Discussion and summary The hypothesis of an impaired transport of neutral fat from the liver of fasting choline deficient animals is sustained by the isotopic data showing a persistently high activity in the liver neutral fat and low plasma triglyceride activity. However, in accord with the in vitro findings of Artom(8), a decreased oxidation of the labeled fatty acids in the liver in choline deficiency might also be a factor of importance for the accumulation of fatty acids. In the refed animals in which oxidation is suppressed to a minimum, there is little difference in rate of disappearance of labeled fatty acids from the livers in both types of experiment. These curves also are rather similar to the liver activity curve in the fasting choline deficient rats. This can also be so expressed that the liver disappearance curves are rather similar for the choline deficient rats whether they have been starved or refed. The specific activity relationship between liver and plasma triglycerides in the choline deficient animals indicates that only a small fraction of the total liver triglycerides is in rapid equilibrium with the plasma triglycerides and that this “actively metabolizing pool”(9) of liver triglycerides is not increased in proportion to the total triglyceride content of the liver in the choline deficient animals. Most of the liver triglycerides which pile up in the livers of choline deficient rats therefore are not easily available for metabolism. The rapid disappearance of neutral fat from the livers of the choline deficient animals on refeeding is not consistent with known data on lipid turnover rates in liver and blood plasma of the rat. The rapid changes in lipid composition and distribution caused by overnight refeeding of control animals maintained on the synthetic diet supplemented with choline has been reproduced in animals reared on ordinary pellet diet.