Brain glucose metabolism is controlled by amplification and desensitization of the neuronal insulin receptor
Glucose metabolism is essential for brain function and structure. Glucose contributes to the formation of neurotransmitters and is normally the only source for energy formation. There is increasing evidence that brain glucose metabolism is under control of the neuronal insulin/insulin receptor signa...
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| Main Authors: | , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
1996
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| In: |
Annals of the New York Academy of Sciences
Year: 1996, Volume: 777, Issue: 1, Pages: 374-379 |
| ISSN: | 1749-6632 |
| DOI: | 10.1111/j.1749-6632.1996.tb34448.x |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1111/j.1749-6632.1996.tb34448.x Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1996.tb34448.x 
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| Author Notes: | S. Hoyer, N. Henneberg, S. Knapp, H. Lannert, and E. Martin |
| Summary: | Glucose metabolism is essential for brain function and structure. Glucose contributes to the formation of neurotransmitters and is normally the only source for energy formation. There is increasing evidence that brain glucose metabolism is under control of the neuronal insulin/insulin receptor signal transduction. The present data clearly show that intracerebroventricularly administered insulin exerts anabolic effects on cerebral glucose/energy metabolism (amplification of the neuronal insulin receptor complex) whereas cortisol (corticosterone) acts antagonistically (desensitization of the neuronal insulin receptor complex). It is also shown that short-term cortisol (corticosterone) enhanced energy turnover in temporoparietal corfex and hippocampus. In contrast, long-term cortisol (corticosterone) reduced energy turnover in both brain structures studied. This metabolic pattern is reminiscent of that found in very old age. Therefore, it is assumed that long-term cortisol accelerates the aging process in the brain and thus the risk for age-related disorders such as dementia. |
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| Item Description: | Elektronische Reproduktion der Druck-Ausgabe 17. Dezember 2006 Gesehen am 27.11.2025 |
| Physical Description: | Online Resource |
| ISSN: | 1749-6632 |
| DOI: | 10.1111/j.1749-6632.1996.tb34448.x |