Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase.
Open accessAbstract
Hypoglycemic coma and brain injury are potential complications of insulin therapy. Certain neurons in the hippocampus and cerebral cortex are uniquely vulnerable to hypoglycemic cell death, and oxidative stress is a key event in this cell death process. Here we show that hypoglycemia-induced oxidative stress and neuronal death are attributable primarily to the activation of neuronal NADPH oxidase during glucose reperfusion. Superoxide production and neuronal death were blocked by the NADPH oxidase inhibitor apocynin in both cell culture and in vivo models of insulin-induced hypoglycemia. Superoxide production and neuronal death were also blocked in studies using mice or cultured neurons deficient in the p47(phox) subunit of NADPH oxidase. Chelation of zinc with calcium disodium EDTA blocked both the assembly of the neuronal NADPH oxidase complex and superoxide production. Inhibition of the hexose monophosphate shunt, which utilizes glucose to regenerate NADPH, also prevented superoxide formation and neuronal death, suggesting a mechanism linking glucose reperfusion to superoxide formation. Moreover, the degree of superoxide production and neuronal death increased with increasing glucose concentrations during the reperfusion period. These results suggest that high blood glucose concentrations following hypoglycemic coma can initiate neuronal death by a mechanism involving extracellular zinc release and activation of neuronal NADPH oxidase.
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Data from a rodent model of extreme hypoglycemia suggest that post-hypoglycemic glucose reperfusion contributes to neuronal death.
“Data from a rodent model of extreme hypoglycemia suggest that post-hypoglycemic glucose reperfusion contributes to neuronal death (188).”
From Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline (2009) · cites this paper as [188]
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- Authors
- Suh, S. W., Gum, E. T., Hamby, A. M., Chan, P. H., & Swanson, R. A.
- Affiliations
- San Francisco VA Medical Center (US)
- Stanford Medicine (US)
- Corresponding author
- Swanson, Raymond A.
- Venue
- Journal of Clinical Investigation
- Published
- 2007-04-02
- Volume
- 117
- Issue
- 4
- Pages
- 910-918
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1838937
- OpenAlex
- W2001637884
- Semantic Scholar
- 0cb14ae531c1e0c4b2a181347d0c97f43bc6c87a
- Cited by
- 419
- References
- 62
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 10 · 2023: 14 · 2022: 18 · 2021: 18 · 2020: 18 · 2019: 15 · 2018: 25 · 2017: 21 · 2016: 22 · 2015: 25 · 2014: 26 · 2013: 26 · 2012: 33
- FWCI
- 13.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health (P50 NS14543, NS14543)
- National Institute of Neurological Disorders and Stroke (P50NS014543, NS051855, R01NS051855, P50NS14543)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- hypoglycemia, neuronal cell death, NADPH oxidase, oxidative stress, superoxide production, insulin-induced hypoglycemia, hypoglycemic coma, hippocampus, cerebral cortex, apocynin, p47phox, extracellular zinc, pentose phosphate pathway, zinc chelation, brain injury
- MeSH terms
- Enzyme Activation, Glucose, Humans, Hypoglycemia, Mitochondria, Neurons, Superoxides, Reperfusion, Cell Death, NADPH Oxidases
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