Disseminated fat necrosis can be produced by intraperitoneal injection of porcine pancreatic lipase. They get detecable by intravital staining with Phosphine 3R about 15 min after injection. The earliest fine structural findings are spotty destruction of the pinocytic invaginations and vesicles, combined with alterations of the cell membrane. Later there is a complete destruction and disintegration of the cytoplasm and its organels as well as the nucleus, whereas the cell membrane partly remains visible. At the same time the central lipid droplet shows cloudy disintegration and clumping as well as cristalline and granular structures. In the beginning the necrosis is limited to single cells. Later the adjacent fat cells also undergo necrosis, even when the applicated lipase has been removed after 30 min. In light microscopic studies fat necrosis are detectable 30 min after the application of lipase. During the first 48 hours they get demarcated by leucocytes. In the following days resorption and organisation take place. Lipolytic drugs facilitate the development of fat necrosis, whereas antilipolytic drugs inhibit it. In starvation the number of fat necrosis rises, after feeding it decreases. In the diurnal rhythm there is a maximum after midnight and a minimum in the early afternoon. The results support the hypothesis that pancreatic lipase only attacks fat cells, which are lipolytically active.