The release of lipoproteins by rat liver slices

1969 ◽  
Vol 47 (1) ◽  
pp. 65-69 ◽  
Author(s):  
A. I. Kook ◽  
D. Rubinstein
Keyword(s):  
Fatty Acids ◽  
Neutral Lipid ◽  
Incubation Medium ◽  
Ringer Solution ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Liver Slices ◽  
Lipid Moiety ◽  
Protein Moiety

The release of the lipid and protein moieties of lipoproteins by liver slices from rats charged in vivo with palmitate-9,10-3H and leucine-1-14C was followed. The replacement of Ringer solution as the incubation medium by serum resulted in an increase in the release of the labelled lipid moiety but had no effect on the radioactivity of the protein moiety. Analysis of the lipoproteins indicated that serum had no effect on the radioactivity of the neutral lipid in the lipoprotein of d < 1.063 or β-lipoproteins prepared by ultracentrifugation or heparin precipitation, respectively. However, the lipoprotein of d < 1.063 released into serum contained considerable amounts of labelled phospholipids and fatty acids which were not present in the β-lipoprotein precipitated by heparin or in the low density lipoproteins prepared by either procedure following incubation in Ringer solution. Following incubation of the slices in serum, but not in Ringer solution, the lipoprotein having d > 1.063 and the supernatant of the heparin precipitate contained considerable amounts of labelled phospholipid. It is concluded that serum may contain a lipoprotein capable of combining with liver phospholipids and that ultracentrifugation results in the separation of low density lipoproteins containing excess lipid.

The metabolism of d < 1.0631 lipoprotein in the rat

1969 ◽  
Vol 47 (11) ◽  
pp. 1033-1041 ◽  
Author(s):  
J. T. Buckley ◽  
A. I. Kook ◽  
D. Rubinstein
Keyword(s):  
Fatty Acids ◽  
Neutral Lipid ◽  
Neutral Lipids ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Perfused Liver ◽  
Phospholipid Synthesis ◽  
Lipid Moiety ◽  
Protein Moiety

The metabolism of d < 1.063 lipoproteins of the rat was studied in perfused liver and in vivo. Perfused livers were used to label the lipoproteins in the lipid and protein moieties with palmitate-3H and leucine-14C, respectively. The lipid moiety of the isolated doubly labelled lipoprotein was removed more rapidly than the protein moiety by perfused liver. The decrease in the ratio of the lipid-3H to protein-14C in the perfusate lipoproteins occurred in three fractions of the very low density as well as the low density lipoproteins but was not accompanied by a shift of the protein among these lipoproteins. These data are consistent with an exchange of neutral lipid between the perfusate lipoproteins and the liver. The uptake and exchange of the lipid moiety of intravenously administered, doubly labelled lipoproteins apparently also occur in vivo, where the decrease in 3H/14C ratio is more rapid.Lipoprotein neutral lipid, labelled with palmitate-3H and glycerol-14C, was taken up by the perfused liver primarily in the unhydrolyzed state, as indicated by a constant 3H/14C ratio. A portion of the neutral lipid was then hydrolyzed and the resulting fatty acids were used preferentially for the synthesis of phospholipids. Unlabelled glycerol diluted the glycerol-14C in the phospholipids further increasing the 3H/14C ratio, but had no effect on this ratio in neutral lipids. It is concluded that the neutral lipid of the d < 1.063 lipoproteins can be exchanged with a small lipid pool in the liver which provides fatty acids for phospholipid synthesis.

Low-Density Lipoproteins in Patients Homozygous for Familial Hyperbetalipoproteinaemia

1976 ◽  
Vol 51 (3) ◽  
pp. 221-231
Author(s):  
G. L. Mills ◽  
C. E. Taylaur ◽  
M. J. Chapman
Keyword(s):  
Fatty Acids ◽  
Molecular Weight ◽  
Healthy Subjects ◽  
Diffusion Constant ◽  
Physicochemical Analysis ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Flotation Rate ◽  
Protein Moiety ◽  
And Diffusion

1. The low-density lipoproteins (LDL; density 1·007–1·063 g/ml) from two patients homozygous for familial hyperbetalipoproteinaemia have been submitted to chemical and physicochemical analysis. 2. The presence of an anomalous lipoprotein with a low proportion of triglyceride and a raised proportion of cholesterol has been confirmed. 3. In one patient, this lipoprotein accounted for about 85% of the LDL, but in the second, the amount varied from about 85% to a point at which it could not be detected among the coexisting normal lipoproteins. 4. The protein moiety of this anomalous LDL has effectively the same amino acid composition as that derived from the LDL of healthy subjects. 5. The proportions of carbohydrate, phospholipid and fatty acids could not be reliably distinguished from those of normal LDL. 6. The molecular weight and diffusion constant of the abnormal lipoprotein, even in the purest preparation, were close to the values determined for normal LDL of similar flotation rate.

