Evidence map›Paper›PMID 31004037›Full record

ArticleThe Journal of biological chemistry2019

Diet-induced hepatic steatosis abrogates cell-surface LDLR by inducing

Paul F Lebeau, Jae Hyun Byun, Khrystyna Platko, Melissa E MacDonald, Samantha V Poon, Mahi Faiyaz, Nabil G Seidah, Richard C Austin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Foods (Basel, Switzerland) · 2026
    Article
  4. Review
  5. Article
  6. Lipid Dysregulation in Tangier Disease: A Case Series and Metabolic Characterization.The Journal of clinical endocrinology and metabolism · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Analytical cellular pathology (Amsterdam) · 2023
    Article
  16. Review
  17. Review
  18. Article
  19. 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

8 authors at 2 institutions in 1 country.

Paul F LebeauFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Jae Hyun ByunFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Khrystyna PlatkoFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Melissa E MacDonaldFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Samantha V PoonFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Mahi FaiyazFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and.
Nabil G Seidahthe Laboratory of Biochemical Neuroendocrinology, Montreal Clinical Research Institute, University of Montreal, Montreal, Quebec H2W 1R7, Canada.
Richard C AustinFrom the Department of Medicine, McMaster University, The Research Institute of St. Joe's Hamilton, Hamilton, Ontario L8N 4A6 and austinr@taari.ca.ORCID 0000-0003-0127-0865
St. Joseph’s Healthcare Hamilton · CAMontreal Clinical Research Institute · CA

Funding

CIHR 74477
6 · The paper itself

Abstract

The worldwide prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing rapidly. Although this condition is generally benign, accumulating evidence now suggests that patients with NAFLD are also at increased risk of cardiovascular disease (CVD); the leading cause of death in developed nations. Despite the well-established role of the liver as a central regulator of circulating low-density lipoprotein (LDL) cholesterol levels, a known driver of CVD, the mechanism(s) by which hepatic steatosis contributes to CVD remains elusive. Interestingly, a recent study has shown that circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) levels correlate positively with liver steatosis grade. Given that PCSK9 degrades the LDL receptor (LDLR) and prevents the removal of LDL from the blood into the liver, in the present study we examined the effect of hepatic steatosis on LDLR expression and circulating LDL cholesterol levels. We now report that in a manner consistent with findings in patients, diet-induced steatosis increases circulating PCSK9 levels as a result of

Indexed as

Diet, High-FatAnimalsApolipoproteins BCholesterol, LDLEndoplasmic Reticulum StressFatty LiverHep G2 CellsHumansLiverMiceMice, Inbred C57BLMice, KnockoutOrganophosphorus CompoundsProprotein Convertase 9Receptors, LDLSterol Regulatory Element Binding Protein 2Apolipoproteins BCholesterol, LDLN-hydroxy-4-phosphonobutanamideOrganophosphorus CompoundsPcsk9 protein, mouseProprotein Convertase 9Receptors, LDLSterol Regulatory Element Binding Protein 2cardiovascular diseasecell biologycell-surface proteinlipidliver metabolism

Identifiers

PMID31004037
PMCPMC6556582
OpenAlexW2938328462

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.