Hydrolysis of human plasma high density lipoprotein2-phospholipids and triglycerides by hepatic lipase

Shirai, Kohji; Barnhart, Roger L.; Jackson, Richard L.

doi:10.1016/s0006-291x(81)80217-3

Cited by 198 publications

(50 citation statements)

References 20 publications

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“…With the increase in HDL triglyceride content, susceptibility to hydrolysis, particularly by hepatic lipase, increases. 27,28 In the current study, HDL triglyceride concentrations increased and cholesteryl ester concentrations fell throughout the postprandial period. In addition, HDL phospholipid concentration fell at 5 hours but then increased, particularly in HDL 2 , by 8 hours.…”

Section: Discussionsupporting

confidence: 45%

“…The relationship between triglyceride level and HDL particle size can be explained in terms of initial triglyceride enrichment of HDL in exchange for cholesterol ester with subsequent lipolysis leading to the production of smaller HDL particles. 27,28 Although the presence of elevated triglyceride levels in subjects with an ⑀4 allele would be expected to facilitate the operation of this mechanism, it appears that other mechanisms must also be operating. It is also of interest to note that the postprandial change in HDL particle size is large enough, despite only a modest degree of lipemia, to result in reclassification of HDL particle subclasses.…”

Section: Discussionmentioning

confidence: 99%

“…12 HDL particles are known to undergo extensive remodelling during their residence in the plasma by processes involving exchange of triglyceride for cholesterol ester with subsequent lipolysis leading to the formation of smaller particles. 27,28 Such processes are also dependent on plasma triglyceride levels and changes in HDL diameters have been seen postprandially coincident with the rise in triglyceride levels. 29 -33 However, associations with apo E phenotypes have apparently not been sought..…”

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confidence: 99%

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Independent Effects of Apo E Phenotype and Plasma Triglyceride on Lipoprotein Particle Sizes in the Fasting and Postprandial States

Dart¹,

Cooper²

1999

ATVB

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Abstract-LDL particle sizes and Apo E phenotypes were determined in 212 subjects of whom 51 had angina. LDL diameter was significantly less in subjects with an ⑀2 allele (24.76Ϯ0.08 vs 24.94Ϯ0.02 nm, Pϭ0.02), and this was evident for both E2/E3 (24.77Ϯ0.09 nm) and E2/E4 (24.69Ϯ0.08 nm) phenotypes. Although there was a negative relation between LDL diameter and plasma triglyceride, the effect of apo E2 was still evident with adjustment for triglyceride. In multiple regression analysis, the significant determinants of LDL diameter were gender (with females having larger particles than males), body mass index, and the presence (or absence) of E2. HDL particle sizes and compositions were determined on fasting samples and, additionally, 5 and 8 hours after a fat-rich meal for 48 coronary heart disease cases and 49 control subjects. Fasting HDL particle sizes were not related to the presence of E2 but were significantly smaller for subjects possessing an ⑀4 allele (8.09Ϯ0.08 vs 8.39Ϯ0.05 nm, Pϭ0.003) and were negatively related to plasma triglyceride. However, the effect of E4 persisted after adjustment for triglyceride. In a multiple regression analysis, the only significant determinant of fasting HDL diameter was the presence (or absence) of E4 with fasting plasma triglyceride just failing to reach significance (Pϭ0.06). There was a postprandial increase in HDL diameter that was less marked in subjects with coronary heart disease. The postprandial increase in HDL diameter was of sufficient magnitude to result in size reclassification of HDL particles. The influence of E4 was also evident at both postprandial time points. Compositional analysis demonstrated that the increase in HDL diameters postprandially could be attributed to triglyceride enrichment, with an accompanying fall in cholesterol ester content. Phospholipid changes postprandially were biphasic with an initial fall followed by a rise in concentration. The increase in triglyceride content was significantly less in those subjects with angina despite an equivalent rise in plasma triglyceride. The present study demonstrates significant, but different, effects of variation in apo E phenotype on the particle sizes of both HDL and LDL. Such effects were still evident with adjustment for differences in plasma triglyceride and suggests that variation in apo E phenotype exerts effects on lipoprotein particle sizes by mechanisms additional to those dependent on change in plasma triglyceride. Key Words: apo E Ⅲ LDL particle size Ⅲ HDL particle size Ⅲ triglyceride Ⅲ coronary heart disease Ⅲ postprandial T here is considerable evidence that variation in apo E phenotype, dependent on the assortment of ⑀4, ⑀3, and ⑀2 alleles, contributes to the variation in occurrence of coronary heart disease (CHD). Thus the possession of an ⑀4 allele has been associated with the CHD in the European Atherosclerosis Research Study. 1 More severe atheroma was found in the coronary vessels of Alzheimer's patients with an ⑀4 allele than in those without, and elderly Finnish men dying of co...

