Hongxia Lei1, 2, Frederic Preitner3, Bernard Thorens3, Rolf Gruetter1, 3
1Ecole Polytechnique Fdrale de Lausanne, Lausanne, Vaud, Switzerland; 2University of Geneva , Geneva, Switzerland; 3University of Lausanne, Lausanne, Vaud, Switzerland
Glucose transporter isoform 2 (GLUT2), one of GLUTs, has been suggested to involve in the glucose sensor mechanism not only in pancreas but also in brain. How GLUT2 affect brain metabolism remained not well understood. We hypothesize that lacking GLUT2 in brain could interfere brain glucose sensor mechanism thus attenuate brain metabolism. In present study, we explored both localized 1H MRS and CASL on GLUT2-/- mice and their countertypes at 9.4T. While at euglyemia and under isoflurane anesthesia, metabolic alterations were consistently observed in hippocampus of GLUT2-/- mice, such as elevated blood flow and selected metabolites including taurine, myo-inositol and total creatine. The observations suggested that GLUT2 indeed affect brain tissue, i.e. hippocampus, substantially.