Because many or most lipid-laden foam cells in atheromas and in xanthomas derive from macrophages, it is important to understand how they accumulate lipids and how they can divest themselves of lipids. The mobilization of stored triglycerides from macrophages was studied in cell cultures. Mouse resident peritoneal macrophages and J774 macrophages increased their triglyceride content six-to tenfold during a 24hour incubation with free fatty acids complexed to albumin. Subsequent incubation in

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... sh medium containing free fatty acid-poor albumin was accompanied by a fall in cell triglyceride content (50% in 20 hours) and a corresponding increase in mediumfree fatty acid. Release of free fatty acid was linear as a function of time, provided fresh medium was added hourly. When medium was not changed, release rates fell off rapidly, probably due to re-uptake of released free fatty acid. Chloroquine did not affect the rate of free fatty acid release. The results suggest that macrophages-foam cells can reduce their triglyceride stores via the action of a nonlysosomal (presumably cytoplasmic) neutral triglyceride lipase. (Arteriosclerosis 4:630-635, November/December 1984) T he lipid accumulating in xanthomas and in early atherosclerotic lesions is largely found in "foam cells" in the form of multiple, large fat droplets. Several lines of evidence indicate that many or most such cells represent monocyte-macrophages. 1 -4 In the case of eruptive xanthomas associated with hyperchylomicronemia, the lesions can appear over a relatively short time and disappear almost as rapidly, 5 presumably because these cells have the capacity to metabolize or mobilize the stored lipids rapidly. The possibility that the cells move out of the lesions back into the circulation should also be considered, but it seems unlikely that this can oc-