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Cited by 103Advanced Glycation End Products researchPancreatic function and diabetesEndoplasmic Reticulum Stress and Disease

Advanced glycation end-products induce injury to pancreatic beta cells through oxidative stress

Lin, N., Zhang, H., Su, Q.·2012·Diabetes & Metabolism
DOI 10.1016/j.diabet.2012.01.003
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Abstract

Aim This study evaluated the direct effects of advanced glycation end-products (AGEs) on pancreatic β cells, including cellular viability, generation of reactive oxygen species (ROS) and insulin secretion, and also looked for the main source of ROS in INS-1 cells and the possible molecular mechanism(s) of cell injury by AGEs.Methods INS-1 cells were cultured with 100, 200 and 500 mg/L of AGEs for specific periods of time. Cell apoptosis was determined by ELISA and real-time PCR assays. ROS were detected by DCFH-DA and MitoSOX Red probes with a flow cytometer, NADPH oxidase activity was measured by lucigenin chemiluminescence and MAPK phosphorylation was measured by Western blot tests.Results Both cell apoptosis and ROS generation increased in AGE-treated cells in a dose-dependent way, and both the mitochondrial electron transport chain and NADPH oxidase pathway participated in ROS generation, although the role of the mitochondrial pathway was earlier and more important. AGEs exerted a toxic effect on insulin secretion that could be largely reversed by inhibiting ROS.Conclusion AGEs injured INS-1 cells by oxidative stress mainly through the mitochondrial pathway, although the JNK and p38 MAPK signaling pathways were also key modulators in ROS-mediated β-cell death.

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Crossref · 10.1016/j.diabet.2012.01.003

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  • Dietary AGEs disrupt and downregulate SIRT1 expression, resulting in acetylation and inactivation of PGC1α.

    “Dietary AGEs have been found to disrupt and downregulate sirtuin1 (SIRT1) expression, resulting in the acetylation and inactivation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC1α), a master regulator of mitochondrial metabolism.”

    From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [52]

  • AGEs stimulate mitochondrial ROS production and JNK and NADPH oxidase activity to induce mitochondrial dysfunction and oxidative stress.

    “AGEs also stimulate mitochondrial ROS production and c-Jun N-terminal protein kinase (JNK) and NADPH oxidase activity to induce mitochondrial dysfunction and oxidative stress51–53.”

    From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [52]

  • The molecular mechanism responsible for AGE-induced oxidative stress relies on increased mitochondrial ROS production and activation of JNK, which in turn activates NADPH oxidase, further fueling oxidative stress.

    “Cell culture studies also showed that the molecular mechanism responsible for AGE-induced oxidative stress relies on increased mitochondrial ROS production as well as the activation of JNK which, in turn, activates NADPH oxidase further fueling oxidative stress.[136]”

    From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [136]

  • AGEs contribute to pancreatic β-cell dysfunction, a key component in the pathogenesis of T2DM.

    “AGEs also contribute to pancreatic 𝛽-cell dysfunction, another key component in the pathogenesis of T2DM.”

    From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [136]

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Authors
Lin, N., Zhang, H., & Su, Q.
Affiliations
Shanghai Jiao Tong University (CN)
Corresponding author
Su, Q.
ORCID
Su, Q.
Venue
Diabetes & Metabolism
Publisher
Elsevier BV
Published
2012-06
Volume
38
Issue
3
Pages
250-257
ISSN
1262-3636 (ISSN-L)
DOI
10.1016/j.diabet.2012.01.003
OpenAlex
W1969047353
Cited by
103
References
38
Citations by year
2026: 3 · 2025: 5 · 2024: 5 · 2023: 12 · 2022: 7 · 2021: 7 · 2020: 5 · 2019: 5 · 2018: 8 · 2017: 12 · 2016: 10 · 2015: 5 · 2014: 8 · 2013: 7 · 2012: 3
FWCI
4.72
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Diabetes & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Keywords
advanced glycation end products, pancreatic beta cells, oxidative stress, reactive oxygen species, beta-cell apoptosis, insulin secretion, NADPH oxidase, mitochondrial electron transport chain, JNK signaling, p38 MAPK, INS-1 cells, diabetes mellitus, beta-cell injury, MAPK phosphorylation, NOX4, NADPH oxidase 5
MeSH terms
Animals, Cell Survival, Cells, Cultured, Phosphorylation, Blotting, Western, Signal Transduction, Glycation End Products, Advanced, Apoptosis, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Insulin-Secreting Cells, Rats, Real-Time Polymerase Chain Reaction

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