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Titlebook: Brain Glycogen Metabolism; Mauro DiNuzzo,Arne Schousboe Book 2019 Springer Nature Switzerland AG 2019 glycogen synthase.phosphorylase.ion

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樓主: SPARK
21#
發(fā)表于 2025-3-25 05:48:24 | 只看該作者
Dysregulation of Glycogen Metabolism with Concomitant Spatial Memory Dysfunction in Type 2 Diabetesl mechanism responsible for memory dysfunction in type 2 diabetes, and showing for the first time that chronic exercise could be an effective therapy for type-2-diabetes-induced hippocampal memory decline.
22#
發(fā)表于 2025-3-25 10:47:37 | 只看該作者
23#
發(fā)表于 2025-3-25 11:48:45 | 只看該作者
24#
發(fā)表于 2025-3-25 16:31:12 | 只看該作者
25#
發(fā)表于 2025-3-25 21:55:13 | 只看該作者
26#
發(fā)表于 2025-3-26 03:24:36 | 只看該作者
27#
發(fā)表于 2025-3-26 07:38:41 | 只看該作者
https://doi.org/10.1007/978-3-642-78980-9ged exhaustive exercise, muscle glycogen was depleted and brain glycogen decreased when associated with decreased blood glucose levels and increased serotonergic activity known as central fatigue factors, suggesting brain glycogen decrease as an integrative factor for central fatigue. Prolonged exha
28#
發(fā)表于 2025-3-26 08:54:43 | 只看該作者
https://doi.org/10.1007/978-3-642-87559-5ns become more vulnerable to depleted glycogen, although aging axons can use lactate as efficiently as young axons. Lactate equally supports function during aglycemia in corpus callosum (CC), which consists of a mixture of myelinated and unmyelinated axons. Moreover, axon function in CC shows greate
29#
發(fā)表于 2025-3-26 13:08:31 | 只看該作者
https://doi.org/10.1007/978-3-642-87559-5l mechanism responsible for memory dysfunction in type 2 diabetes, and showing for the first time that chronic exercise could be an effective therapy for type-2-diabetes-induced hippocampal memory decline.
30#
發(fā)表于 2025-3-26 19:13:37 | 只看該作者
Peter G. Elliott BSc, Mb ChB, DRCOG, MRCGPturnover of pathways that intersect with glycogen mobilization. A series of equations is developed to describe the stoichiometric relationships between net glycogen consumption that is predominantly in astrocytes with the rate of the glutamate-glutamine cycle, rates of astrocytic and neuronal glycol
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