Evidence map›Paper›PMID 19715772›Full record

ReviewBiochimica et biophysica acta2010

Glucolipotoxicity of the pancreatic beta cell.

Vincent Poitout, Julie Amyot, Meriem Semache, Bader Zarrouki, Derek Hagman, Ghislaine Fontés

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
13.8field-weighted citation impact, top 1% 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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 372 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mechanism of Obesity-Related Lipotoxicity and Clinical Perspective.Advances in experimental medicine and biology · 2024
    Review
  19. Article
  20. Frontiers in immunology · 2024
    Review

117 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

6 authors at 1 institution in 1 country.

Vincent PoitoutMontreal Diabetes Research Center, CRCHUM, Department of Medicine, University of Montreal, Montreal, QC, Canada. Vincent.poitout@umontreal.ca
Julie Amyot
Meriem Semache
Bader Zarrouki
Derek Hagman
Ghislaine Fontés
Université de Montréal · CA

Funding

Neutral lipid dysregulation of the pancreatic beta-cellR01DK058096 · NIDDK · UNIVERSITY OF MONTREAL HOSPITAL · PI POITOUT, VINCENT · 2001 to 2020
$3.9M
Mechanisms of Fatty-Acid Inhibition of the Insulin GeneR56DK058096 · NIDDK · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI POITOUT, VINCENT · 2005 to 2005
$53k
CIHR 77686CIHR MOP 77686NIDDK NIH HHS R01 DK058096NIDDK NIH HHS R01-DK58096NIDDK NIH HHS R56 DK058096
6 · The paper itself

Abstract

The concept of glucolipotoxicity refers to the combined, deleterious effects of elevated glucose and fatty acid levels on pancreatic beta-cell function and survival. Significant progress has been made in recent years towards a better understanding of the cellular and molecular basis of glucolipotoxicity in the beta cell. The permissive effect of elevated glucose on the detrimental actions of fatty acids stems from the influence of glucose on intracellular fatty acid metabolism, promoting the synthesis of cellular lipids. The combination of excessive levels of fatty acids and glucose therefore leads to decreased insulin secretion, impaired insulin gene expression, and beta-cell death by apoptosis, all of which probably have distinct underlying mechanisms. Recent studies from our laboratory have identified several pathways implicated in fatty acid inhibition of insulin gene expression, including the extracellular-regulated kinase (ERK1/2) pathway, the metabolic sensor Per-Arnt-Sim kinase (PASK), and the ATF6 branch of the unfolded protein response. We have also confirmed in vivo in rats that the decrease in insulin gene expression is an early defect which precedes any detectable abnormality in insulin secretion. While the role of glucolipotoxicity in humans is still debated, the inhibitory effects of chronically elevated fatty acid levels has been clearly demonstrated in several studies, at least in individuals genetically predisposed to developing type 2 diabetes. It is therefore likely that glucolipotoxicity contributes to beta-cell failure in type 2 diabetes as well as to the decline in beta-cell function observed after the onset of the disease.

Indexed as

AnimalsFatty AcidsFemaleGlucoseHumansInsulin ResistanceInsulin-Secreting CellsLipid Metabolism DisordersMaleObesityFatty AcidsGlucose

Identifiers

PMID19715772
PMCPMC2824006
OpenAlexW2101369715

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.