Cited by 114Pancreatic function and diabetesMitochondrial Function and PathologyAutophagy in Disease and Therapy

The sensitivity of pancreatic β-cells to mitochondrial injuries triggered by lipotoxicity and oxidative stress.

Open access
Li, Ning, Frigerio, Francesca, Maechler, Pierre·2008·Biochemical Society Transactions

Abstract

Pancreatic beta-cells are essential for the maintenance of glucose homoeostasis, and dysfunction of these insulin-secreting cells results in the development of diabetes. In the course of events leading from obesity to Type 2 diabetes, several mechanisms are currently envisaged. Among them, lipids and oxidative stress are considered as toxic candidates for the beta-cell. The cellular link between fatty acids and ROS (reactive oxygen species) is essentially the mitochondrion, a key organelle for the control of insulin secretion. Mitochondria are the main source of ROS and are also the primary target of oxidative attacks. The present review presents the current knowledge of lipotoxicity related to oxidative stress in the context of mitochondrial function in the beta-cell.

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Registry

Crossref · 10.1042/bst0360930

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  • Nonesterified fatty acids associated with obesity and type 2 diabetes may impair islet function by mechanisms including fatty acid-induced apoptosis, malonyl-CoA accumulation, cytoplasmic fatty acyl-CoA accumulation, decreased insulin gene transcription, and ROS induction.

    “Nonesterified fatty acids associated with obesity and type 2 diabetes may impair islet function by several mechanisms, as recently reviewed (194). These include fatty acid–induced apoptosis, accumulation of malonyl-CoA, and consequent accumulation of cytoplasmic fatty acyl-CoA molecules, decreased insulin gene transcription, and induction of ROS.”
  • Low levels of ROS are necessary for insulin secretion, but chronic, high mitochondrial ROS production can have a deleterious effect on β-cell function.

    “Low levels of ROS are necessary for insulin secretion, but chronic, high mitochondrial ROS production can have a deleterious effect on ␤-cell function (254 -256).”

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Authors
Li, N., Frigerio, F., & Maechler, P.
Affiliations
University of Geneva (CH)
Venue
Biochemical Society Transactions
Published
2008-09-19
Volume
36
Issue
5
Pages
930-934
ISSN
  • 0300-5127 (ISSN-L)
  • 1470-8752
OpenAlex
W1990045305
Cited by
114
References
65
Citations by year
2026: 2 · 2025: 3 · 2024: 7 · 2023: 8 · 2022: 5 · 2021: 7 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 3 · 2016: 8 · 2015: 4 · 2014: 8 · 2013: 4 · 2012: 11
FWCI
1.42
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Biochemical Society Transactions (publishedVersion)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
pancreatic beta cells, lipotoxicity, oxidative stress, mitochondrial dysfunction, reactive oxygen species, insulin secretion, type 2 diabetes, obesity, fatty acids, glucose homeostasis
MeSH terms
Animals, Diabetes Mellitus, DNA, Mitochondrial, Humans, Lipids, Mitochondria, Reactive Oxygen Species, Oxidative Stress, Insulin-Secreting Cells

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