1. Lipoprotein lipase was separated from normal human post-heparin plasma by affinity chromatography and assayed with a 14 C-labelled triolein emulsion. No enzyme activity was detected unless whole serum was included in the assay as a source of cofactor, apolipoprotein C-II. 2. After a 10 h fast, serum obtained from 46 normal subjects, eight patients with hypertriglyceridaemia but normal renal function, patients with chronic renal failure (24 undialysed, 20 haemodialysed) and 14 recipients of renal allografts, was added to incubation medium for the assay of lipoprotein lipase to determine the maximum activation of the enzyme. 3. When serum was obtained from normal subjects, maximum activation of the enzyme correlated positively with the concentration of triacylglycerol in the sample. Neither sex nor age had a significant effect on the maximum activation achieved by serum from control subjects. 4. The maximum lipoprotein lipase-activating capacity of serum from uraemic and transplant patients was significantly reduced when compared with serum from healthy controls or from the non-uraemic hypertriglyceridaemic patients. 5. Maximum enzyme activation correlated positively with high-density lipoprotein cholesterol in serum from undialysed patients, but did not correlate positively with total serum triacylglycerols in any of the patient groups. Only in transplant recipients was there a significant inverse relationship between serum creatinine concentrations and maximum enzyme activation. 6. Although lipoprotein lipase activation was impaired in uraemic subjects and renal transplant recipients, this appeared to be due more to the presence of an inhibitor than to cofactor deficiency.
1. Post-heparin plasma from normal subjects, patients with chronic renal failure and recipients of renal allografts were subjected to affinity chromatography on heparin—agarose (Sepharose 4B) columns to separate two fractions representing hepatic lipase and lipoprotein lipase respectively. 2. The optimum conditions for assay of each fraction were determined for both normal and uraemic plasma. 3. Normal males had activities of hepatic lipase which were higher, and activities of lipoprotein lipase which were lower, than normal females. There was no consistent relationship to age for either enzyme. 4. Thirty patients with chronic renal failure untreated by dialysis had significantly elevated serum triacylglycerol concentrations, and significantly lowered lipoprotein lipase activities when compared with control groups with similar ages for each sex. However, only in uraemic males was hepatic lipase activity significantly reduced. 5. In a study of female patients with chronic renal failure, there were no significant differences in activities of hepatic lipase or lipoprotein lipase or concentrations of serum triacylglycerols between eight patients receiving dialysis treatment and eight untreated by dialysis. 6. Although serum triacylglycerol concentrations were raised in the group of 15 renal transplant recipients, lipase activities were not diminished. The only significant change was elevation of hepatic lipase activity in female graft recipients. 7. No relationship was found between the enzyme activities and fasting serum triacylglycerol concentrations in any group. However, there was a weak inverse correlation between serum creatinine and hepatic lipase in female patients from both renal failure and transplant groups. 8. Similar results were obtained when the enzymes were assayed with, as substrate, a laboratory-prepared emulsion of 14 C-labelled triolein in water with soya-bean lecithin as emulsifier, or commercially prepared soya-bean oil in water, emulsified with egg-yolk lecithin and containing glycerol (Intralipid).