The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Reactive Oxygen Species as a Signal in Glucose-Stimulated Insulin Secretion
Open accessAbstract
One of the unique features of β-cells is their relatively low expression of many antioxidant enzymes. This could render β-cells susceptible to oxidative damage but may also provide a system that is sensitive to reactive oxygen species as signals. In isolated mouse islets and INS-1(832/13) cells, glucose increases intracellular accumulation of H2O2. In both models, insulin secretion could be stimulated by provision of either exogenous H2O2 or diethyl maleate, which raises intracellular H2O2 levels. Provision of exogenous H2O2 scavengers, including cell permeable catalase and N-acetyl-l-cysteine, inhibited glucose-stimulated H2O2 accumulation and insulin secretion (GSIS). In contrast, cell permeable superoxide dismutase, which metabolizes superoxide into H2O2, had no effect on GSIS. Because oxidative stress is an important risk factor for β-cell dysfunction in diabetes, the relationship between glucose-induced H2O2 generation and GSIS was investigated under various oxidative stress conditions. Acute exposure of isolated mouse islets or INS-1(832/13) cells to oxidative stressors, including arsenite, 4-hydroxynonenal, and methylglyoxal, led to decreased GSIS. This impaired GSIS was associated with increases in a battery of endogenous antioxidant enzymes. Taken together, these findings suggest that H2O2 derived from glucose metabolism is one of the metabolic signals for insulin secretion, whereas oxidative stress may disturb its signaling function.
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Citations
Cites
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
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H 2 O 2 , a Necessary Evil for Cell Signaling
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“For example, a persistently elevated level of antioxidant enzymes might quickly and efficiently eliminate any ROS that is generated (47).”
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Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure
Liesa, M., & Shirihai, O. S. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.03.002 · Cited by 1,341
Glucolipotoxicity: fuel excess and β-cell dysfunction
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Oxidative stress in obesity: A critical component in human diseases
Marseglia, L., Manti, S., D’Angelo, G., Nicotera, A., Parisi, E., Di Rosa, G., Gitto, E., & Arrigo, T. (2014) · International Journal of Molecular Sciences · doi:10.3390/ijms16010378 · Cited by 933
“Additionally, it has been reported that β-cells have relatively low expression of many antioxidant enzymes, making these cells susceptible to ROS-induced damage [86].”
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Metabolic Signaling in Fuel-Induced Insulin Secretion
Prentki, M., Matschinsky, F. M., & Madiraju, S. R. M. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.05.018 · Cited by 548
Metadata
- Authors
- Pi, J., Bai, Y., Zhang, Q., Wong, V., Floering, L. M., Daniel, K., Reece, J. M., Deeney, J. T., Andersen, M. E., Corkey, B. E., & Collins, S.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-07-01
- Volume
- 56
- Issue
- 7
- Pages
- 1783-1791
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2109069544
- Cited by
- 574
- References
- 11
- FWCI
- 25.68
- Type
- journal article
- Language
- en
- Open access
- bronze
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