Post-heparin lipolytic activity

Reduction of dietary fat intake to 5-20 gm per day significantly lowered the lipolytic activity of post-heparin plasma within 7-10 days from the time of fat restriction. Return to normal values was observed upon restoration of regular fat intake. Extension of these careful studies to a large-scale population is likely to provide a better insight into the correlation between hyperlipemias and post-heparin lipolytic activity in plasma. 

Jones (1974) compiled a list of parameters influenced by polyunsaturated dietary fat compared to eucaloric amounts of saturated dietary fat. A number of the observed effects were regarded as being beneficial. These include Reductions in serum cholesterol level, in triglyceride response to dietary carbohydrate, in blood clotting time and in platelet aggregation, as well as enhancement of post-heparin lipolytic activity, clearance of particulate lipid, and platelet survival time. Other parameters, including those already discussed, could have harmful effects. 

Bobek, P., and Ginter, E., 1978, 8erum triglycerides and post-heparin lipolytic activity in guinea pigs with latent vitamin C deficiency, Experientia 34 1554-1555. 

I. Familial fat-induced hyperlipemia. Plasma creamy Xanthomatosis eruptive, tuberous Hepato-splenomegaly Chylomicrons on any fat intake Post-heparin lipolytic activity low Glucose tolerance normal. 

III. Familial Hyper-/8- and Pre-/8-Lipoproteinemia ( Familial Hypercholesterolemia with Hyper-glyceridemia ). Plasma clear, cloudy or milky Xanthomatosis Tuberous, tendon, plane Arcus Post-heparin lipolytic activity normal Glucose tolerance abnormal Carbohydrate inducible Atheromatosis. 

V. Familial Hyperchylomicronemia and Hyper-Pre-/8-Lipoproteinemia. Plasma creamy AU manifestations seen in type I Post-heparin lipolytic activity low or normal Glucose tolerance abnormal Fat and carbohydrate inducible. 

Lipoprotein lipase (post-heparin lipolytic activity) The enzyme(s), extracted by Korn (1955) from a variety of tissues, particularly adipose tissue, and probably identical with the heparin-induced clearing principle (Hahn 1943), is thought to play a significant role in removal of triglyceride from the circulation. Its release by human liver has only recently been demonstrated (Condon et al. 1965). 

Early research on lipolytic enzymes in cows milk suggested that at least two major lipases were present a plasma lipase in the skim portion and a membrane lipase associated with the milk fat globule membrane (Tarassuk and Frankel, 1957) while later research indicated that there might be up to six different molecular species with lipase activity (Downey and Andrews, 1969). However, work by Korn (1962) showed that milk contained a lipoprotein lipase (EC 3.1.1.34) (LPL) with properties very similar to those of post-heparin plasma, adipose tissue and heart LPLs, particularly the enhancement of its activity on emulsified triglycerides by blood serum lipoproteins. It is now accepted that LPL is the major, if not the only, lipase in cows milk. Its properties have been reviewed by Olivecrona et al. (2003). 

The rate of triglyceride output from the plasma is mainly controlled by the lipoprotein lipase activity of peripheral tissues. Post-heparin plasma lipolytic activity in vitamin-C-deficient guinea pigs decreases considerably. In addition, in some of the animals the response of the plasma lipolytic activity to intravenously administered heparin is also prolonged (45). Similar results have been reported in vitamin-C-deficient baboons (46). 

K. Ono, and L. L. Davis Lipolytic activity of post-heparin plasma in hyperglyceridemia. 

The lipolytic activity of post-heparin plasma is usually assessed by in vitro hydrolysis of a fat emulsion and conveniently expressed as Eq FFA released per ml per minute (Fredrickson et al. 1963). Low values are, as mentioned, quite consistently found in exogenous hyperlipemia and normal levels in endogenous hyperlipemias. Table 1 presents such data from the literature. If the test is performed during periods of fat restriction, low values may be found in normal individuals as well as in endogenous hyperlipemia (Fredrickson et al. 1963, Kuo et al. 1965). 

The diagnosis of primary hyperlipoproteinaemia can usually be confirmed, after exclusion of secondary causes, by an investigation of medical history, analysis (by electrophoresis and determination of blood lipids) of lipoprotein patterns and screening of near relatives. Further ambiguities may be removed by such procedures as the measurement of post-heparin plasma lipolytic activity or assay of LDL receptor function in cultured fibroblasts or blood lymphocytes. 

---