1. Post-heparin lipolytic activity was determined in the plasma of thirteen patients with malabsorption and fourteen healthy controls, with a coconut-oil emulsion (Ediol), triolein and very-low-density lipoprotein (VLDL) as substrates.
2. Significantly lower post-heparin lipolytic activities were found in malabsorbers, whichever substrate was used. Lipolysis was inhibited by 0–5 mol/l sodium chloride when VLDL was the substrate but not when the two artificial substrates were used.
3. Plasma post-heparin lipolytic activities rose in malabsorbers after therapeutic doses of an intravenous fat emulsion (Intralipid), especially when assayed against VLDL.
4. The abnormal fatty acid composition of VLDL from malabsorbers did not affect its properties as a substrate for lipolysis by post-heparin plasma from normal subjects.
5. These findings support the concept that PHLA is heterogeneous in origin. They also suggest that if reduced clearance is a factor in the hypertriglyceridaemia sometimes seen in malabsorption, it is due to an enzyme deficit rather than a substrate defect.