Quinidine and propranolol binding to very low and low density lipoproteins of human plasma

1984 ◽  
Vol 62 (5) ◽  
pp. 589-595 ◽  
Author(s):  
A. Ho Ngoc-Ta Trung ◽  
G. Sirois
Keyword(s):  
Binding Sites ◽  
Phosphate Buffer ◽  
In Vitro Study ◽  
Low Density Lipoproteins ◽  
Drug Binding ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Vldl Fraction ◽  
Scatchard Plots

The interaction of quinidine (Q) and propranolol (P) with human very low density lipoproteins (VLDL) and low density lipoproteins (LDL) was determined by ultrafiltration in phosphate buffer (pH 7.4) for Q and in phosphate and Tris buffers (pH 7.4–7.5) for P, respectively. The Scatchard plots of Q are curved and were best described by a model assuming two independent classes of binding sites on lipoproteins. When working with P, the Scatchard plots were also nonlinear, but positive cooperativity was observed for the VLDL fraction in phosphate buffer and apparently also for the LDL fraction in Tris buffer. These nonlinear curves were described by the model used for Q, excluding any data falling in the cooperating region. The binding parameters, primary (K1) and secondary (K2) affinity constants and the number of sites in each class of independent binding sites, were generated by a computer program. The results of this in vitro study suggest that drug binding (and possibly distribution) to lipoproteins may be affected by the nature and concentration of some ions present in serum.

scholarly journals Catabolism of human very low density lipoproteins in vitro: a fluorescent phospholipid method for monitoring lipolysis.

1981 ◽  
Vol 22 (2) ◽  
pp. 382-386
Author(s):  
M R Taskinen ◽  
J D Johnson ◽  
M L Kashyap ◽  
K Shirai ◽  
C J Glueck ◽  
...  
Keyword(s):  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins

scholarly journals Sirtuin 3 Restores Synthesis and Secretion of Very Low-Density Lipoproteins in Cow Hepatocytes Challenged with Nonesterified Fatty Acids In Vitro

2021 ◽  
Vol 8 (7) ◽  
pp. 121
Author(s):  
Dongmei Xing ◽  
Baogen Wang ◽  
Hong Lu ◽  
Tao Peng ◽  
Jianming Su ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dairy Cows ◽  
Low Density Lipoproteins ◽  
Mrna Abundance ◽  
Low Density ◽  
Sirtuin 3 ◽  
Very Low Density Lipoproteins ◽  
Nonesterified Fatty Acids ◽  
Tag Accumulation

Fatty liver is closely associated with elevated concentrations of nonesterified fatty acids (NEFA) and a low level of very low-density lipoproteins (VLDL) in blood of dairy cows. High NEFA inhibit the VLDL synthesis and assembly, and cause hepatic triacylglycerol (TAG) deposition. Sirtuin 3 (SIRT3), a mitochondrial deacetylase, antagonizes NEFA-induced TAG accumulation through modulating expressions of fatty acid synthesis and oxidation genes in cow hepatocytes. However, the role of SIRT3 in the VLDL synthesis and assembly was largely unknown. Here we aimed to test whether SIRT3 would recover the synthesis and assembly of VLDL in cow hepatocytes induced by high NEFA. Primary cow hepatocytes were isolated from 3 Holstein cows. Hepatocytes were infected with SIRT3 overexpression adenovirus (Ad-SIRT3), SIRT3-short interfering (si) RNA, or first infected with Ad-SIRT3 and then incubated with 1.0 mM NEFA (Ad-SIRT3 + NEFA). Expressions of key genes in VLDL synthesis and the VLDL contents in cell culture supernatants were measured. SIRT3 overexpression significantly increased the mRNA abundance of microsomal triglyceride transfer protein (MTP), apolipoprotein B100 (ApoB100) and ApoE (p < 0.01), and raised VLDL contents in the supernatants (p < 0.01). However, SIRT3 silencing displayed a reverse effect in comparison to SIRT3 overexpression. Compared with NEFA treatment alone, the Ad-SIRT3 + NEFA significantly upregulated the mRNA abundance of MTP, ApoB100 and ApoE (p < 0.01), and increased VLDL contents in the supernatants (p < 0.01). Our data demonstrated that SIRT3 restored the synthesis and assembly of VLDL in cow hepatocytes challenged with NEFA, providing an in vitro basis for further investigations testing its feasibility against hepatic TAG accumulation in dairy cows during the perinatal period.

scholarly journals Decreased Susceptibility of Glycated Very Low Density Lipoproteins to Lipoprotein Lipase in vitro and Prevention by Glutathione

1994 ◽  
Vol 1 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Shuichi Saheki ◽  
Kohji Shishino ◽  
Yasuo Hitsumoto ◽  
Mitsuharu Murase ◽  
Nozomu Takeuchi ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins

The disappearance rate of human versus rat intermediate density lipoproteins from rat liver perfusion

1991 ◽  
Vol 69 (8) ◽  
pp. 537-543 ◽  
Author(s):  
Robert Dupras ◽  
Louise Brissette ◽  
Paul D. Roach ◽  
Sylvain Begin ◽  
André Tremblay ◽  
...  
Keyword(s):  
Liver Perfusion ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Disappearance Rate ◽  
Very Low Density Lipoproteins ◽  
Rat Liver Perfusion ◽  
Heparin Plasma ◽  
Intermediate Density

The aim of this work was to compare the disappearance rate of human and rat intermediate density lipoproteins (IDL) using the rat liver perfusion system. Human and rat IDL were produced in vitro by incubating human or rat very low density lipoproteins (VLDL) with either rat post-heparin plasma (method I) or a resolubilized isopropanol precipitate of rat post-heparin plasma (method II). With both methods, the degree of triacylglycerol lipolysis was approximately 55%. The different preparations of IDL were labelled with 125I and added to perfusates of rat livers. The disappearance rates of 125I-labelled IDL were monitored by measuring the radioactivity associated with apolipoprotein (apo) B in the perfusate during a 15-min period. Both human and rat IDL prepared with method I had an increased apoE to apoC ratio as compared with their native counterparts. Furthermore, human IDL had a significantly higher apoE to apoC ratio than rat IDL. However, when IDL were produced in the absence of exchangeable apolipoproteins (method II), no change in the apoE to apoC ratios was observed for the transformation of VLDL to IDL and the ratios were similar for human and rat IDL. Despite these differences, human IDL were always removed at a lower rate than rat IDL. The only striking difference between the two types of IDL made by method II was that the apoB100 to apoB48 ratio was considerably higher in human than in rat IDL. These results suggest that the apoB100 to apoB48 ratio is likely to be responsible for the observed differences in liver uptake between rat and human IDL.Key words: very low density lipoproteins, intermediate density lipoproteins, low density lipoproteins, hepatic lipoprotein receptors, intermediate density lipoprotein uptake, in vitro lipolysis, very low density lipoprotein remnants, apolipoproteins.

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