Effects of plasma apolipoproteins on lipoprotein lipase-mediated lipolysis of small and large lipid emulsions

Yamamoto, Mayumi; Morita, Shin; Kumon, Michiko; Kawabe, Misa; Nishitsuji, Kazuchika; Saito, Hiroyuki; Vertut-Doı̈, Aline; Nakano, Minoru; Handa, Tetsurou

doi:10.1016/s1388-1981(03)00058-1

Cited by 28 publications

(23 citation statements)

References 57 publications

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“…It is possible that apoA-I, as a structural component of intestinally secreted chylomicrons, modulates their rate of assembly and subsequent secretion in the circulation. Likewise, because excess apoA-I is a known inhibitor of lipoprotein lipase (33), it is possible that deficiency in apoA-I accelerates lipoprotein lipase-mediated lipolysis of chylomicrons, thus promoting their catabolism. These possibilities warrant further investigation in future studies.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Karavia

Papachristou

Liopeta

et al. 2012

Mol Med

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Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Karavia

Papachristou

Liopeta

et al. 2012

Mol Med

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“…Both large and small emulsions are hydrolyzed at similar rates in the presence of apoC-II. 264) ApoC-III and apoE work as LPL-inhibitors of the lipolysis activated by apoC-II.…”

Section: )mentioning

confidence: 99%

“…264) The inhibition by apoE in small emulsions is more effective than for large emulsions. 264) ApoA-I inhibits the LPL-mediated lipolysis of small emulsions more effectively.…”

Section: )mentioning

confidence: 99%

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Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

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133

108

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Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies.

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“…A possible biological explanation of how this gene variation elevates plasma TG levels is that the binding capacity of the protein to lipases is impaired, resulting in decreased lipolysis and elevated plasma TG levels. On the other hand, Yamamoto et al 38 showed that apolipoprotein C-III, apolipoprotein E and apolipoprotein A-I work as a potential inhibitor for the LPL-mediated lipolysis of TG-rich emulsions. This implies that elevated lipoprotein levels in blood lead to elevated TG levels.…”

Section: Polymorphisms Associated With Triglyceride Levelsmentioning

confidence: 99%

Polymorphisms in APOA1 and LPL genes are statistically independently associated with fasting TG in men with CAD

et al. 2005

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The objective of this paper was to identify the single nucleotide polymorphisms (SNPs) that show unshared effects on plasma triglyceride (TG) levels and to investigate whether these SNPs show statistically independent effects on plasma TG levels. In total, 59 polymorphisms in 20 genes involved in lipid metabolism were investigated. Polymorphisms were selected for a multivariate ANOVA model if they showed an univariate association with TG (after adjustment for HDL-C and LDL-C) in more than 50% of bootstrap samples that were made from the original data. The multivariate model included 512 men with coronary artery disease from the REGRESS study who were completely genotyped for eight polymorphisms selected in the univariate procedure (ie, APOA1 G(À75)A, ABCA1 C(À477)T, ABCA1 G1051A, APOC3 T3206G, APOE Arg158Cys, LIPC C(À514)T, LPL Asn291Ser and LPL Ser447Stop). The gene variants APOA1 G(À75)A (P ¼ 0.04) and LPL Asn291Ser (P ¼ 0.03) were significantly associated with plasma TG levels in this multivariate analysis. The eight polymorphisms explained 8.9% of the variation in plasma TG levels. In conclusion, this study showed statistically independent effects of gene variants in the APOA1 and LPL genes on fasting plasma levels of TG. Nevertheless, only a small part of variation in TG levels could be explained by the polymorphisms.

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Effects of plasma apolipoproteins on lipoprotein lipase-mediated lipolysis of small and large lipid emulsions

Cited by 28 publications

References 57 publications

Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Apolipoprotein A-I Modulates Processes Associated with Diet-Induced Nonalcoholic Fatty Liver Disease in Mice

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Polymorphisms in APOA1 and LPL genes are statistically independently associated with fasting TG in men with CAD

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