TY - CHAP
T1 - Dysregulation of Glycogen Metabolism with Concomitant Spatial Memory Dysfunction in Type 2 Diabetes
T2 - Potential Beneficial Effects of Chronic Exercise
AU - Soya, Mariko
AU - Jesmin, Subrina
AU - Shima, Takeru
AU - Matsui, Takashi
AU - Soya, Hideaki
N1 - Publisher Copyright:
© Springer Nature Switzerland AG 2019.
PY - 2019
Y1 - 2019
N2 - Cognitive dysfunction is one of the comorbidities of diabetes mellitus, but hippocampus-dependent learning and memory, a component of cognitive function, shows particular decline in type 2 diabetes, suggesting an increased risk for dementia and Alzheimer’s disease. Cognitive function is related to dysregulated glucose metabolism, which is the typical cause of type 2 diabetes; however, hippocampal glycogen and its metabolite lactate are also crucial for hippocampus-dependent memory function. Type 2 diabetes induced hippocampus-dependent learning and memory dysfunction can be improved by chronic exercise and this improvement may possibly mediate through an adaptation of the astrocyte-neuron lactate shuttle (ANLS). This chapter focuses on the dysregulation of hippocampal glycometabolism in type 2 diabetes examining both existing evidence as well as the potential underlying pathophysiological 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.
AB - Cognitive dysfunction is one of the comorbidities of diabetes mellitus, but hippocampus-dependent learning and memory, a component of cognitive function, shows particular decline in type 2 diabetes, suggesting an increased risk for dementia and Alzheimer’s disease. Cognitive function is related to dysregulated glucose metabolism, which is the typical cause of type 2 diabetes; however, hippocampal glycogen and its metabolite lactate are also crucial for hippocampus-dependent memory function. Type 2 diabetes induced hippocampus-dependent learning and memory dysfunction can be improved by chronic exercise and this improvement may possibly mediate through an adaptation of the astrocyte-neuron lactate shuttle (ANLS). This chapter focuses on the dysregulation of hippocampal glycometabolism in type 2 diabetes examining both existing evidence as well as the potential underlying pathophysiological 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.
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U2 - 10.1007/978-3-030-27480-1_13
DO - 10.1007/978-3-030-27480-1_13
M3 - Chapter
C2 - 31667816
AN - SCOPUS:85074404527
T3 - Advances in Neurobiology
SP - 363
EP - 383
BT - Advances in Neurobiology
PB - Springer New York LLC
ER -