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.

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.

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 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.

Increase in hydroxy fatty acids in human low density lipoproteins with age

1996 ◽  
Vol 84 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Wolfgang Jira ◽  
Gerhard Spiteller ◽  
Axel Schramm
Keyword(s):  
Fatty Acids ◽  
Low Density Lipoproteins ◽  
Hydroxy Fatty Acids ◽  
Low Density

Effect of feeding protected lipid to dairy cows in early lactation on the composition of blood lipoproteins and secretion of fatty acids in milk

1980 ◽  
Vol 94 (3) ◽  
pp. 503-516 ◽  
Author(s):  
J. E. Storry ◽  
P. E. Brumby ◽  
B. Tuckley ◽  
V. A. Welch ◽  
D. Stead ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Milk Fat ◽  
Low Density Lipoproteins ◽  
Total Serum ◽  
Low Density ◽  
Dietary Intakes ◽  
Vldl Triglyceride

SummaryEffects of 0, 1·7, 3·3 or 5·0 kg/day of a protected soya bean – tallow supplement, incorporated into a hay:concentrate diet (25:75) and fed ad libitumto Friesian cows, on intake and digestion of fatty acids, on output of milk fatty acids and on blood lipoprotein composition were measured.Most of the increased intake of fatty acids, approximately 1 kg/day, was accounted for by increased intakes of C16:0, C18:0 and C18:1. At low intakes, amounts of all fatty acids apparently digested were linearly related to their respective intakes. At high intakes of C16 and C18 acids, curvilinear relationships were established.Yield of total milk fat was related positively to dietary intakes of total fatty acid and carbohydrate and negatively to live-weight change. Yields of short and intermediate chain acids in milk, synthesized within the mammary gland, were negatively correlated and yields of C18 fatty acids positively correlated with respective dietary intakes of these acids. Decreased proportions of C4–16 and increased proportions of C18:0 and C18:1 fatty acids in milk were associated with increased protected tallow in the diet. Yields of C16:1 and C18:1 were positively related to corresponding outputs of saturated acids and negatively to weeks of lactation. The proportion of C18:1 in milk was positively related to the corresponding proportion of C18:0.The increased intake of fatty acids resulted in increased concentrations of very low density lipoproteins (VLDL, d < 1·019 g/ml), low density lipoproteins (LDL1 + LDL2, 1·019 < d < 1·06 g/ml), high density lipoproteins (d > 1·060 g/ml) and serum free fatty acids. Most of the increase in low density lipoproteins was accounted for by a very large increase in LDL1, whose proportion increased from 17 to 75% (2 to 22% of total serum lipid). The proportion of triglyceride in the combined low density lipoprotein fraction decreased from 11 to 2% whilst phospholipids increased from 29 to 36%. These changes were attributed to the increased proportion of LDL1 present.The proportions of VLDL and LDL triglyceride taken up by the mammary gland averaged 0·79 and 0·34 respectively. The proportion of VLDL+LDL triglyceride taken up by the gland decreased with increased amounts of fatty acid digested. Yields of C18 fatty acids in milk tended to be positively related to apparent uptakes of VLDL triglyceride and to VLDL C18 fatty acids, but negatively related to apparent uptakes of LDL triglycerides and LDL C18 fatty acids. It is suggested that the increased LDL1 resulted from the utilization of VLDL triglyceride for milk fat formation.Protected lipid feeding increased the proportion of C14:0, C16:0 C16:1 and C18:1 and decreased the proportions of C14:1 and C18:0 fatty acids in jugular serum triglycerides. Similar changes were observed in jugular VLDL triglycerides. Differences in the compositions of VLDL and LDL triglycerides across the mammary gland were observed and attributed either to selective uptake or to interchange of fatty acids between triglycerides and free fatty acids.

scholarly journals Differential Effects of Delivery of Omega-3 Fatty Acids to Human Cancer Cells by Low-Density Lipoproteins versus Albumin

2004 ◽  
Vol 10 (24) ◽  
pp. 8275-8283 ◽  
Author(s):  
Iris J. Edwards ◽  
Isabelle M. Berquin ◽  
Haiguo Sun ◽  
Joseph T. O’Flaherty ◽  
Larry W. Daniel ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cancer Cells ◽  
Human Cancer ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Differential Effects ◽  
Human Cancer Cells

scholarly journals Stimulation of triacylglycerol synthesis in rat adipocytes by plasma very-low-density lipoproteins

1978 ◽  
Vol 176 (1) ◽  
pp. 169-174 ◽  
Author(s):  
P Thomopoulos ◽  
M Berthelier ◽  
D Lagrange ◽  
M J Chapman ◽  
M H Laudat
Keyword(s):  
Fatty Acids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
High Density Lipoproteins ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Rat Adipocytes ◽  
Triacylglycerol Synthesis

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.

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