Evidence map›Paper›PMID 18509206›Full record

Trial reportDiabetes care2008

Dose-dependent effect of rosuvastatin on VLDL-apolipoprotein C-III kinetics in the metabolic syndrome.

Esther M M Ooi, Gerald F Watts, Dick C Chan, Meifania M Chen, Paul J Nestel, Dmitri Sviridov, P Hugh R Barrett

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Diabetes care, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Metabolism of Triglyceride-Rich Lipoproteins.Handbook of experimental pharmacology · 2022
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Targeting ApoC-III to Reduce Coronary Disease Risk.Current atherosclerosis reports · 2016
    Review
  14. The metabolic vascular syndrome - guide to an individualized treatment.Reviews in endocrine & metabolic disorders · 2016
    Review
  15. Article
  16. 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

7 authors at 3 institutions in 1 country.

Esther M M OoiMetabolic Research Centre, School of Medicine and Pharmacology, Royal Perth Hospital, Universityof Western Australia, Perth, Western Australia.
Gerald F Watts
Dick C Chan
Meifania M Chen
Paul J Nestel
Dmitri Sviridov
P Hugh R Barrett
University of Western Australia · AUThe Heart Research Institute · AURoyal Perth Hospital · AU

Funding

Resource Facility for Population KineticsP41EB001975 · NIBIB · UNIVERSITY OF WASHINGTON · PI FOSTER, DAVID M · 2003 to 2007
$4.9M
NIBIB NIH HHS P41 EB-001975NIBIB NIH HHS P41 EB001975
6 · The paper itself

Abstract

objectiveDysregulated apolipoprotein (apo)C-III metabolism may account for hypertriglyceridemia and increased cardiovascular risk in the metabolic syndrome. This study investigated the dose-dependent effect of rosuvastatin on VLDL apoC-III transport in men with the metabolic syndrome. RESEARCH DESIGN AND

methodsTwelve men with the metabolic syndrome were studied in a randomized double-blind crossover trial of 5-week intervention periods with placebo, 10 mg rosuvastatin, or 40 mg rosuvastatin, with 2-week placebo washouts between each period. VLDL apoC-III kinetics were examined using a stable isotope method and compartmental modeling at the end of each intervention period.

resultsCompared with placebo, there was a significant dose-dependent reduction with rosuvastatin in plasma triglyceride and VLDL apoC-III concentrations. Rosuvastatin significantly (P < 0.05) increased VLDL apoC-III fractional catabolic rate (FCR) and decreased its production rate, with a significant (P < 0.05) dose-related effect. With 40 mg rosuvastatin, changes in VLDL apoC-III concentration were inversely associated with changes in VLDL apoC-III FCR and positively associated with VLDL apoC-III production rate (P < 0.05). Changes in VLDL apoC-III concentration and production rate were positively correlated with changes in VLDL apoB concentration and production rate and inversely correlated with VLDL apoB FCR (P < 0.05). Similar associations were observed with 10 mg rosuvastatin but were either less or not statistically significant.

conclusionsIn this study, rosuvastatin decreased the production and increased the catabolism of VLDL apoC-III, a mechanism that accounted for the significant reduction in VLDL apoC-III and triglyceride concentrations. This has implications for the management of cardiometabolic risk in obese subjects with the metabolic syndrome.

Indexed as

Apolipoprotein C-IIICholesterol, HDLCholesterol, LDLDose-Response Relationship, DrugDouble-Blind MethodFluorobenzenesHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLeucineLipoproteins, VLDLMaleMetabolic SyndromePlacebosPyrimidinesRosuvastatin CalciumSulfonamidesApolipoprotein C-IIICholesterol, HDLCholesterol, LDLFluorobenzenesHydroxymethylglutaryl-CoA Reductase InhibitorsLeucineLipoproteins, VLDLPlacebosPyrimidinesRosuvastatin CalciumSulfonamidesTriglycerides

Identifiers

PMID18509206
PMCPMC2494658
OpenAlexW2031581250

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.