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Independent Effects of Apo E Phenotype and Plasma Triglyceride on Lipoprotein Particle Sizes in the Fasting and Postprandial States

Dart¹,

Cooper²

1999

ATVB

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“…Thus, patients with LPL deficiency accumulate primarily chylomicrons as well as very low density lipoproteins in plasma (11), whereas HL deficiency results in elevated plasma concentrations of intermediate density lipoproteins and HDL (26,27). Characterization of these patients demonstrates that in vivo, the preferred substrate of LPL are the large triglyceride-rich lipoproteins, whereas HL is more active in the hydrolysis of smaller lipoproteins such as HDL (28,29), especially HDL 2 (30), and intermediate density lipoproteins (26,31,32). Another physiologically important difference in the function of HL and LPL is the relative phospholipase versus triacylglycerol hydrolase activity of the two enzymes.…”

mentioning

confidence: 99%

Human Hepatic and Lipoprotein Lipase: The Loop Covering the Catalytic Site Mediates Lipase Substrate Specificity

Dugi

Dichek

Santamarina-Fojo

1995

Journal of Biological Chemistry

124

104

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“…By using native polyacrylamide gradient gel electrophoresis, at least five distinct subfractions of HDLs have been identified. 23 Hepatic lipase, 24 -25 lipoprotein lipase, 26 LCAT, 2728 and CETP 29 . *) have been implicated in the size redistribution of HDL subpopulations.…”

mentioning

confidence: 99%

Influence of plasma cholesteryl ester transfer activity on the LDL and HDL distribution profiles in normolipidemic subjects.

Lagrost¹,

Gandjini²,

Athias³

et al. 1993

Arterioscler Thromb

114

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The relations of cholesteryl ester transfer protein (CETP) activity to the distribution of low density lipoproteins (LDLs) and high density lipoproteins (HDLs) were investigated in fasting plasma samples from 27 normolipidemic subjects. LDL and HDL subtractions were separated by electrophoresis on 20-160 g/L and 40-300 g/L polyacrylamide gradient gels, respectively. Subjects were subdivided into two groups according to their LDL pattern. Monodisperse patterns were characterized by the presence of a single LDL band, whereas polydisperse patterns were characterized by the presence of several LDL bands of different sizes. To investigate the influence of lipid transfers on LDL patterns, total plasma was incubated at 37°C in the absence of lecithin: cholesterol acyltransferase (LCAT) activity. The incubation induced a progressive transformation of polydisperse patterns into monodisperse patterns. Under the same conditions, initially monodisperse patterns remained unchanged. Measurements of the rate of radiolabeled cholesteryl esters transferred from HDL 3 s to very low density lipoproteins (VLDLs) and LDLs revealed that subjects with a monodisperse LDL pattern presented a significantly higher plasma CETP activity than subjects with a polydisperse LDL pattern (301±85%/hr per milliliter versus 216±47%/hr per milliliter, respectively; p<0.02). In addition, when total plasma was incubated for 24 hours at 37°C in the absence of LCAT activity, the relative mass of cholesteryl esters transferred from

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Hydrolysis of human plasma high density lipoprotein2-phospholipids and triglycerides by hepatic lipase

Cited by 198 publications

References 20 publications

Independent Effects of Apo E Phenotype and Plasma Triglyceride on Lipoprotein Particle Sizes in the Fasting and Postprandial States

Independent Effects of Apo E Phenotype and Plasma Triglyceride on Lipoprotein Particle Sizes in the Fasting and Postprandial States

Human Hepatic and Lipoprotein Lipase: The Loop Covering the Catalytic Site Mediates Lipase Substrate Specificity

Influence of plasma cholesteryl ester transfer activity on the LDL and HDL distribution profiles in normolipidemic subjects.

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