Comparison of the triacylglycerol hydrolase activity of human post-heparin plasma lipoprotein lipase and hepatic triacylglycerol lipase. A monolayer study

Lipoprotein lipase activity has been measured in both pre- and post-heparin plasma samples from 6 patients with Primary Type IV hyperlipoproteinaemia and from 6 normal subjects. Post-heparin lipoprotein lipase activity was of the same order in plasma from both groups. Appreciable activity was, however, noted in plasma collected from the Type IV patients prior to administration of heparin. Lipase activity was minimal in such samples from normal individuals.

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Effect of an antimitotic agent (cyclophosphamide) on post-heparin plasma lipoprotein lipase activity in rabbit

Biochemical Pharmacology ◽

10.1016/0006-2952(85)90739-7 ◽

1985 ◽

Vol 34 (19) ◽

pp. 3597-3599 ◽

Cited By ~ 3

Author(s):

Anne-Marie Loudet ◽

Nicole Dousset ◽

Michel Carton ◽

Louis Douste-Blazy

Keyword(s):

Lipoprotein Lipase ◽

Lipase Activity ◽

Plasma Lipoprotein ◽

Lipoprotein Lipase Activity ◽

Antimitotic Agent ◽

Heparin Plasma

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Intralipid administration induces a lipoprotein lipase-like activity in the livers of starved adult rats

Biochemical Journal ◽

10.1042/bj2360273 ◽

1986 ◽

Vol 236 (1) ◽

pp. 273-278 ◽

Cited By ~ 24

Author(s):

S Vilaró ◽

M Reina ◽

I Ramírez ◽

M Llobera

Keyword(s):

Lipoprotein Lipase ◽

Adult Rats ◽

Protamine Sulphate ◽

Triacylglycerol Lipase ◽

Apolipoprotein C ◽

Hepatic Triacylglycerol

The administration of Intralipid to starved adult rats induces the appearance of lipoprotein lipase (LPL)-like activity in the liver, whereas the so-called hepatic triacylglycerol lipase is unaffected. This LPL-like activity is eluted by 1.5 M-NaCl from heparin-Sepharose columns. This partially purified fraction is inhibited by 1.0 M-NaCl (91%) and by 1.0 mg of protamine sulphate/ml (79%), whereas it is stimulated 69-fold by the presence of 8.0 micrograms of apolipoprotein C-II/ml and inhibited by anti-LPL antibodies. We conclude that Intralipid administration induces the appearance of LPL activity in livers of starved adult rats. Its possible origin is discussed.

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Triacylglycerol kinetics in endotoxic rats with suppressed lipoprotein lipase activity

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1987.253.1.e59 ◽

1987 ◽

Vol 253 (1) ◽

pp. E59-E64 ◽

Cited By ~ 4

Author(s):

G. J. Bagby ◽

C. B. Corll ◽

R. R. Martinez

Keyword(s):

Skeletal Muscle ◽

Lipoprotein Lipase ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Metabolic Clearance ◽

Endotoxin Administration ◽

Heparin Plasma ◽

Plasma Ffa ◽

Extrahepatic Tissues ◽

Hepatic Triacylglycerol

Hypertriglyceridemia observed in animals after bacterial endotoxin administration and some forms of sepsis can result from increased hepatic triacylglycerol (TG) output or decreased TG clearance by extrahepatic tissues. To differentiate between these two possibilities, TG and free fatty acid (FFA) kinetics were determined in control and endotoxin-injected (0.1–0.5 mg/100 g) rats 18 h after treatment. Plasma TG and FFA kinetics were assessed by a constant intravenous infusion with [9,10-3H]palmitate-labeled very low-density lipoprotein and [1–14C]palmitate bound to albumin, respectively. In addition, lipoprotein lipase (LPL) activity was determined in heart, skeletal muscle, and adipose tissue as well as in postheparin plasma of functionally hepatectomized, adrenalectomized, and gonadectomized rats. Plasma FFA acid concentrations were slightly increased in endotoxin-treated rats but their turnover did not differ from control. Endotoxin-treated rats had a threefold increase in plasma TG concentrations and decreased heart, skeletal muscle, and post-heparin plasma LPL activity. Plasma TG turnover was decreased, indicating that hypertriglyceridemia was not due to an increased TG output by the liver. Instead, the endotoxin-induced increase in plasma TG concentration was a consequence of the 80% reduction in TG metabolic clearance rate. Thus, suppression of LPL activity in endotoxic animals impairs TG clearance resulting in hypertriglyceridemia. Furthermore, endotoxin administration reduced the delivery of TG-FFA to extrahepatic tissues because hepatic synthesis and secretion of TG from plasma FFA was decreased and LPL activity was suppressed.

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