Glucose transport rates are estimated non-invasively in physiological and pathological states by kinetic imaging using positron emission tomography (PET). The glucose analog most often used is ¹⁸F labeled 2-fluoro-2-deoxy-D-glucose (2FDG). It is poorly transported by intestine and kidney compared to glucose. We examined 6-fluoro-6-deoxy-D-glucose (6FDG) as a tracer of glucose transport. Lacking a hydroxyl at its 6^th position 6FDG cannot be phosphorylated as 2FDG. Prior studies have shown 6FDG competes with glucose for transport in yeast and is actively transported by intestine. We found insulin stimulated 6FDG uptake 1.6-fold in 3T3-L1 adipocytes and azide stimulated the uptake 3.7-fold in Clone 9 cells. Stimulations of 3-0-methyl D-glucose, uptake was similar and the uptakes were inhibited by cyclochalasin B. Glucose transport is by Glut 1 and Glut 4 transporters which cytochalasin B inhibits. Rats were imaged in vivo by PET using 6¹⁸FDG. There was no excretion of ¹⁸F into the urinary bladder unless phlorizin, a renal transport inhibitor, was also injected. ¹⁸F activity in brain, liver, and heart reached a constant level in keeping with the 6FDG being distributed in body water. In contrast, ¹⁸F from 2¹⁸FDG was excreted and ¹⁸F activity increased in heart and brain in accord with 2¹⁸FDG -6-P accumulation. In conclusion: 6FDG is actively transported by kidney and intestine and is insulin responsive. In trace quantity it appears to be distributed unchanged in body water. These results support for 6FDG as a valid tracer of glucose transport.