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 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.
Hoyer
S
S
Department of Pathochemistry & General Neurochemistry, University of Heidelberg, Germany.
Henneberg
N
N
Knapp
S
S
Lannert
H
H
Martin
E
E
D000818:Animals; D001921:Brain / Q000378:metabolism*; D003345:Corticosterone / Q000494:pharmacology; D004734:Energy Metabolism / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011972:Receptor, Insulin / Q000378:metabolism*; D013311:Streptozocin / Q000494:pharmacology
D010710:Phosphates; D013311:Streptozocin; D011972:Receptor, Insulin; D005947:Glucose; D003345:Corticosterone