Composition and distribution of low density lipoprotein fractions in hyperapobetalipoproteinemia, normolipidemia, and familial hypercholesterolemia.

Teng, Babie; Thompson, Gilbert R.; Sniderman, Allan D.; Forte, Trudy M.; Krauss, Ronald M.; Kwiterovich, Peter O.

doi:10.1073/pnas.80.21.6662

Cited by 195 publications

(68 citation statements)

References 36 publications

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“…The percent content of cholesterol was significantly lower in survivors than in controls, whereas the percent content of apolipoprotein was rather higher in survivors, resulting in a lower cholesterol to apolipoprotein ratio of LDL in survivors (1.08±0.17) than that in controls (1.20±0.13) (Teng et al 1983), although not statistically significant. The percent content of either phospholipid or triglyceride did not differ between survivors and controls (Table 4).…”

Section: Low Density Lipoprotein (Ldl)mentioning

confidence: 77%

“…On the other hand, LDL, a major cholesterol transporting lipoprotein, is considered not to be homogeneous. Sniderman et al (1980) claimed that the plasma concentration of LDL apolipoprotein (apo B) may frequently be increased in patients with coronary heart disease despite their having an LDL cholesterol within the normal range and this abnormality is pronounced in not heavy but light LDL particles (Sniderman et al 1980;Teng et al 1983). It was shown by these investigators that cholesterol to apolipoprotein B ratio in coronary heart disease is significantly lower than that in control when light subfraction of LDL was examined (Teng et al 1983).…”

Section: Discussionmentioning

confidence: 99%

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Characterization of plasma lipoproteins in survivors of cerebral infarction.

Murai¹,

Miyahara

Tanaka

et al. 1986

Tohoku J. Exp. Med.

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To characterize the plasma lipoproteins in survivors of cerebral infarction, plasma lipoproteins were ultracentrifugally fractionated into VLDL, LDL, HDLZ and HDL3, and the concentrations of cholesterol, phospholipid, apolipoprotein and triglyceride in each lipoprotein class were determined. Subjects examined were 15 male healthy controls and 15 male survivors of cerebral infarction situated in the distribution of cerebral cortical artery. The concentrations of VLDL-cholesterol and VLDL-triglyceride and the percent content of VLDL-cholesterol were higher in survivors than in controls. The concentration of LDL-triglyceride was higher and the percent content of LDL-cholesterol was lower in survivors than in controls. While the plasma concentration of triglyceride was higher in survivors than in controls, those of HDL, HDLZ and HDL3 were lower in survivors. The concentrations of cholesterol, phospholipid and apolipoprotein in either HDLZ or HDL3 were also reduced in survivors as compared with controls. In either HDLZ or HDL3, the percent content of triglyceride was higher and that of phospholipid was lower in survivors than in controls. These results were in good agreement with those reported for survivors of myocardial infarction, suggesting that the underlying derangement in lipoprotein metabolism is common to myocardial and cerebral infarction, cerebral infarction ; atherosclerosis ; plasma lipoprotein ; high density lipoprotein subfraction ; chemical composition

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Section: Low Density Lipoprotein (Ldl)mentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Characterization of plasma lipoproteins in survivors of cerebral infarction.

Murai¹,

Miyahara

Tanaka

et al. 1986

Tohoku J. Exp. Med.

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“…The first feature of hyperapoB to be recognized was the elevated LDL particle number, many of which are smaller and denser than normal [4]. In reality, though, the metabolism of all the lipoprotein classes is demonstrably abnormal.…”

mentioning

confidence: 99%

The pathogenetic role of impaired fatty acid trapping by adipocytes in generating the pleiotropic features of hyperapoB

