Nonenzymatic glycosylation of low density lipoproteins in vitro. Effects on cell-interactive properties

Diabetes ◽  
1981 ◽  
Vol 30 (10) ◽  
pp. 875-878 ◽  
Author(s):  
B. Gonen ◽  
J. Baenziger ◽  
G. Schonfeld ◽  
D. Jacobson ◽  
P. Farrar
Keyword(s):  
Low Density Lipoproteins ◽  
Low Density ◽  
Nonenzymatic Glycosylation ◽  
In Vitro Effects

scholarly journals Nonenzymatic Glycosylation of Low Density Lipoproteins In Vitro: Effects on Cell-interactive Properties

Diabetes ◽  
1981 ◽  
Vol 30 (10) ◽  
pp. 875-878 ◽  
Author(s):  
B. Gonen ◽  
J. Baenziger ◽  
G. Schonfeld ◽  
D. Jacobson ◽  
P. Farrar
Keyword(s):  
Low Density Lipoproteins ◽  
Low Density ◽  
Nonenzymatic Glycosylation ◽  
In Vitro Effects

Observations on the in vitro Effects of Chylomicra, Low-Density Lipoproteins and Phospholipids on Human Plasma Euglobulin Lysis

1963 ◽  
Vol 09 (01) ◽  
pp. 164-174 ◽  
Author(s):  
Albert R Pappenhagen ◽  
J. L Koppel ◽  
John H Olwin
Keyword(s):  
Human Plasma ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Inositol ◽  
Plasma Lipoproteins ◽  
Low Density ◽  
Inhibitory Effects ◽  
Soybean Phospholipids ◽  
In Vitro Effects ◽  
Complete Precipitation

SummaryData have been presented on the in vitro effects of human chylomicra, low-density human plasma lipoproteins, and partially purified preparations of various phospholipids on human plasma euglobulin lysis. Euglobulin lysis was found to be accelerated by preparations of mixed soybean phospholipids (aso-lectin), cephalin, phosphatidyl inositol, phophatidyl serine and phosphatidyl ethanolamine. In contrast, it was found to be inhibited by preparations of human chylomicra, low-density human plasma liproproteins and lecithin. Inhibition of euglobulin lysis produced by any of these three agents could be diminished or completely overcome by the simultaneous presence of suitable levels of any one of the accelerating agents. In all cases studied, both inhibitory and accelerating effects were observed to be concentration-dependent. Evidence has been obtained to suggest that in the case of the accelerating agents the observed increased rate of euglobulin lysis is not a direct effect on lysis itself, but rather is due to more complete precipitation of plasminogen in the presence of these substances. On the other hand, it appears that the inhibitory effects observed are not related to the extent of plasminogen precipitation, but are actually true inhibitions of euglobulin lysis. The possible clinical significance of some of these observations has been briefly discussed.

scholarly journals Selective modification of apoB-100 in the oxidation of low density lipoproteins by myeloperoxidase in vitro

1999 ◽  
Vol 40 (4) ◽  
pp. 686-698 ◽  
Author(s):  
Chao-yuh Yang ◽  
Zi-Wei Gu ◽  
Manlan Yang ◽  
Shen-Nan Lin ◽  
Anthony J. Garcia-Prats ◽  
...  
Keyword(s):  
Low Density Lipoproteins ◽  
Low Density

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.

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