Evidence map›Paper›PMID 18640390›Full record

ArticleMetabolism: clinical and experimental2008

Proteomic analysis of fructose-induced fatty liver in hamsters.

Lihe Zhang, German Perdomo, Dae Hyun Kim, Shen Qu, Steven Ringquist, Massimo Trucco, H Henry Dong

Open access · greenAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.2field-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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
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  10. Review
  11. Article
  12. Article
  13. Article
  14. High Fat Diet-Induced Changes in Hepatic Protein Abundance in Mice.Journal of proteomics & bioinformatics · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. FoxO1 integrates insulin signaling to VLDL production.Cell cycle (Georgetown, Tex.) · 2008
    Review
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.

Lihe ZhangDivision of Immunogenetics, Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Rangos Research Center, Pittsburgh, PA 15213, USA.
German Perdomo
Dae Hyun Kim
Shen Qu
Steven Ringquist
Massimo Trucco
H Henry Dong
University of Pittsburgh · USChildren's Hospital of Pittsburgh · US

Funding

Humoral And Cellular Tolerization Approaches Against AutoimmunityU19AI056374 · NIAID · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI TRUCCO, MASSIMO M. · 2003 to 2007
$3.3M
Foxo1 in Triglyceride MetabolismR01DK066301 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DONG, HENGJIANG HENRY · 2006 to 2010
$1.3M
NIAID NIH HHS U19 AI056374NIAID NIH HHS U19-AI056374-01NIDDK NIH HHS DK066301NIDDK NIH HHS R01 DK066301
6 · The paper itself

Abstract

High fructose consumption is associated with the development of fatty liver and dyslipidemia with poorly understood mechanisms. We used a matrix-assisted laser desorption/ionization-based proteomics approach to define the molecular events that link high fructose consumption to fatty liver in hamsters. Hamsters fed high-fructose diet for 8 weeks, as opposed to regular-chow-fed controls, developed hyperinsulinemia and hyperlipidemia. High-fructose-fed hamsters exhibited fat accumulation in liver. Hamsters were killed, and liver tissues were subjected to matrix-assisted laser desorption/ionization-based proteomics. This approach identified a number of proteins whose expression levels were altered by >2-fold in response to high fructose feeding. These proteins fall into 5 different categories including (1) functions in fatty acid metabolism such as fatty acid binding protein and carbamoyl-phosphate synthase; (2) proteins in cholesterol and triglyceride metabolism such as apolipoprotein A-1 and protein disulfide isomerase; (3) molecular chaperones such as GroEL, peroxiredoxin 2, and heat shock protein 70, whose functions are important for protein folding and antioxidation; (4) enzymes in fructose catabolism such as fructose-1,6-bisphosphatase and glycerol kinase; and (5) proteins with housekeeping functions such as albumin. These data provide insight into the molecular basis linking fructose-induced metabolic shift to the development of metabolic syndrome characterized by hepatic steatosis and dyslipidemia.

Indexed as

AnimalsApolipoprotein A-ICarbamoyl-Phosphate Synthase (Ammonia)Chaperonin 60CricetinaeDietary CarbohydratesFatty Acid-Binding ProteinsFatty LiverFructoseFructose-BisphosphataseGlucose Tolerance TestGlycerol KinaseHistocytochemistryHSP70 Heat-Shock ProteinsHyperinsulinismHyperlipidemiasApolipoprotein A-ICarbamoyl-Phosphate Synthase (Ammonia)Chaperonin 60Dietary CarbohydratesFatty Acid-Binding ProteinsFructoseFructose-BisphosphataseGlycerol KinaseHSP70 Heat-Shock ProteinsPeroxiredoxinsProtein Disulfide-Isomerases

Identifiers

PMID18640390
PMCPMC2553352
OpenAlexW2002437472

What OpenQuestion holds

Textmetadata
LicenceTDM
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.