Evidence map›Paper›PMID 22001232›Full record

ReviewBiochimica et biophysica acta2012

Hepatic ABCA1 and VLDL triglyceride production.

Mingxia Liu, Soonkyu Chung, Gregory S Shelness, John S Parks

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Glucocorticoid-Induced Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Hepatic ABC transporters and triglyceride metabolism.Current opinion in lipidology · 2012
    Review
  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

4 authors at 2 institutions in 1 country.

Mingxia LiuDepartment of Pathology/Section on Lipid Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Soonkyu Chung
Gregory S Shelness
John S Parks
Wake Forest University · USUniversity of Florida · US

Funding

TISSUE CULTURE COREP01HL049373 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RUDEL, LAWRENCE L · 1993 to 2012
$23.8M
UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
Macrophage, ABCA1, Inflammation, and AtherosclerosisR01HL094525 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARKS, JOHN S · 2009 to 2012
$1.5M
NCATS NIH HHS UL1 TR000064NHLBI NIH HHS P01 HL049373NHLBI NIH HHS P01 HL 49373NHLBI NIH HHS R01 HL094525NHLBI NIH HHS R01 HL94525
6 · The paper itself

Abstract

Elevated plasma triglyceride (TG) and reduced high density lipoprotein (HDL) concentrations are prominent features of metabolic syndrome (MS) and type 2 diabetes (T2D). Individuals with Tangier disease also have elevated plasma TG concentrations and a near absence of HDL, resulting from mutations in ATP binding cassette transporter A1 (ABCA1), which facilitates the efflux of cellular phospholipid and free cholesterol to assemble with apolipoprotein A-I (apoA-I), forming nascent HDL particles. In this review, we summarize studies focused on the regulation of hepatic very low density lipoprotein (VLDL) TG production, with particular attention on recent evidence connecting hepatic ABCA1 expression to VLDL, LDL, and HDL metabolism. Silencing ABCA1 in McArdle rat hepatoma cells results in diminished assembly of large (>10nm) nascent HDL particles, diminished PI3 kinase activation, and increased secretion of large, TG-enriched VLDL1 particles. Hepatocyte-specific ABCA1 knockout (HSKO) mice have a similar plasma lipid phenotype as Tangier disease subjects, with a two-fold elevation of plasma VLDL TG, 50% lower LDL, and 80% reduction in HDL concentrations. This lipid phenotype arises from increased hepatic secretion of VLDL1 particles, increased hepatic uptake of plasma LDL by the LDL receptor, elimination of nascent HDL particle assembly by the liver, and hypercatabolism of apoA-I by the kidney. These studies highlight a novel role for hepatic ABCA1 in the metabolism of all three major classes of plasma lipoproteins and provide a metabolic link between elevated TG and reduced HDL levels that are a common feature of Tangier disease, MS, and T2D. This article is part of a Special Issue entitled: Triglyceride Metabolism and Disease.

Indexed as

ATP-Binding Cassette TransportersLiverTangier DiseaseAnimalsApolipoprotein A-IATP Binding Cassette Transporter 1Diabetes Mellitus, Type 2HumansLipoproteins, HDLLipoproteins, VLDLMetabolic SyndromeMiceTriglyceridesABCA1 protein, humanApolipoprotein A-IATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersLipoproteins, HDLLipoproteins, VLDLTriglycerides

Identifiers

PMID22001232
PMCPMC3272310
OpenAlexW2017084907

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.