Evidence map›Paper›PMID 17437081›Full record

ArticleDiabetologia2007

Human high-density lipoprotein particles prevent activation of the JNK pathway induced by human oxidised low-density lipoprotein particles in pancreatic beta cells.

A Abderrahmani, G Niederhauser, D Favre, S Abdelli, M Ferdaoussi, J Y Yang, R Regazzi, C Widmann, G Waeber

Registry-linked trialOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05072587 (Dietary Oxysterols and β-Cell Function Among African Americans), which is not on this map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
9.3field-weighted citation impact, top 2% 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.

NCT05072587 nacompletednot on this mapstarted 2021, after this paper: background citation

Dietary Oxysterols and β-Cell Function Among African Americans

TypeinterventionalSponsorMorehouse School of MedicineRan2021 to 2023Enrolled12ConditionsType 2 DiabetesArmsPlant-based diet with no oxysterols, Standard ADA Diet (SADA)
3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 150 citations in OpenAlex.

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  17. Observational
  18. Oxidized LDLs as Signaling Molecules.Antioxidants (Basel, Switzerland) · 2021
    Review
  19. Review
  20. Article

13 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

A AbderrahmaniService of Internal Medicine, CHUV-Hospital, Rue du Bugnon 9, 1005 Lausanne, Switzerland. Amar.Abderrahmani@unil.ch
G Niederhauser
D Favre
S Abdelli
M Ferdaoussi
J Y Yang
R Regazzi
C Widmann
G Waeber
University of Lausanne · CHUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisWe explored the potential adverse effects of pro-atherogenic oxidised LDL-cholesterol particles on beta cell function. MATERIALS AND

methodsIsolated human and rat islets and different insulin-secreting cell lines were incubated with human oxidised LDL with or without HDL particles. The insulin level was monitored by ELISA, real-time PCR and a rat insulin promoter construct linked to luciferase gene reporter. Cell apoptosis was determined by scoring cells displaying pycnotic nuclei.

resultsProlonged incubation with human oxidised LDL particles led to a reduction in preproinsulin expression levels, whereas the insulin level was preserved in the presence of native LDL-cholesterol. The loss of insulin production occurred at the transcriptional levels and was associated with an increase in activator protein-1 transcriptional activity. The rise in activator protein-1 activity resulted from activation of c-Jun N-terminal kinases (JNK, now known as mitogen-activated protein kinase 8 [MAPK8]) due to a subsequent decrease in islet-brain 1 (IB1; now known as MAPK8 interacting protein 1) levels. Consistent with the pro-apoptotic role of the JNK pathway, oxidised LDL also induced a twofold increase in the rate of beta cell apoptosis. Treatment of the cells with JNK inhibitor peptides or HDL countered the effects mediated by oxidised LDL. CONCLUSIONS/

interpretationThese data provide strong evidence that oxidised LDL particles exert deleterious effects in the progression of beta cell failure in diabetes and that these effects can be countered by HDL particles.

Indexed as

AnimalsApoptosisCell LineDiabetes MellitusDisease ProgressionEnzyme ActivationGenes, ReporterHumansInsulinInsulin-Secreting CellsInsulin SecretionLipoproteins, HDLLipoproteins, LDLMaleMAP Kinase Kinase 4Polymerase Chain ReactionInsulinLipoproteins, HDLLipoproteins, LDLMAP Kinase Kinase 4oxidized low density lipoproteinRNA

Identifiers

PMID17437081
OpenAlexW1983012279

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.