Post-heparin plasma hepatic triacylglycerol lipase-catalyzed hydrolysis of tributyrin Effect of lipid interface

Author(s):  
Shirai Kohji ◽  
Matsuoka Nobuo ◽  
Saito Yasushi ◽  
Yoshida Sho
Author(s):  
Shuichi Nozaki ◽  
Iichiro Shimomura ◽  
Tohru Funahashi ◽  
Masakazu Menju ◽  
Masaharu Kubo ◽  
...  

1977 ◽  
Vol 162 (2) ◽  
pp. 367-377 ◽  
Author(s):  
A Nilsson

1. Post-heparin plasma that promoted rapid hydrolysis of about 90% of the triacylglycerol markedly stimulated the uptake or binding of chylomicron cholesteryl ester by suspended hepatocytes. The net hydrolysis of chyle cholesteryl ester after the uptake by the cells was, however, slower than in vivo. 2. The cholesteryl ester uptake in the presence of post-heparin plasma was larger if the cells had been preincubated for 2h. It was inhibited by the presence of colchicine, vinblastine or cycloheximide during the preincubation, and by mild trypsin treatment of the preincubated cells. 3. The results suggested that the anti-microtubular agents, but not cycloheximide, also inhibited the hydrolysis of chyle cholesteryl ester after uptake or binding to the cells. 4. The uptake of isolated chylomicron remnant particles was more efficient than that of native chyle lipoproteins. It was, however, still stimulated by heparin alone and by post-heparin plasma. The heparin-stimulated uptake was markedly decreased if cycloheximide was present during the preincubation period.


1986 ◽  
Vol 236 (1) ◽  
pp. 273-278 ◽  
Author(s):  
S Vilaró ◽  
M Reina ◽  
I Ramírez ◽  
M Llobera

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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