PT - JOURNAL ARTICLE AU - Koon-Pong Wong AU - Xiaoli Zhang AU - Wei Sha AU - Sung-Cheng Huang TI - Effects of elevated plasma glucose levels on FDG rate constants in mouse brain DP - 2011 May 01 TA - Journal of Nuclear Medicine PG - 2060--2060 VI - 52 IP - supplement 1 4099 - http://jnm.snmjournals.org/content/52/supplement_1/2060.short 4100 - http://jnm.snmjournals.org/content/52/supplement_1/2060.full SO - J Nucl Med2011 May 01; 52 AB - 2060 Objectives To investigate the impact of variations in plasma glucose levels on the FDG rate constants in mouse brain using intravenous (IV) and intraperitoneal (IP) injections. Methods Dynamic PET scans were performed for 60 min on 23 C57BL/6 isoflurane anesthetized male mice (23.8±3.1 g) after IV (14.2±3.8 MBq; n=11) or IP (10.5±0.8 MBq; n=12) injection of FDG. Five and 6 mice were fasted overnight (18±2 h) in IV and IP groups, respectively, and the rest were fed ad libitum. Serial blood samples were drawn from the femoral artery to measure FDG and plasma glucose concentrations. Image data were reconstructed using filtered backprojection with CT-based attenuation correction. Volume of interest was assigned to the brain and the tissue time-activity curve (TAC) was then calculated and fitted to the FDG model to derive the rate constant parameters (K1, k2, k3 and k4) and cerebral metabolic rate of glucose (CMRglc), assuming 3% of blood volume in the brain and a lumped constant of 0.6. Results The rate constant for the transport of FDG from plasma to brain (K1) and the phosphorylation rate constant (k3) were found to decline with increasing plasma glucose levels (K1: R=-0.592, P<0.01; k3: R=-0.494, P<0.05). Conversely, the rate constant for the efflux from brain to plasma had no correlation with the plasma glucose levels (R=-0.138, P=NS). Mean CMRglc calculated from the rate constants remained relatively constant, independent of plasma glucose levels. Conclusions Elevated plasma glucose levels caused down-regulation of both FDG transport from plasma to brain and phosphorylation in brain tissue, but the cerebral metabolic rate of glucose of the whole brain remained unchanged. Research Support NIBIB grant R01-EB00194