New insights into ER stress-induced insulin resistance
Open accessAbstract
Insulin resistance is a major characteristic of obesity and type 2 diabetes (T2DM). During the last decade, endoplasmic reticulum (ER) stress has emerged as a new player in this field and a considerable number of recent studies have pointed out its role in the onset of insulin resistance (IR). ER stress appears to act directly as a negative modulator of the insulin signaling pathway but also indirectly by promoting lipid accumulation. This review aims to summarize and decipher the abundant new literature concerning the emerging and multifaceted involvement of ER stress in the development of metabolic dysfunctions in insulin target tissues.
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Dysregulation of interactions between mitochondria and the ER is implicated in the pathogenesis of insulin resistance.
“Particularly, the dysregulation of the interactions between mitochondria and the ER has been reported to be implicated in the pathogenesis of insulin resistance (Flamment et al., 2012; Sebastian et al., 2012; Tubbs et al., 2018).”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Flamment et al., 2012
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Mechanisms of Insulin Action and Insulin Resistance
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- Authors
- Flamment, M., Hajduch, E., Ferré, P., & Foufelle, F.
- Affiliations
- Inserm (FR)
- Corresponding author
- Foufelle, Fabienne
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2012-08
- Volume
- 23
- Issue
- 8
- Pages
- 381-390
- ISSN
- 1043-2760 (ISSN-L)
- OpenAlex
- W1974719515
- Cited by
- 306
- References
- 100
- Citations by year
- 2026: 7 · 2025: 21 · 2024: 11 · 2023: 18 · 2022: 20 · 2021: 34 · 2020: 23 · 2019: 21 · 2018: 26 · 2017: 29 · 2016: 23 · 2015: 20 · 2014: 29 · 2013: 23 · 2012: 1
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- green
- zenodo.org
- Licence
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Funders
- European Commission
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- endoplasmic reticulum stress, insulin resistance, type 2 diabetes, obesity, insulin signaling pathway, lipid accumulation, insulin target tissues, metabolic dysfunction
- MeSH terms
- Adipose Tissue, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Liver, Obesity, Transcription Factors, Signal Transduction, Muscle, Skeletal, Lipid Metabolism, Unfolded Protein Response, Endoplasmic Reticulum Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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