Hyper-insulinemia increases the glutamate-excitotoxicity in cortical neurons: A mechanistic study
European Journal of Pharmacology, ISSN: 0014-2999, Vol: 833, Page: 524-530
2018
- 10Citations
- 19Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations10
- Citation Indexes10
- 10
- CrossRef7
- Captures19
- Readers19
- 19
Article Description
Insulin resistance in type-2 diabetic condition increases the risk of stroke and cognitive deficits in which involvement of glutamate has been postulated. It has been hypothesized that hyper-insulinemia in cortical neurons increases the vulnerability towards glutamate-induced excitotoxicity. To mimic insulin resistance, cortical neurons were incubated with high insulin (1 µM) and high glucose (50 mM final concentration) in in-vitro condition for 24 h. Pre-treatment of cortical neurons with high insulin blocked acute insulin-induced activation of Akt and GSK-3β but not in the case of high glucose. Our results demonstrate that chronic high insulin exposure increases glutamate-induced excitotoxity, which was blocked by insulin receptor antagonist (S961) and GSK-3β inhibitor (SB216763). These inhibitors also ameliorated pAkt (Ser473) and pGSK-3β(Ser9) levels after chronic insulin exposure. Increase in glutamate-excitotoxicity in insulin-resistant cortical neurons was found to be associated with increased expression of PICK1. However, GluR2 did not get altered in hyper-insulinemia condition. This study demonstrates that hyper-insulinemia increases glutamate excitotoxicity which could be attributed to activation of GSK-3β and increased expression of PICK1.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0014299918303686; http://dx.doi.org/10.1016/j.ejphar.2018.07.001; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85050120756&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/30017861; https://linkinghub.elsevier.com/retrieve/pii/S0014299918303686; https://dx.doi.org/10.1016/j.ejphar.2018.07.001
Elsevier BV
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