LIPOLYSIS IN VERY LOW DENSITY LIPOPROTEINS - LOCUS MINORIS RESISTENTIAE - IN THE PATHOGENESIS OF HYPERTRIGLYCERIDEMIA. POSITIVE EFFECTS OF DIET, POLYENIC FATTY ACIDS, STATINS AND FIBRATES

2019 ◽  
Vol 64 (7) ◽  
pp. 388-396
Author(s):  
V. N. Titov ◽  
T. A. Rozhkova ◽  
V. A. Amelyshkina ◽  
V. V. Kukharchuk ◽  
M. Yu. Kotlovsky ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Biological Effects ◽  
Low Density Lipoproteins ◽  
Moderate Increase ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Positive Effects ◽  
Trans Fa ◽  
Prevention Of Atherosclerosis

Inhibition of hydrolysis of palmitic and oleic triglycedires (TG) in very low density lipoproteins (VLDL), slow formation of active apoВ-100 conformation, blockade of апоЕ/В-100 ligand formation in VLDL and their reduced uptake by insulin-dependent cells cause hypertriglyceridemia (HTG). Palmitic and oleic VLDL (>80% total VLDL) are not converted in low density lipoproteins (LDL). Atherosclerosis is not an alimentary deficiency of polyenic fatty acids (PFA), but results from low in vivo bioavailability of PFA in LDL against the background of high dietary palmitic FA and palmitic LDL. Plasma PFA content and cellular PFA deficiency are as high as LDL cholesterol (CL). Primary prevention of atherosclerosis should be based on a decrease in dietary content of palmitic saturated FA, trans FA and a moderate increase in PFA. It seems highly unlikely that the xeobiotics statins, fibrates and probucol produce pleiotropic biological effects in vivo. These effects are brought about by phylogenetically early humoral mediators eicosanoids: prostacyclins, prostaglandins, thromboxanes, leukotrienes, and resolvins. It is reasonable to suggest that all preparations which act according to the same algorithm activate TG hydrolysis in VLDL and normalize cellular uptake of PFA in linoleic and linolenic LDL via apoВ-100 endocytosis. Atherosclerosis is a syndrome of cellular deficiency of essential polyenic FA.

Nature of the interaction between low-density lipoproteins and polyanions and metal ions, as exemplified by heparin and Ca2+.

1976 ◽  
Vol 22 (11) ◽  
pp. 1812-1816 ◽  
Author(s):  
B E Cham
Keyword(s):  
Chemical Composition ◽  
Metal Ions ◽  
Small Proportion ◽  
Metal Ion ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Total Precipitation ◽  
Lipid Concentration ◽  
Lipid Moiety ◽  
Protein Moiety

Abstract I examined the effect of lipid concentration on the interaction of the very-low density and low-density lipoproteins in serum with heparin and calcium. A precipitate forms when partly delipidated serum is subjected to the polyanion-metal ion system. Although this precipitate is less turbid than the complexed lipoprotein-polyanion-metal ion in undelipidated serum, the two precipitates contain identical amounts of apolipoprotein. Totally delipidated serum produces only a slight precipitate with heparin and calcium, and this precipitate contains only a fraction of the appolipoproteins. Cholesterol and triglycerides are the major determinants of turbidity when serum is mixed with heparin and calcium, but have no effect on the precipitation of the protein moiety. Phospholipids contribute a small proportion of the turbidity in the lipoprotein-polyanion-metal ion interaction. Precipitation of the low-density lipoproteins by heparin and calcium depends on the protein moiety and on the chemical composition of the lipid moiety. Phospholipid is required, but cholesterol and triglyceride are not, for total precipitation of the complex.

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.

Effects of oxidized low-density lipoproteins on the hepatic microvasculature

2011 ◽  
Vol 301 (4) ◽  
pp. G684-G693 ◽  
Author(s):  
Ana Oteiza ◽  
Ruomei Li ◽  
Robert S. McCuskey ◽  
Bård Smedsrød ◽  
Karen Kristine Sørensen
Keyword(s):  
Electron Microscopy ◽  
Linear Trend ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Intercellular Adhesion Molecule ◽  
Organ Distribution ◽  
Low Density ◽  
Hepatic Microcirculation ◽  
Oxidized Low Density Lipoproteins

