Evidence map›Paper›PMID 30213825›Full record

ArticleDiabetes2018

CETP Inhibition Improves HDL Function but Leads to Fatty Liver and Insulin Resistance in CETP-Expressing Transgenic Mice on a High-Fat Diet.

Lin Zhu, Thao Luu, Christopher H Emfinger, Bryan A Parks, Jeanne Shi, Elijah Trefts, Fenghua Zeng, Zsuzsanna Kuklenyik, Raymond C Harris, David H Wasserman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Cardiovascular Benefits of Menopause Hormone Treatment is Age-Dependent.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
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  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. HDL and Cholesterol Ester Transfer Protein (CETP).Advances in experimental medicine and biology · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 4 institutions in 1 country.

Lin ZhuVeterans Administration Tennessee Valley Healthcare System, Vanderbilt University School of Medicine, Nashville, TN.
Thao LuuDivision of Diabetes, Endocrinology, and Metabolism, Vanderbilt University School of Medicine, Nashville, TN.
Christopher H EmfingerVeterans Administration Tennessee Valley Healthcare System, Vanderbilt University School of Medicine, Nashville, TN.
Bryan A ParksDivision of Laboratory Sciences, Centers for Disease Control and Prevention, Atlanta, GA.
Jeanne ShiDivision of Diabetes, Endocrinology, and Metabolism, Vanderbilt University School of Medicine, Nashville, TN.
Elijah TreftsDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN.
Fenghua ZengDivision of Nephrology and Hypertension, Vanderbilt University School of Medicine, Nashville, TN.ORCID 0000-0003-1087-7634
Zsuzsanna KuklenyikDivision of Laboratory Sciences, Centers for Disease Control and Prevention, Atlanta, GA.
Raymond C HarrisDivision of Nephrology and Hypertension, Vanderbilt University School of Medicine, Nashville, TN.ORCID 0000-0001-8025-0883
David H WassermanDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN.
Sergio FazioThe Center for Preventive Cardiology at the Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR.
John M StaffordVeterans Administration Tennessee Valley Healthcare System, Vanderbilt University School of Medicine, Nashville, TN john.stafford@vanderbilt.edu.ORCID 0000-0001-6527-959X
Vanderbilt University · USCenters for Disease Control and Prevention · USDuke University · USOregon Health & Science University · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Vanderbilt O'Brien Kidney Center - Core D - Clinical and Translational CoreP30DK114809 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, MATTHEW H · 2017 to 2021
$5.9M
Functional and structural correlates of PCSK9 association with lipoproteinsR01HL132985 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI PAMIR, NATHALIE · 2016 to 2024
$4.2M
Sex-Specific Risk of Metabolic and Cardiovascular DiseaseR01HL144846 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI John Michael Stafford · 2019 to 2026
$4.1M
Therapeutic Potential of Estrogen-Regulated Metabolism and Cardiovascular RiskR01DK109102 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STAFFORD, JOHN MICHAEL · 2016 to 2024
$3.6M
Cholesteryl ester transfer protein, a novel mediator of insulin sensitivityI01BX002223 · VA · VETERANS HEALTH ADMINISTRATION · PI STAFFORD, JOHN MICHAEL · 2014 to 2017
–
BLRD VA I01 BX002223NHLBI NIH HHS R01 HL132985NHLBI NIH HHS R01 HL144846NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK109102NIDDK NIH HHS U24 DK059637NIDDK NIH HHS U2C DK059637
6 · The paper itself

Abstract

In clinical trials, inhibition of cholesteryl ester transfer protein (CETP) raises HDL cholesterol levels but does not robustly improve cardiovascular outcomes. Approximately two-thirds of trial participants are obese. Lower plasma CETP activity is associated with increased cardiovascular risk in human studies, and protective aspects of CETP have been observed in mice fed a high-fat diet (HFD) with regard to metabolic outcomes. To define whether CETP inhibition has different effects depending on the presence of obesity, we performed short-term anacetrapib treatment in chow- and HFD-fed CETP transgenic mice. Anacetrapib raised HDL cholesterol and improved aspects of HDL functionality, including reverse cholesterol transport, and HDL's antioxidative capacity in HFD-fed mice was better than in chow-fed mice. Anacetrapib worsened the anti-inflammatory capacity of HDL in HFD-fed mice. The HDL proteome was markedly different with anacetrapib treatment in HFD- versus chow-fed mice. Despite benefits on HDL, anacetrapib led to liver triglyceride accumulation and insulin resistance in HFD-fed mice. Overall, our results support a physiologic importance of CETP in protecting from fatty liver and demonstrate context selectivity of CETP inhibition that might be important in obese subjects.

Indexed as

Diet, High-FatAnimalsAnticholesteremic AgentsCholesterol Ester Transfer ProteinsCholesterol, HDLFatty LiverInsulin ResistanceMiceMice, TransgenicOxazolidinonesanacetrapibAnticholesteremic AgentsCholesterol Ester Transfer ProteinsCholesterol, HDLOxazolidinones

Identifiers

PMID30213825
PMCPMC6245220
OpenAlexW2892170508

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.