Abstract
Weanling male mice fed rac-1(3)-palmitoyl glycerol at levels of 30 mmoles/100 g of diet or higher develop, within a few days, a severe pulmonary inflammation characterized by marked infiltration of the interstitium by macrophages and few polymorphonuclear leukocytes. This results in severe vascular stasis, alveolar collapse and death of the animal. Adult mice and weanling rats also show the syndrome, but only at higher levels of palmitoyl glycerol. Neither the position of palmitate on the glycerol nor the level of myo-inositol in the diet affects the toxicity of palmitoyl glycerol. Supplementation of the diet with small amounts of linoleate or oleate prevents the toxicity although oleate is less effective than linoleate. There are no differences between mice fed linoleate and those that were not in: the rate of absorption of palmitoyl glycerol, oxidative phosphorylation by liver or heart mitochondria, excretion of carbon dioxide and tissue distribution of radioactivity following gavage of rac-1(3)-[1-14C]palmitoyl glycerol.
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