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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 295/5/E1084    most recent 90491.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schmidt, S. Articles by Schürmann, A. Search for Related Content PubMed PubMed Citation Articles by Schmidt, S. Articles by Schürmann, A.

Neuronal functions, feeding behavior, and energy balance in Slc2a3^+/– mice

¹Department of Pharmacology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal; ²Research Group Neurogenetics, Leibniz-Institute for Neurobiology, Magdeburg; ³Department of Pharmacology and Toxicology, Pharmaceutical Institute of the University of Tübingen; ⁴Department of Internal Medicine, Division of Endocrinology, Nephrology, Vascular Disease and Clinical Chemistry, University of Tübingen, Tubingen; ⁵Max Planck Institute for Molecular Genetics, Berlin-Dahlem, Germany; and ⁶Centre for Genomic Regulation, Barcelona, Spain

Submitted 5 June 2008 ; accepted in final form 2 September 2008

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.

glucose transporter 3; knockout; glucose sensing; food in take; neurons and astrocytes

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