Total plasma lipase activity comprises the activities of three endothelial lipases, lipoprotein lipase (LPL) from the peripheral circulation, hepatic lipase (HL) from the microcirculation of the liver and the newly discovered endothelial lipase (EL) of unknown significance. LPL hydrolyses chylomicron- and VLDL- triglycerides to di and mono-glycerides and free fatty acids in the capillaries of skeletal muscle and adipose tissue. The free fatty acids are used either for resynthesis of triglycerides subsequently stored in adipose tissue, or as a source of energy. HL has similar actions to LPL on smaller lipoprotein particles and EL has more phospholipid lipase activity than triglyceride lipase activity.
LPL and HL are adsorbed to capillary endothelial surface oligosaccharides and do not normally circulate in the blood, but may be released by heparin and measured in plasma. This forms the basis of the test for post-heparin lipolytic activities of total and hepatic lipase.
Low LPL activity is associated with gross hypertriglyceridaemia. It may be due to decreased activation, to a rare mutation of the LPL gene, or to a deficiency of apo C-II, an activator for LPL. Apo C-III and apo C-1 inhibit LPL activity. Apoprotein C-II and C-III can be measured by immunoturbidimetry or by gel electrophoresis, using isoelectric focusing followed by protein staining and quantitation. It is usual to measure apo C-II at the same time as LPL activity.
Clinical indications:
Measurement is useful when a decrease in LPL activity in plasma is suspected to underlie a gross hypertriglyceridaemia and the E2/2 phenotype has been excluded. Low LPL activity may result from a relative deficiency of LPL or its co-factor apo C-II. Type I hyperlipidaemia, a rare genetic condition, results from a genetic deletion of the LPL or C-II gene and presents as a severe hypertriglyceridaemia (chylomicronaemia).
Approximate reference range:
LPL: 2-12 µmol fatty acid/ml/hr
Type I hyperlipidaemia < 0.2 µmol fatty acid/ml/hr
Apo CII: 1.9 – 4.1 mg/dl
These ranges are method dependent. Please refer to laboratory report.
Patient preparation:
The test should not be performed in subjects who have a sensitivity to heparin, are taking aspirin, have a history of bleeding diathesis, proliferative retinopathy, or CVA, or have rheumatic fever or a peptic ulcer. The patient should have fasted overnight, and refrained from alcohol in the previous 24 hours and heavy exercise in the previous 48 hours.
Sample details:
Detailed sample collection protocols should be obtained from the appropriate laboratory.
Plasma lipase activities are measured in post-heparin plasma (PHP).
Samples must be transported to laboratory on dry ice as soon as possible – analysis should be within 7 days
Information required:
Age, sex, Hospital/NHS No.
Medication
Plasma triglyceride and HDL-cholesterol
Reference:
Brunzell JD, Deeb SS (2001) Familial lipoprotein lipase deficiency, apo CII deficiency and hepatic lipase deficiency. In: Scriver CR, Beaudet AL, Sly WS, Valle D (eds) The Metabolic and Molecular Bases of Inherited Disease, 8 ed. McGraw-Hill, New York, pp2789-2816.
Otarod JK, Goldberg IJ. Lipoprotein lipase and its role in regulation of plasma lipoproteins and cardiac risk. Curr Atheroscler Rep 2004; 6(5):335-342
Jansen H. Hepatic lipase: friend or foe and under what circumstances? Curr Atheroscler Rep 2004; 6(5):343-347.
Henderson AD, Richmond W, Elkeles RS. Hepatic and lipoprotein lipases selectively assayed in postheparin plasma. Clin Chem 1993; 39(2):218-223
Watson TD, Tan CE, McConnell M, Clegg SK, Squires LF, Packard CJ. Measurement and physiological significance of lipoprotein and hepatic lipase activities in preheparin plasma. Clin Chem 1995; 41(3): 405-412.