Oxidized low-density lipoproteins (oxLDLs) are involved in proinflammatory and cytotoxic events in different microcirculatory systems. The liver is an important scavenger organ for circulating oxLDLs. However, the interaction of oxLDL with the hepatic microcirculation has been poorly investigated. The present study was conducted to examine the effects of differently modified oxLDLs on the hepatic microvasculature. C57Bl/6J mice were injected intravenously with low-density lipoprotein (LDL), or LDL oxidized for 3 h (oxLDL3) or 24 h (oxLDL24), at doses resembling oxLDL plasma levels in cardiovascular disease patients. Radioiodinated ligands were used to measure blood decay and organ distribution, and nonlabeled ligands to evaluate microcirculatory responses, examined by in vivo microscopy 30–60 min after ligand injection, immunohistochemistry, and scanning and transmission electron microscopy. Mildly oxLDL (oxLDL3) was cleared from blood at a markedly slower rate than heavily oxLDL (oxLDL24), but significantly faster than LDL ( P < 0.01). Injected oxLDLs distributed to liver. OxLDL effects were most pronounced in central areas of the liver lobules where oxLDL3elicited a significant ( P < 0.05) reduction in perfused sinusoids, and both oxLDL3and oxLDL24significantly increased the numbers of swollen endothelial cells and adherent leukocytes compared with LDL ( P < 0.05). OxLDL-treated livers also exhibited increased intercellular adhesion molecule (ICAM)-1 centrilobular staining. Electron microscopy showed a 30% increased thickness of the liver sinusoidal endothelium in the oxLDL3group ( P < 0.05) and a reduced sinusoidal fenestration in centrilobular areas with increased oxidation of LDL ( P for linear trend <0.05). In conclusion, OxLDL induced several acute changes in the liver microvasculature, which may lead to sinusoidal endothelial dysfunction.

scholarly journals Antioxidant and Protective Effects of Artemisia campestris Essential Oil Against Chlorpyrifos-Induced Kidney and Liver Injuries in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Mongi Saoudi ◽  
Riadh Badraoui ◽  
Fatma Rahmouni ◽  
Kamel Jamoussi ◽  
Abdelfattah El Feki
Keyword(s):  
Essential Oil ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Protective Effects ◽  
Liver Injuries ◽  
Liver And Kidney ◽  
Artemisia Campestris ◽  
Morphologic Changes ◽  
Histopathologic Features

This study is aimed to elucidate the possible antioxidant and protective effects of Artemisia campestris essential oil (ACEO) against the deleterious effects of chlorpyrifos (CPF) in rats. The in vivo study revealed increases in aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) activities and the serum contents of creatinine, urea, uric acid, cholesterol, triglycerides, low density lipoproteins (LDL), and glucose in rats treated with CPF as compared to controls. Meanwhile, hepatic and renal activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in liver and kidney decreased and the content of malondialdehyde (MDA) increased. Some histopathologic features were noticed in liver and kidney of the CPF group. Interestingly, ACEO alleviated the biochemical disruptions and reduced these hepato-renal morphologic changes.

scholarly journals Maternal loading with very low-density lipoproteins stimulates fetal surfactant synthesis

2002 ◽  
Vol 283 (2) ◽  
pp. L310-L318 ◽  
Author(s):  
Alan J. Ryan ◽  
Jheem D. Medh ◽  
Diann M. McCoy ◽  
Ronald G. Salome ◽  
Rama K. Mallampalli
Keyword(s):  
Fatty Acids ◽  
Knockout Mice ◽  
Low Density Lipoproteins ◽  
Alveolar Epithelial Cells ◽  
Type Ii Cells ◽  
Low Density ◽  
Type Ii ◽  
Very Low Density Lipoproteins ◽  
Pregnant Rat ◽  
Apolipoprotein E Knockout Mice

We examined whether administration of very low-density lipoproteins (VLDL) to pregnant rats increases surfactant phosphatidylcholine (PtdCho) content in fetal pre-type II alveolar epithelial cells. VLDL-triglycerides are hydrolyzed to fatty acids by lipoprotein lipase (LPL), an enzyme activated by heparin. Fatty acids released by LPL can incorporate into the PtdCho molecule or activate the key biosynthetic enzyme cytidylyltransferase (CCT). Dams were given BSA, heparin, VLDL, or VLDL with heparin intravenously. Radiolabeled VLDL given to the pregnant rat crossed the placenta and was distributed systemically in the fetus and incorporated into disaturated PtdCho (DSPtdCho) in pre-type II cells. Maternal administration of VLDL with heparin increased DSPtdCho content in cells by 45% compared with control ( P < 0.05). VLDL produced a dose-dependent, saturable, and selective increase in CCT activity. VLDL did not significantly alter immunoreactive CCT content but increased palmitic, stearic, and oleic acids in pre-type II cells. Furthermore, hypertriglyceridemic apolipoprotein E knockout mice contained significantly greater levels of DSPtdCho content in alveolar lavage and CCT activity compared with either LDL receptor knockout mice or wild-type controls that have normal serum triglycerides. Thus the nutritional or genetic modulation of serum VLDL-triglycerides provides specific fatty acids that stimulate PtdCho synthesis and CCT activity thereby increasing surfactant content.

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