title: β2-adrenergic receptor and astrocyte glucose metabolism.
abstract: Astrocyte glucose metabolism functions to maintain brain activity in both normal and stress conditions. Dysregulation of astrocyte glucose metabolism relates to development of neuronal disease, such as multiple sclerosis and Alzheimer's disease. In response to acute stress, beta2-adrenergic receptor is activated and initiates multiple signaling events mediated by Gs, Gi, arrestin, or other effectors depending on specific cellular contexts. In astrocytes, beta2-adrenergic receptor promotes glucose uptake through GLUT1 and accelerates glycogen degradation via coupling to Gs and second messenger cAMP-dependent pathway. Beta2-adrenergic receptor may regulate other steps in astrocyte glucose metabolism, such as lactate production or transduction. Inappropriate regulation of beta2-adrenergic receptor activity can disrupt normal glucose metabolism, and leads to accelerate neuronal disease development. It was demonstrated that the absence of beta2-adrenergic receptor in astrocytes occurred in multiple sclerosis patients, and the increased beta2-adrenergic receptor activity relates to Alzheimer's disease. A clear view of beta2-adrenergic receptor-mediated signaling pathways in regulating astrocyte glucose metabolism could help us to develop neuronal diseases treatment by targeting to the beta2-adrenergic receptor.
authors.affiliation: Key Laboratory for Experimental Teratology of the Ministry of Education, Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan, Shandong 250012, People's Republic of China.
authors.forename: Jun-hong
authors.initials: JH
authors.lastname: Dong
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.forename: Min
authors.initials: M
authors.lastname: Cui
authors.forename: Xiao
authors.initials: X
authors.lastname: Yu
authors.forename: Qi
authors.initials: Q
authors.lastname: Pang
authors.forename: Jin-peng
authors.initials: JP
authors.lastname: Sun
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D002450:Cell Communication / Q000502:physiology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D009103:Multiple Sclerosis / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D018343:Receptors, Adrenergic, beta-2 / Q000502:physiology*; D015854:Up-Regulation / Q000502:physiology
chemical_list: D018343:Receptors, Adrenergic, beta-2; D005947:Glucose