title: Neuronal functions, feeding behavior, and energy balance in Slc2a3+/- mice.
abstract: 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.
authors.affiliation: Department of Pharmacology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Schmidt
authors.forename: Miriam
authors.initials: M
authors.lastname: Richter
authors.forename: Dirk
authors.initials: D
authors.lastname: Montag
authors.forename: Tina
authors.initials: T
authors.lastname: Sartorius
authors.forename: Verena
authors.initials: V
authors.lastname: Gawlik
authors.forename: Anita M
authors.initials: AM
authors.lastname: Hennige
authors.forename: Stephan
authors.initials: S
authors.lastname: Scherneck
authors.forename: Heinz
authors.initials: H
authors.lastname: Himmelbauer
authors.forename: Stefan Z
authors.initials: SZ
authors.lastname: Lutz
authors.forename: Robert
authors.initials: R
authors.lastname: Augustin
authors.forename: Reinhart
authors.initials: R
authors.lastname: Kluge
authors.forename: Peter
authors.initials: P
authors.lastname: Ruth
authors.forename: Hans-Georg
authors.initials: HG
authors.lastname: Joost
authors.forename: Annette
authors.initials: A
authors.lastname: Schürmann
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D004041:Dietary Fats / Q000008:administration & dosage / Q000494:pharmacology; D004435:Eating / Q000187:drug effects; D004569:Electroencephalography; D004734:Energy Metabolism / Q000502:physiology*; D005247:Feeding Behavior / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics; D051274:Glucose Transporter Type 3 / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D006579:Heterozygote; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009424:Nervous System Physiological Phenomena
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D051246:Glucose Transport Proteins, Facilitative; D051274:Glucose Transporter Type 3; D007328:Insulin; D008055:Lipids; C495689:Slc2a3 protein, mouse; D019344:Lactic Acid