Evidence map›Paper›PMID 31628942›Full record

ReviewJournal of molecular biology2020

Recent Insights Into Mechanisms of β-Cell Lipo- and Glucolipotoxicity in Type 2 Diabetes.

Maria Lytrivi, Anne-Laure Castell, Vincent Poitout, Miriam Cnop

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed
31.4field-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

243 citing papers in PubMed, 382 citations in OpenAlex.

  1. Trial
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  4. Metabolic Stress Shifts the Function of KArchiv der Pharmazie · 2026
    Article
  5. Review
  6. Review
  7. Article
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  14. Review
  15. Review
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  18. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  19. Article
  20. Article

183 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

4 authors at 2 institutions in 2 countries.

Maria LytriviULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium; Division of Endocrinology, Erasmus Hospital, Université Libre de Bruxelles, Brussels, Belgium.
Anne-Laure CastellCRCHUM, Montréal, QC, Canada; Department of Medicine, Université de Montréal, Montréal, QC, Canada.
Vincent PoitoutCRCHUM, Montréal, QC, Canada; Department of Medicine, Université de Montréal, Montréal, QC, Canada. Electronic address: Vincent.poitout@umontreal.ca.
Miriam CnopULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium; Division of Endocrinology, Erasmus Hospital, Université Libre de Bruxelles, Brussels, Belgium. Electronic address: mcnop@ulb.ac.be.
Université de Montréal · CAUniversité Libre de Bruxelles · BE

Funding

Neutral lipid dysregulation of the pancreatic beta-cellR01DK058096 · NIDDK · UNIVERSITY OF MONTREAL HOSPITAL · PI POITOUT, VINCENT · 2001 to 2020
$3.9M
CIHR MOP 77686NIDDK NIH HHS R01 DK058096
6 · The paper itself

Abstract

The deleterious effects of chronically elevated free fatty acid (FFA) levels on glucose homeostasis are referred to as lipotoxicity, and the concurrent exposure to high glucose may cause synergistic glucolipotoxicity. Lipo- and glucolipotoxicity have been studied for over 25 years. Here, we review the current evidence supporting the role of pancreatic β-cell lipo- and glucolipotoxicity in type 2 diabetes (T2D), including lipid-based interventions in humans, prospective epidemiological studies, and human genetic findings. In addition to total FFA quantity, the quality of FFAs (saturation and chain length) is a key determinant of lipotoxicity. We discuss in vitro and in vivo experimental models to investigate lipo- and glucolipotoxicity in β-cells and describe experimental pitfalls. Lipo- and glucolipotoxicity adversely affect many steps of the insulin production and secretion process. The molecular mechanisms underpinning lipo- and glucolipotoxic β-cell dysfunction and death comprise endoplasmic reticulum stress, oxidative stress and mitochondrial dysfunction, impaired autophagy, and inflammation. Crosstalk between these stress pathways exists at multiple levels and may aggravate β-cell lipo- and glucolipotoxicity. Lipo- and glucolipotoxicity are therapeutic targets as several drugs impact the underlying stress responses in β-cells, potentially contributing to their glucose-lowering effects in T2D.

Indexed as

Diabetes Mellitus, Type 2AnimalsAutophagyEndoplasmic Reticulum StressFatty Acids, NonesterifiedGlucagon-Like Peptide-1 ReceptorGlucoseHumansHypoglycemic AgentsInflammationInsulinInsulin-Secreting CellsMetforminMitochondriaOxidative StressSignal TransductionFatty Acids, NonesterifiedGLP1R protein, humanGlucagon-Like Peptide-1 ReceptorGlucoseHypoglycemic AgentsInsulinMetforminThiazolidinedionesInsulinIsletLipotoxicityPalmitatePancreatic β-cell

Identifiers

PMID31628942
PMCPMC7073302
OpenAlexW2980342819

What OpenQuestion holds

Texttitle and abstract
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.