Evidence map›Paper›PMID 34943836›Full record

ReviewCells2021

Lipotoxicity and β-Cell Failure in Type 2 Diabetes: Oxidative Stress Linked to NADPH Oxidase and ER Stress.

Eloisa Aparecida Vilas-Boas, Davidson Correa Almeida, Leticia Prates Roma, Fernanda Ortis, Angelo Rafael Carpinelli

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
11.5field-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

83 citing papers in PubMed, 116 citations in OpenAlex.

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23 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

5 authors at 2 institutions in 2 countries.

Eloisa Aparecida Vilas-BoasDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo 05508-000, Brazil.ORCID 0000-0003-1565-1618
Davidson Correa AlmeidaDepartment of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo 05508-000, Brazil.ORCID 0000-0003-4285-0081
Leticia Prates RomaCenter for Human and Molecular Biology (ZHMB), Department of Biophysics, Saarland University, 66424 Homburg, Germany.ORCID 0000-0001-9527-0529
Fernanda OrtisDepartment of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo 05508-000, Brazil.
Angelo Rafael CarpinelliDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo 05508-000, Brazil.ORCID 0000-0002-0781-4934
Universidade de São Paulo · BRSaarland University · DE

Funding

National Council for Scientific and Technological Development CNPq 142008/2016-8National Council for Scientific and Technological Development CNPq 465389/2014-7São Paulo Research Foundation FAPESP 2017/04580-2São Paulo Research Foundation FAPESP 2017/26339-5São Paulo Research Foundation FAPESP 2019/26062-9São Paulo Research Foundation FAPESP 2020/06184-0São Paulo Research Foundation Instituto Nacional de Ciência e Tecnologia em Bioanalítica (INCTBio) - FAPESP 2014/50867-3
6 · The paper itself

Abstract

A high caloric intake, rich in saturated fats, greatly contributes to the development of obesity, which is the leading risk factor for type 2 diabetes (T2D). A persistent caloric surplus increases plasma levels of fatty acids (FAs), especially saturated ones, which were shown to negatively impact pancreatic β-cell function and survival in a process called lipotoxicity. Lipotoxicity in β-cells activates different stress pathways, culminating in β-cells dysfunction and death. Among all stresses, endoplasmic reticulum (ER) stress and oxidative stress have been shown to be strongly correlated. One main source of oxidative stress in pancreatic β-cells appears to be the reactive oxygen species producer NADPH oxidase (NOX) enzyme, which has a role in the glucose-stimulated insulin secretion and in the β-cell demise during both T1 and T2D. In this review, we focus on the acute and chronic effects of FAs and the lipotoxicity-induced β-cell failure during T2D development, with special emphasis on the oxidative stress induced by NOX, the ER stress, and the crosstalk between NOX and ER stress.

Indexed as

Endoplasmic Reticulum StressOxidative StressAnimalsDiabetes Mellitus, Type 2HumansInsulin-Secreting CellsLipidsNADPH OxidasesLipidsNADPH OxidasesER stresslipotoxicityNADPH oxidaseoxidative stresspancreatic β-celltype 2 diabetes

Identifiers

PMID34943836
PMCPMC8699655
OpenAlexW3216856793

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.