Sniderman¹,

Cianflone²,

Frayn

1997

Diabetologia

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HyperapoB is the commonest dyslipoproteinaemia associated with coronary disease [1,2] and is characterized by an increased LDL particle number due to increased secretion of B100 lipoproteins by the liver [3]. The first feature of hyperapoB to be recognized was the elevated LDL particle number, many of which are smaller and denser than normal [4]. In reality, though, the metabolism of all the lipoprotein classes is demonstrably abnormal.At the onset, however, it must be appreciated that hyperapoB is a phenotype, not a genotype, and there are multiple causes which produce increased hepatic secretion of B100 lipoprotein particles. The focus in this review, however, will be to outline how a reduced rate of fatty acid trapping by adipocytes can produce the pleiotropic features which characterize hyperapoB. At the end of this line of reasoning lies the conclusion that faults in fatty acid metabolism, not errors in the LDL pathway, are the commonest causes for the atherogenic dyslipoproteinaemias seen clinically.The features of hyperapoB to be explicated are: 1) increased hepatic VLDL secretion; 2) increased LDL particle number; 3) smaller denser LDL particles; 4) reduced HDL cholesterol levels; 4) postprandial hyperlipaemia with accumulation of triglyceride-rich remnants; 5) elevated plasma non-esterified fatty acid levels (NEFA); and 6) insulin resistance. Regulation of the rate of fatty acid storage by adipocytesThe normal sequence involved in the uptake by adipocytes of fatty acids released from chylomicrons can be summarized as follows: chylomicrons attach to endothelial cells and the triglyceride within them is rapidly hydrolysed by lipoprotein lipase (LPL) [5]. The rate at which chylomicron triglyceride hydrolysis proceeds is determined by the number of LPL molecules involved and by the rate at which the NEFA which are generated are removed from the capillary microenvironment.The NEFA which are liberated from the chylomicrons can enter the adipocyte to be trapped within it as triglyceride. Alternatively, they may bind to albumin, leave the capillary, and enter the general circulation. The proportion of NEFA released from chylomicrons which enter adipocytes is necessarily the reciprocal of the proportion which are not trapped by adipocytes and which then leave the microenvironment. Under normal circumstance, the proportions are about equal [6]. The proportion of NEFA which are trapped by adipocytes is determined by their rate of triglyceride synthesis, the major determinant of which is the acylation stimulating protein (ASP) pathway [7].ASP is the product of the ASP pathway and, as just noted, is the major determinant of the rate of triglyceride synthesis within adipocytes. The major features of the pathway are described elsewhere [8]. In brief, human adipocytes synthesize and secrete the three proteins of the alternate complement pathway which interact to form a 77 amino terminal fragment of C3, the terminal arginine of which is removed by carboxypeptidases to produce ASP. ASP then interacts specifically with a ...

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“…The less dense subtraction was enriched in triglycerides, and the more dense subtraction was poor in lipids and had an unusually high ratio of apo B to cholesterol. Previously, Teng et al 11 had reported that denser LDL in patients with hyperapobetalipoproteinemia has a high content of apo B. Many patients with hyperapobetalipoproteinemia probably have familial combined hyperiipidemia -a condition in which very dense LDL have also been reported.…”

Section: Metabolism Of Polydlsperse Ldlmentioning

confidence: 99%

Kinetic heterogeneity of low density lipoproteins in primary hypertriglyceridemia.

Vega¹,

Grundy²

1986

Arteriosclerosis

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The kinetics of two subfractions of low density lipoproteins (LDL) were examined in nine patients with primary hypertriglyceridemia. LDL was subjected to equilibrium ultracentrifugation, and three patterns of LDL subfractions were noted. The LDL of five patients with moderate hypertriglyceridemia (plasma triglycerides (TG) ranging from 333 to 580 mg/dl) appeared to contain two distinct subfractions. One was less dense and had a high TG content; the other was more dense and had a reduced content of all lipids, particularly cholesterol. Each subfraction was labeled separately and was reinjected into the patient. Of the two subfractions, the more dense LDL usually had a higher fractional catabolic rate (FCR), although the turnover rates of both subfractions for these hypertriglyceridemic patients were higher than normal. Two other patients with mild hypertriglyceridemia had only a single LDL after gradient equilibrium ultracentrifugation. This fraction was divided into less dense and more dense subfractions, and their FCR was determined. In both patients, turnover rates of the two subfractions were similar and both were in the normal range. Finally, two more patients with mildly elevated TG had a very dense LDL, besides having a single, less dense band. For both patients, the FCR for the less dense and very dense subfractions were similar, although the denser LDL had a greater fraction in the extravascular compartment. Thus, patients with primary moderate hypertriglyceridemia often have distinct subfractions that have different turnover rates. For patients with mild hypertriglyceridemia, the LDL is more homogeneous, and its subfractions are kinetically similar.

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Composition and distribution of low density lipoprotein fractions in hyperapobetalipoproteinemia, normolipidemia, and familial hypercholesterolemia.

Cited by 195 publications

References 36 publications

Characterization of plasma lipoproteins in survivors of cerebral infarction.

Characterization of plasma lipoproteins in survivors of cerebral infarction.

The pathogenetic role of impaired fatty acid trapping by adipocytes in generating the pleiotropic features of hyperapoB

Kinetic heterogeneity of low density lipoproteins in primary hypertriglyceridemia.

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