Lipid changes in the plasma lipoproteins of baboons given an atherogenic diet

An, Howard; Blaton,; Vandamme, Dries; N, Van Landschoot; Peeters, H.

doi:10.1016/0021-9150(72)90060-3

Cited by 28 publications

(6 citation statements)

References 18 publications

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“…Although limited information is available concerning the FC/P in the serum of hyperlipemic individuals, a recent study has demonstrated a 35% increase in the FC/P of the LDL of 16 patients heterozygous for type Iha hypercholesterolemia and a 40% increase in 3 type Iha homozygotes (41). Values greater than normal for the FC/P of Ila LDL have been reported by three other laboratories (42)(43)(44); although in one, this abnormality was found only in Ila homozygotes (44). The results reported herein demonstrate that elevations in the exogenous FC/P ratio can elicit cholesteryl ester accumulation in the Fu5AH cells.…”

Section: Methodssupporting

confidence: 54%

Cellular cholesterol ester accumulation induced by free cholesterol-rich lipid dispersions.

Arbogast¹,

Rothblat²,

Leslie³

et al. 1976

Proc. Natl. Acad. Sci. U.S.A.

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The influence of lipoprotein composition on free cholesterol (FC) esterification and accumulation of esterified cholesterol (EC) was studied in cells of Fu5AH rat hepatoma exposed to culture media supplemented with FC-lecithin dispersions having mole ratios of FC to phospholipid (FC/P) ranging from 0.6 to 2.8. In the presence of normal human serum, FC-lecithin dispersions with a FC/P greater than one stimulated both the We sought to determine if variations in the exogenous FC/P composition could influence the accumulation of EC by tissue culture cells. The Fu5AH rat hepatoma cell line was selected because these cells are capable of accumulating large quantities of EC when grown in the presence of hyperlipemic animal sera (11), and because the accumulation of EC correlates closely with the extent of esterification of FC (12). Thus, this cell, with its high capacity for cholesterol esterification and EC accumulation, can serve as a sensitive experimental tool for the quantitation of cholesterol flux between the cells and the culture medium. MATERIALS AND METHODSCholesterol/Lecithin Dispersions. Cholesterol/lecithin dispersions of various molar ratios were prepared as previously described (5, 6). L-a-Dipalmitoyl lecithin (General Biochemicals, Div. Mogul Corp., Chagrin Falls, Ohio) and FC (Sigma Chemical Co., St. Louis, Mo.) were added to 10 ml of physiological saline and subjected to 70 W with a Branson sonifier for 60 min at 450 under N2. Cholesterol dispersions prepared with 40 mg of lecithin and 23 mg of cholesterol resulted in a free cholesterol-to-phospholipid mole ratio (FC/P) of approximately one. Cholesterol rich dispersions (40 mg of lecithin, plus 30-80 mg of cholesterol) had a FC/P of greater than one. Cholesterol poor dispersions (FC/P less than one) were prepared with 40 mg of lecithin and less than 20 mg of cholesterol. Albumin (5 mg/ml) was added to the sonicated dispersions and the mixture was centrifuged at 26,000 X g for 30 min to sediment the undispersed lipid. Dispersions were sterilized by filtration through a 0.45 ,um Millipore filter and mixed at various concentrations, with tissue culture medium supplemented with either albumin (bovine fraction V powder, fatty acid-free, Miles Laboratories, Inc., Kankakee, Ill.), normal human serum, or human serum lipoproteins.Cells and Incubation Conditions. The Fu5AH rat hepatoma cell line has been described previously (11,12

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Section: Methodssupporting

confidence: 54%

Cellular cholesterol ester accumulation induced by free cholesterol-rich lipid dispersions.

Arbogast¹,

Rothblat²,

Leslie³

et al. 1976

Proc. Natl. Acad. Sci. U.S.A.

