Broad-β disease versus endogenous hypertriglyceridemia: Levels and lipid composition of chylomicrons and very low density lipoproteins during fat-free feeding and alimentary lipemia

Hazzard, William R.; Bierman, Edwin L.

doi:10.1016/0026-0495(75)90128-6

Cited by 25 publications

(4 citation statements)

References 24 publications

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“…1 B ); in contrast, 3/3 plasma shows virtually no lipid staining at the ␤ -position. ␤ -VLDL particles from the 2/2 mice are highly enriched in cholesterol ester (67% in 2/2 compared with Ͻ 1% in 3/3 mice), and have a VLDL cholesterolto-triglyceride ratio of 0.76 compared with 0.03 in the 3/3 mice (a ratio Ͼ 0.3 is diagnostic for type III HLP in humans [15]). Accumulation of ␤ -VLDL in 2/2 plasma is further illustrated by fast protein liquid chromatography (FPLC), which shows that ‫ف‬ 65% of the total cholesterol is in lipoproteins that elute in the VLDL-intermediate density lipoprotein (IDL) range (fractions 15-23, Fig.…”

Section: Resultsmentioning

confidence: 99%

Type III hyperlipoproteinemia and spontaneous atherosclerosis in mice resulting from gene replacement of mouse Apoe with human Apoe*2.

Sullivan¹,

Mezdour²,

Quarfordt³

et al. 1998

J. Clin. Invest.

221

186

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Section: Resultsmentioning

confidence: 99%

Type III hyperlipoproteinemia and spontaneous atherosclerosis in mice resulting from gene replacement of mouse Apoe with human Apoe*2.

Sullivan¹,

Mezdour²,

Quarfordt³

et al. 1998

J. Clin. Invest.

221

186

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“…2, is shown in Table I. In the perfusates of livers from the hypercholesterolemic rats the initial release represents -30% ofthe total apoE collected in 4 h, but is negligible in perfusates of normal livers. To restrict the studies to lipoproteins actively secreted by the livers, the perfusates were routinely replaced after the first 15 min in all subsequent experiments, resulting in initial releases which were close to zero.…”

Section: Resultsmentioning

confidence: 99%

“…Based on these properties and a number of metabolic studies, it has been suggested that the abnormal VLDL found in familial dysbetalipoproteinemia represents an accumulation of remnants of VLDL and chylomicron catabolism which have not been efficiently removed (2)(3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Secretion of Cholesterol-Rich Lipoproteins by Perfused Livers of Hypercholesterolemic Rats

Noël¹,

Wong²,

Dolphin³

et al. 1979

J. Clin. Invest.

102

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A B S T R A C T Rats maintained on a high-fat diet supplemented with propylthiouracil develop a hypercholesterolemia, an increased serum level of apolipoprotein (apo) E, abnormal very low density lipoproteins (VLDL) and low density lipoproteins (LDL), and a fatty liver which contains cholesterol ester as its major lipid. The fatty liver secretes apoE into a recirculating perfusate at a significantly higher rate and produces cholesterol ester-rich, apoC-deficient VLDL with slower electrophoretic mobility than the triacylglycerol-rich VLDL produced by perfused normal livers. LDL

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“…54150 ' 51 The fact that remnant lipoproteins formed from chylomicrons and hepatogenous VLDL in F. dys. are heavily enriched in cholesteryl esters suggests that the long residence time in blood attendant to impaired receptor-mediated endocytosis allows the transfer of cholesteryl esters generated by lecithin-cholesterol acyltransferase (LCAT) to proceed further.…”

Section: Discussionmentioning

confidence: 99%

Remnants of lipoproteins of intestinal and hepatic origin in familial dysbetalipoproteinemia.

Kane¹,

Chen²,

Hamilton³

et al. 1983

Arteriosclerosis

102

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We used the low molecular weight form of apolipoprotein B (B-48) as a marker for the identification of remnant particles formed from chyiomicrons in the plasma of patients with familial dysbetalipoproteinemia. In the serum of patients fasted 14 hours, the d < 1.006 g/cm 3 lipoproteins of prebeta mobility, separated by starch block electrophoresis, contained only the primary hepatogenous species of apolipoprotein B (B-100), and their llpld composition resembled that of normal prebeta very low density lipoproteins. In contrast, the fraction with beta mobility contained both the B-48 and B-100 proteins; the B-48 protein was found primarily among the largest particles. All fractions of beta mobility were greatly enriched with choiesteryi esters. The beta fraction thus contains remnant particles which appear to originate both from chyiomicrons and hepatogenous very low density lipoproteins. It appears that these remnant particles share a common removal mechanism which is impaired in familial dysbetalipoproteinemia. (Arteriosclerosis 3:47-56, January/February 1983) amilial dysbetalipoproteinemia (F. dys.) (type III hyperlipoproteinemia) is now recognized as a disorder in which remnant-like particles, formed from triglyceride-rich lipoproteins, accumulate in plasma.12 Clinically, it is associated with arteriosclerosis of both the coronary and peripheral circulations. 3These remnant-like lipoprotein particles are enriched with choiesteryi esters 1 2 ' 4 and have beta mobility upon electrophoresis in agarose gel, in contrast with normal very low density lipoproteins (VLDL), which have prebeta mobility. The electrophoretic mobility of remnant particles is accounted for principally by deficiency of the C-apoproteins, which are normally the preponderant species in VLDL, with retention of appreciable quantities of less anionic apolipoprotein E (apo E). 5 The initial stages of intravascular lipolysis appear to proceed relatively normally. Removal of remnant particles from the plasma normally occurs rapidly by means of receptor-mediated endocytosis in the liver.2 In F. dys., however, there is

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Broad-β disease versus endogenous hypertriglyceridemia: Levels and lipid composition of chylomicrons and very low density lipoproteins during fat-free feeding and alimentary lipemia

Cited by 25 publications

References 24 publications

Type III hyperlipoproteinemia and spontaneous atherosclerosis in mice resulting from gene replacement of mouse Apoe with human Apoe*2.

Type III hyperlipoproteinemia and spontaneous atherosclerosis in mice resulting from gene replacement of mouse Apoe with human Apoe*2.

Secretion of Cholesterol-Rich Lipoproteins by Perfused Livers of Hypercholesterolemic Rats

Remnants of lipoproteins of intestinal and hepatic origin in familial dysbetalipoproteinemia.

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