Evidence map›Paper›PMID 26112886›Full record

Trial reportEuropean heart journal2015

Potent peroxisome proliferator-activated receptor-α agonist treatment increases cholesterol efflux capacity in humans with the metabolic syndrome.

Amit V Khera, John S Millar, Giacomo Ruotolo, Ming-Dauh Wang, Daniel J Rader

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Observational
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Observational
  11. Article
  12. Novel Approaches for HDL-Directed Therapies.Current atherosclerosis reports · 2017
    Review
  13. Review
  14. βDrug design, development and therapy · 2017
    Article
  15. Cholesterol efflux capacity of high-density lipoprotein correlates with survival and allograft vasculopathy in cardiac transplant recipients.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2016
    Article
  16. New Era of Lipid-Lowering Drugs.Pharmacological reviews · 2016
    Review
  17. 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

5 authors at 2 institutions in 1 country.

Amit V KheraCardiology Division, Department of Medicine, Massachusetts General Hospital, 55 Fruit Street, Yawkey 5B, Boston, MA 02114, USA avkhera@mgh.harvard.edu rader@mail.med.upenn.edu.
John S MillarDepartment of Medicine and Cardiovascular Institute, Perelman School of Medicine, Philadelphia, PA, USA.
Giacomo RuotoloCardiovascular Unit, Eli Lilly and Company, Indiannapolis, IN, USA.
Ming-Dauh WangCardiovascular Unit, Eli Lilly and Company, Indiannapolis, IN, USA.
Daniel J RaderDepartment of Medicine and Cardiovascular Institute, Perelman School of Medicine, Philadelphia, PA, USA avkhera@mgh.harvard.edu rader@mail.med.upenn.edu.
Eli Lilly (United States) · USCardiovascular Institute of the South · US

Funding

ZDV VS ZDV + DDL VS ZDV + DDL + NVP IN ASYMPTOMATIC HIV PATIENTSM01RR000040 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 1985 to 2006
$21.1M
NCRR NIH HHS M01-RR00040
6 · The paper itself

Abstract

aimsFibrate medications weakly stimulate the nuclear receptor peroxisome proliferator-activated receptor-α (PPAR-α) and are currently employed clinically in patients with dyslipidaemia. The potent and selective agonist of PPAR-α LY518674 is known to substantially increase apolipoprotein A-I (apoA-I) turnover without major impact on steady-state levels of apoA-I or high-density lipoprotein-cholesterol (HDL-C). We sought to determine whether therapy with a PPAR-α agonist impacts cholesterol efflux capacity, a marker of HDL function. METHODS AND

resultsCholesterol efflux capacity was measured at baseline and after 8 weeks of therapy in a randomized, placebo-controlled trial involving participants with metabolic syndrome treated with either LY518674 100 μg daily (n = 13) or placebo (n = 15). Efflux capacity assessment was quantified using a previously validated ex vivo assay that measures the ability of apolipoprotein-B depleted plasma to mobilize cholesterol from macrophages. LY518674 led to a 15.7% increase from baseline (95% CI 3.3-28.1%; P = 0.02, P vs. placebo = 0.01) in efflux capacity. The change in apoA-I production rate in the active treatment arm was strongly linked to change in cholesterol efflux capacity (r = 0.67, P = 0.01).

conclusionsPotent stimulation of PPAR-α leads to accelerated turnover of apoA-I and an increase in cholesterol efflux capacity in metabolic syndrome patients despite no change in HDL-C or apoA-I levels. This finding reinforces the notion that changes in HDL-C levels may poorly predict impact on functionality and thus has implications for ongoing pharmacologic efforts to enhance apoA-I metabolism.

Indexed as

Apolipoprotein A-IApolipoproteins BCholesterol, HDLFemaleHumansMaleMetabolic SyndromeMiddle AgedPPAR alphaPropionatesTriazolesAPOA1 protein, humanApolipoprotein A-IApolipoproteins BCholesterol, HDLLY 518674PPAR alphaPropionatesTriazolesCholesterol efflux capacityHDL-cholesterolLipid metabolismPPAR-α

Identifiers

PMID26112886
PMCPMC4644252
OpenAlexW2105822415

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.