scholarly journals Effects of Insulin and Glucose on Very Low Density Lipoprotein Triglyceride Secretion by Cultured Rat Hepatocytes

1982 ◽  
Vol 70 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Paul N. Durrington ◽  
Roger S. Newton ◽  
David B. Weinstein ◽  
Daniel Steinberg
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Rat Hepatocytes ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Triglyceride Secretion ◽  
Cultured Rat Hepatocytes

scholarly journals Calcium-antagonists inhibit secretion of very-low-density lipoprotein from cultured rat hepatocytes

1987 ◽  
Vol 247 (2) ◽  
pp. 433-439 ◽  
Author(s):  
J O Nossen ◽  
A C Rustan ◽  
C A Drevon
Keyword(s):  
Calcium Antagonists ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Rat Hepatocytes ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Triacylglycerol Synthesis ◽  
Cultured Rat Hepatocytes

The effects of different calcium-antagonists on secretion of very-low-density lipoprotein (VLDL) from cultured rat hepatocytes were examined. Verapamil (an inhibitor of voltage-dependent calcium channels) and EGTA (a calcium chelator) decreased VLDL-triacylglycerol secretion in a concentration-dependent manner, with maximum inhibition (about 90%) at 0.2 mM-verapamil and 5 mM-EGTA. Inorganic calcium-antagonists such as lanthanum, nickel, cobalt and manganese decreased secretion of VLDL-triacylglycerol by 55-95%, whereas the calcium-agonist barium did not affect secretion. Inhibition of VLDL-triacylglycerol secretion appeared within 30 min, without inhibition of triacylglycerol synthesis. Pulse-chase experiments revealed that verapamil and cobalt inhibited the secretory pathway itself. Cobalt showed a concentration-dependent inhibition of VLDL-triacylglycerol secretion, with maximal effect at 8 mM. Although inhibition by cobalt was not completely reversible, Trypan Blue exclusion and lactate dehydrogenase leakage indicated that the hepatocytes were not injured by cobalt or any of the other calcium-antagonists tested. Inhibition of protein synthesis by cycloheximide did not affect triacylglycerol secretion (up to 2 h), and the observed effects were therefore probably not due to impaired production of apolipoproteins. Taken together, these results suggest that calcium is important for secretion of VLDL particles.

scholarly journals Very low density lipoprotein synthesis and secretion by cultured rat hepatocytes.

1979 ◽  
Vol 254 (6) ◽  
pp. 2010-2016 ◽  
Author(s):  
R.A. Davis ◽  
S.C. Engelhorn ◽  
S.H. Pangburn ◽  
D.B. Weinstein ◽  
D. Steinberg
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Rat Hepatocytes ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Synthesis ◽  
Cultured Rat Hepatocytes

scholarly journals Lysophosphatidylcholine metabolism and lipoprotein secretion by cultured rat hepatocytes deficient in choline

1989 ◽  
Vol 260 (1) ◽  
pp. 207-214 ◽  
Author(s):  
B S Robinson ◽  
Z Yao ◽  
D J Baisted ◽  
D E Vance
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Rat Hepatocytes ◽  
Cellular Protein ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Phosphatidylcholine Biosynthesis ◽  
Cultured Rat Hepatocytes ◽  
Phosphatidylcholine Synthesis

The metabolism of lysophosphatidylcholine was studied in cultured rat hepatocytes deficient in choline and methionine. Even though the cells were defective in phosphatidylcholine biosynthesis, the albumin-stimulated release of lysophosphatidylcholine (1.9 nmol/h per mg of cellular protein) was similar to that in hepatocytes supplemented with choline. Albumin also stimulated (1.4-fold) the release of phosphatidylcholine from the deficient cells. The extra phosphatidylcholine and lysophosphatidylcholine in the medium were largely recovered in the albumin fraction (density greater than 1.18 g/ml), suggesting that albumin released these lipids from hepatocytes because of binding to this protein. The secretion of glycerophosphocholine was decreased by about 40% by the addition of albumin. When choline-deficient hepatocytes were supplemented with lysophosphatidylcholine, it was transported into the cells and mainly acylated to form phosphatidylcholine, which increased in mass by 30-35% in the first 4 h of incubation. Lysophosphatidylcholine was shown to be as effective as choline in restoring the secretion of very-low-density lipoproteins to normal amounts, as judged by the secretion of triacylglycerol, phosphatidylcholine and the apolipoproteins associated with very-low-density lipoproteins. Thus phosphatidylcholine synthesis via reacylation of lysophosphatidylcholine, via the CDP-choline pathway or via methylation of phosphatidylethanolamine, will satisfy the requirements for secretion of very-low-density lipoprotein from hepatocytes.

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