Brain glucose metabolism is controlled by amplification and desensitization of the neuronal insulin receptor
Brain glucose metabolism is controlled by amplification and desensitization of the neuronal insulin receptor
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DOI：
10.1111/j.1749-6632.1996.tb34448.x
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发表时间：
1996-01-01
期刊：
影响因子：
--
通讯作者：
Martin, E
中科院分区：
文献类型：
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作者：
Hoyer, S;Henneberg, N;Martin, E
葡萄糖代谢对大脑功能和结构至关重要。葡萄糖有助于神经递质的形成，通常是能量形成的唯一来源。越来越多的证据表明，脑葡萄糖代谢受神经元胰岛素/胰岛素受体信号转导的控制。目前的数据清楚地表明，脑室内注射胰岛素对大脑葡萄糖/能量代谢产生合成代谢作用（神经元胰岛素受体复合物的放大），而皮质醇（皮质酮）则具有拮抗作用（神经元胰岛素受体复合物的脱敏）。研究还表明，短期皮质醇（皮质酮）增强颞顶皮层和海马的能量周转。相比之下，长期的皮质醇（皮质酮）减少了研究的两种大脑结构的能量周转。这种代谢模式使人想起在非常年老时发现的。因此，人们认为长期的皮质醇会加速大脑的衰老过程，从而增加患老年性疾病（如痴呆症）的风险。
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.