Zingone, A.Seidel, J.Aloj, L.Caraco, C.Vaquero López, Juan JoséJagoda, E. M.Chou, J. Y.Green, M. V.Eckelman, William C.2010-10-052010-10-052002-08-02Life Sciences, 2002, vol. 71, n. 11, p. 1293-13010024-3205https://hdl.handle.net/10016/9344Monitoring gene therapy of glycogen storage disease type 1a in a mouse model was achieved using [18F]FDG and a dedicated animal scanner. The G6Pase knockout (KO) mice were compared to the same mice after infusion with a recombinant adenovirus containing the murine G6Pase gene (Ad-mG6Pase). Serial images of the same mouse before and after therapy were obtained and compared with wild-type (WT) mice of the same strain to determine the uptake and retention of [18F]FDG in the liver. Image data were acquired from heart, blood pool and liver for twenty minutes after injection of [18F]FDG. The retention of [18F]FDG was lower for the WT mice compared to the KO mice. The mice treated with adenovirus-mediated gene therapy had retention similar to that found in age-matched WT mice. These studies show that FDG can be used to monitor the G6Pase concentration in liver of WT mice as compared to G6Pase KO mice. In these mice, gene therapy returned the liver function to that found in age matched WT controls as measured by the FDG kinetics in the liver compared to that found in age matched wild type controlsapplication/pdfeng© ElsevierGlycogen storage disease type 1aMouse[18F]FDGG6Paseresearch articleBiología y Biomedicina10.1016/S0024-3205(02)01831-3open access1293111301Life Sciences71