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          Document History for Document ID 411614

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Document Version Version Comment Date Status
411614.0 Automatic journal name synchronization 14.03.2009 20:15 Released

ID: 411614.0, MPI für molekulare Genetik / Department of Vertebrate Genomics
Neuronal functions, feeding behavior, and energy balance in Slc2a3+/– mice
Authors:Schmidt, Stefan; Richter, Miriam; Montag, Dirk; Sartorius, Tina; Gawlik, Verena; Hennige, Anita M.; Scherneck, Stephan; Himmelbauer, Heinz; Lutz, Stefan Z.; Augustin, Robert; Kluge, Reinhart; Ruth, Peter; Joost, Hans-Georg; Schürmann, Annette
Language:English
Date of Publication (YYYY-MM-DD):2008-11
Title of Journal:American Journal of Physiology / Endocrinology and Metabolism
Journal Abbrev.:Am J Physiol Endocrinol Metab
Volume:295
Start Page:E1084
End Page:E1094
Copyright:© 2008 by the American Physiological Society
Review Status:not specified
Audience:Experts Only
Abstract / Description:Homozygous deletion of the gene of the neuronal glucose transporter GLUT3 (Slc2a3) in mice results in embryonic lethality, whereas heterozygotes (Slc2a3+/–) are viable. Here, we describe the characterization of heterozygous mice with regard to neuronal function, glucose homeostasis, and, since GLUT3 might be a component of the neuronal glucose-sensing mechanism, food intake and energy balance. Levels of GLUT3 mRNA and protein in brain were reduced by 50% in Slc2a3+/– mice. Electrographic features examined by electroencephalographic recordings give evidence for slightly but significantly enhanced cerebrocortical activity in Slc2a3+/– mice. In addition, Slc2a3+/– mice were slightly more sensitive to an acoustic startle stimulus (elevated startle amplitude and reduced prepulse inhibition). However, systemic behavioral testing revealed no other functional abnormalities, e.g., in coordination, reflexes, motor abilities, anxiety, learning, and memory. Furthermore, no differences in body weight, blood glucose, and insulin levels were detected between wild-type and Slc2a3+/– littermates. Food intake as monitored randomly or after intracerebroventricular administration of 2-deoxyglucose or D-glucose, or food choice for carbohydrates/fat was not affected in Slc2a3+/– mice. Taken together, our data indicate that, in contrast to Slc2a1, a single allele of Slc2a3 is sufficient for maintenance of neuronal energy supply, motor abilities, learning and memory, and feeding behavior.
Comment of the Author/Creator:Glucose transporter 3, Knockout, Glucose sensing, Food in take, Neurons and astrocytes
External Publication Status:published
Document Type:Article
Version Comment:Automatic journal name synchronization
Communicated by:Hans Lehrach
Affiliations:MPI für molekulare Genetik
External Affiliations:Department of Pharmacology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal
Research Group Neurogenetics, Leibniz-Institute for Neurobiology, Magdeburg
Department of Pharmacology and Toxicology, Pharmaceutical Institute of the University of Tübingen
Department of Internal Medicine, Division of Endocrinology, Nephrology, Vascular Disease and Clinical Chemistry, University of Tübingen, Tubingen
Centre for Genomic Regulation, Barcelona, Spain
Identifiers:ISSN:0193-1849
DOI:10.1152/ajpendo.90491.2008