The work of N.H. was supported by a grant from the Graduate Program in Molecular and Cellular Neurobiology, University of Heidelberg.
Brain Glucose Metabolism Is Controlled by Amplification and Desensitization of the Neuronal Insulin Receptora
Article first published online: 17 DEC 2006
Annals of the New York Academy of Sciences
Volume 777, The Neurobiology of Alzheimer's Disease pages 374–379, January 1996
How to Cite
HOYER, S., HENNEBERG, N., KNAPP, S., LANNERT, H. and MARTIN, E. (1996), Brain Glucose Metabolism Is Controlled by Amplification and Desensitization of the Neuronal Insulin Receptor. Annals of the New York Academy of Sciences, 777: 374–379. doi: 10.1111/j.1749-6632.1996.tb34448.x
- Issue published online: 17 DEC 2006
- Article first published online: 17 DEC 2006
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.