. Do thrifty genes exist? Revisiting uricase.Obesity (Silver Spring, Md.) · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Fructose metabolism and metabolic disease.The Journal of clinical investigation · 2018
    Review
  19. Article
  20. Article
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

13 authors at 2 institutions in 2 countries.

Edilia TapiaLaboratory of Renal Physiopathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Magdalena Cristóbal
Fernando E García-Arroyo
Virgilia Soto
Fabiola Monroy-Sánchez
Ursino Pacheco
Miguel A Lanaspa
Carlos A Roncal-Jiménez
David Cruz-Robles
Takuji Ishimoto
Magdalena Madero
Richard J Johnson
Laura-Gabriela Sánchez-Lozada
Instituto Nacional de Cardiología · MXUniversity of Colorado Denver · 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-068607-10
6 · The paper itself

Abstract

Fructose in sweetened beverages (SB) increases the risk for metabolic and cardiorenal disorders, and these effects are in part mediated by a secondary increment in uric acid (UA). Rodents have an active uricase, thus requiring large doses of fructose to increase plasma UA and to induce metabolic syndrome and renal hemodynamic changes. We therefore hypothesized that the effects of fructose in rats might be enhanced in the setting of uricase inhibition. Four groups of male Sprague-Dawley rats (n = 7/group) were studied during 8 wk: water + vehicle (V), water + oxonic acid (OA; 750 mg/k BW), sweetened beverage (SB; 11% fructose-glucose combination) + V, and SB + OA. Systemic blood pressure, plasma UA, triglycerides (TG), glucose and insulin, glomerular hemodynamics, renal structural damage, renal cortex and liver UA, TG, markers of oxidative stress, mitDNA, fructokinase, and fatty liver synthase protein expressions were evaluated at the end of the experiment. Chronic hyperuricemia and SB induced features of the metabolic syndrome, including hypertension, hyperuricemia, hyperglycemia, and systemic and hepatic TG accumulation. OA alone also induced glomerular hypertension, and SB alone induced insulin resistance. SB + OA induced a combined phenotype including metabolic and renal alterations induced by SB or OA alone and in addition also acted synergistically on systemic and glomerular pressure, plasma glucose, hepatic TG, and oxidative stress. These findings explain why high concentrations of fructose are required to induce greater metabolic changes and renal disease in rats whereas humans, who lack uricase, appear to be much more sensitive to the effects of fructose.

Indexed as

AnimalsBeveragesFatty LiverFructokinasesFructoseGlucoseHypertrophyHyperuricemiaInsulin ResistanceKidneyKidney DiseasesLiverMaleMetabolic SyndromeOxidative StressOxonic AcidFructokinasesFructoseGlucoseketohexokinaseOxonic AcidUrate OxidaseUric Acid

Identifiers

PMID23303409
PMCPMC3602695
OpenAlexW2126764959

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.