Brain Glucose Metabolism Is Controlled by Amplification and Desensitization of the Neuronal Insulin Receptora
| Autor: | Eike Martin, Siegfried Hoyer, S. Knapp, N. Henneberg, Heinrich Lannert |
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| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty medicine.medical_treatment Carbohydrate metabolism Streptozocin General Biochemistry Genetics and Molecular Biology Phosphates chemistry.chemical_compound History and Philosophy of Science Desensitization (telecommunications) Corticosterone Internal medicine medicine Animals Rats Wistar Receptor Neurons biology General Neuroscience Insulin Brain Insulin receptor complex Receptor Insulin Rats Insulin receptor Glucose Endocrinology chemistry biology.protein Signal transduction Energy Metabolism |
| Zdroj: | Annals of the New York Academy of Sciences. 777:374-379 |
| ISSN: | 0077-8923 |
| DOI: | 10.1111/j.1749-6632.1996.tb34448.x |
| Popis: | 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 cortex 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. |
| Databáze: | OpenAIRE |
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