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“…Slack & Mills [4] reported an increased proportion of cholesterol ester and a decreased proportion of triglyceride, and Mills et al [5] subsequently noted that the 1ecithin:sphingomyelin ratio was abnor- mally low in two homozygotes. An increase in the cholestero1:phospholipid ratio and a decrease in the lecithin :sphingomyelin ratio of LDL had previously been described in three patients with type I1 hyperlipoproteinaemia, but it was not made clear whether the latter was familial in origin [6]. Recently, Shattil et al 171 investigated a large group of patients with proven FH and confirmed the increased LDL cholesterol: protein ratio originally described by Beaumont et al [8].…”

Section: Introductionmentioning

confidence: 82%

Reversible abnormalities of low density lipoprotein composition in familial hypercholesterolaemia

Jadhav

Thompson

1979

Eur J Clin Investigation

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Low density lipoprotein (LDL) composition was analysed in twenty-one patients with familial hypercholesterolaemia, including six homozygotes. By comparison with nineteen controls the patients' LDL had an increased ratio of cholesterol:phospholipid and a decreased ratio of lecithin:sphingomyelin; these changes were more marked in homozygotes than in heterozygotes. Treatment of sevel patients with plasma exchange temporarily resulted in near-normalization of the composition of their LDL. These results suggest that abnormalities of LDL composition in familial hypercholesterolaemia are secondary to hypocatabolism of LDL, which prolongs the half-life of LDL and thus increases the mean age of the population of particles circulating in plasma.

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“…Experiments with red blood cells and vesicles have suggested that cholesterol loading and depletion by exchange depends primarily on the cholesterol: phospholipid molar ratio in the donor and acceptor membranes (or lipoprotein) (Slotte & Lundberg, 1983;Clejan & Bittman, 1984). An increased cholesterol: phospholipid ratio has been documented in LDL of individuals with familial hypercholesterolaemia (Howard et al, 1972;Brown et al, 1973;Shattil et al, 1977). Such LDL may cause a net movement of cholesterol into the arterial cells.…”

Section: Discussionmentioning

confidence: 99%

Physicochemical transfer of [3H]cholesterol from plasma lipoproteins to cultured human fibroblasts

Lundberg¹,

Suominen²

1985

Biochemical Journal

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The transfer of free cholesterol from [3H]cholesterol-labelled plasma lipoproteins to cultured human lung fibroblasts was studied in a serum-free medium. The uptake of [3H]cholesterol depended upon time of incubation, concentration of lipoprotein in the medium, and temperature. Modified (reduced and methylated) low-density lipoprotein (LDL), which did not enter the cells by the receptor pathway, gave a somewhat lower transfer rate than unmodified LDL, but if the transfer values for native LDL were corrected for the receptor-mediated uptake of cholesterol the difference was eliminated. The initial rates of transfer of [3H]cholesterol from LDL and high-density lipoprotein (HDL) were of the same order of magnitude (0.67 +/- 0.05 and 0.75 +/- 0.06 nmol of cholesterol/h per mg of cell protein, respectively) while that from very-low-density lipoprotein (VLDL) was much lower (0.23 +/- 0.02 nmol of cholesterol/h per mg) (means +/- S.D., n = 5). The activation energy for transfer of cholesterol from reduced, methylated LDL to fibroblasts was determined to be 57.5 kJ/mol. If albumin was added to the incubation medium the transfer of [3H]cholesterol was enhanced, while that of [14C]dipalmitoyl phosphatidylcholine was decreased compared with the protein-free system. The results demonstrate that, in spite of its low water solubility, free cholesterol can move from lipoproteins to cellular membranes, probably by aqueous diffusion. We propose that physicochemical transfer of free cholesterol may be a significant mechanism for net uptake of the sterol into the artery during atherogenesis.

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Lipid changes in the plasma lipoproteins of baboons given an atherogenic diet

Cited by 28 publications

References 18 publications

Cellular cholesterol ester accumulation induced by free cholesterol-rich lipid dispersions.

Cellular cholesterol ester accumulation induced by free cholesterol-rich lipid dispersions.

Reversible abnormalities of low density lipoprotein composition in familial hypercholesterolaemia

Physicochemical transfer of [3H]cholesterol from plasma lipoproteins to cultured human fibroblasts

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