Association of Lp(a) rather than integrally-bound apo(a) with triglyceride-rich lipoproteins of human subjects

Marcoux, Caroline; Lussier‐Cacan, Suzanne; Davignon, Jean; Cohn, Jeffrey S.

doi:10.1016/s0005-2760(97)00049-0

Cited by 15 publications

(12 citation statements)

References 39 publications

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“…It has been documented that the apo(a) found in the d <1.006 g/mL fraction occurs on slow preβ-migrating particles; and when apo(a) in this fraction was dissociated from chylomicrons and VLDL particles with 100 mM proline and ultracentrifugation, the majority of the apo(a) was in the form of Lp(a) particles [49,50]. In our own studies we have observed that much of apo(a) in whole plasma, as determined by gradient gel electrophoresis and specific immunoblotting, is found in a wide range of lipoprotein particle size, with virtually none in the lipoprotein free state [51].…”

Section: Discussionmentioning

confidence: 99%

Distinct metabolism of apolipoproteins (a) and B-100 within plasma lipoprotein(a)

et al. 2016

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Objectives Lipoprotein(a) [Lp(a)] is mainly similar in composition to LDL, but differs in having apolipoprotein (apo) (a) covalently linked to apoB-100. Our purpose was to examine the individual metabolism of apo(a) and apoB-100 within plasma Lp(a). Materials and methods The kinetics of apo(a) and apoB-100 in plasma Lp(a) were assessed in four men with dyslipidemia [Lp(a) concentration: 8.9-124.7 nmol/L]. All subjects received a primed constant infusion of [5,5,5-2H3] L-leucine while in the constantly fed state. Lp(a) was immunoprecipitated directly from whole plasma; apo(a) and apoB-100 were separated by gel electrophoresis; and isotopic enrichment was determined by gas chromatography/mass spectrometry. Results Multicompartmental modeling analysis indicated that the median fractional catabolic rates of apo(a) and apoB-100 within Lp(a) were significantly different at 0.104 and 0.263 pools/day, respectively (P=0.04). The median Lp(a) apo(a) production rate at 0.248 nmol/kg·day-1 was significantly lower than that of Lp(a) apoB-100 at 0.514 nmol/kg·day-1 (P=0.02). Conclusion Our data indicate that apo(a) has a plasma residence time (11 days) that is more than twice as long at that of apoB-100 (4 days) within Lp(a), supporting the concept that apo(a) and apoB-100 within plasma Lp(a) are not catabolized from the bloodstream as a unit in humans in the fed state.

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Section: Discussionmentioning

confidence: 99%

Distinct metabolism of apolipoproteins (a) and B-100 within plasma lipoprotein(a)

et al. 2016

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“…The majority of apo(a) in plasma is characteristically associated with Lp(a). In the postprandial state, a small proportion of plasma apo(a) is found in the d Ͻ1.006 kg/L fraction of plasma by density gradient ultracentrifugation, associated with larger and less dense TRLs (26 ). Moreover, apo(a) in the TRLs fraction increased, whereas apo(a) in the d Ͼ1.006 fraction decreased after fat intake, suggesting a transfer of apo(a) from the d Ͼ1.006 fraction to the TRLs (2 ).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, apo(a) in the TRLs fraction increased, whereas apo(a) in the d Ͼ1.006 fraction decreased after fat intake, suggesting a transfer of apo(a) from the d Ͼ1.006 fraction to the TRLs (2 ). Evidence supports that apo(a) in the TRL fraction of individuals with postprandial hypertriglyceridemia is not an integral component of plasma VLDL or chylomicrons, but represents the presence of noncovalently bound Lp(a) (26 ). Recently, Nassir et al (27 ) observed that apo(a) secretion from hepatoma cells may be linked to elements of cellular triglyceride assembly and secretion, which raises the idea that the Lp(a) concentration in humans may be affected by alterations in the hepatic synthesis of TRLs.…”

Section: Discussionmentioning

confidence: 99%

Xuezhikang Decreases Serum Lipoprotein(a) and C-reactive Protein Concentrations in Patients with Coronary Heart Disease

Liu¹,

Zhao²,

Cheng³

et al. 2003

Clinical Chemistry

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Background: Increased serum lipoprotein(a) [Lp(a)] andhigh-sensitivity C-reactive protein (hsCRP) concentrations are independent risk factors for coronary heart disease (CHD). Xuezhikang, an extract of cholestin, effectively lowers fasting cholesterol and triglyceride concentrations. We studied whether xuezhikang lowered Lp(a) and hsCRP concentrations. Methods: We randomly divided 60 CHD patients into two groups to receive xuezhikang (1200 mg daily) or placebo for 6 weeks. The fasting hsCRP concentration and the postprandial changes of serum lipid concentrations at 2, 4, and 6 h after a high-fat meal (800 calories; 50 g of fat) were measured before and after the 6-week protocol. Results: The two groups had similar baseline fasting lipid and hsCRP concentrations. The postprandial triglyceride and Lp(a) concentrations were significantly increased (P <0.05). After 6 weeks, the fasting and postprandial lipid concentrations decreased significantly in the xuezhikang group, accompanied by a significant reduction in fasting hsCRP concentration (P <0.001). The placebo group had no significant change in lipid concentrations, whereas the fasting serum hsCRP concentration was reduced significantly (P <0.05). The reduction in hsCRP was closely related to the changes in fasting Lp(a) concentration (r ‫؍‬ 0.402; P <0.05) and triglyceride area under the curve (r ‫؍‬ 0.441; P <0.001). Conclusions: Xuezhikang effectively decreased fasting Lp(a) and postprandial triglyceride concentrations, which were associated with reductions of fasting hsCRP concentrations in CHD patients.

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“…No other quantitative trait is as influenced by sequence differences at a single locus as is Lp(a) [33]. is gene is accountable for the substantial size heterogeneity of apo(a) isoforms [34], which is associated with the variable number of copies (repeats) of kringle KIV 2 , ranging from 2 to more than 50 repeats with substantial size polymorphism (200-800 kilodaltons) [35] (see Figure 2). e largest apo(a) isoform described so far has 52-54 KIV repeats [36].…”

Section: 4mentioning

confidence: 99%

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

2020

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Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

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Association of Lp(a) rather than integrally-bound apo(a) with triglyceride-rich lipoproteins of human subjects

Cited by 15 publications

References 39 publications

Distinct metabolism of apolipoproteins (a) and B-100 within plasma lipoprotein(a)

Distinct metabolism of apolipoproteins (a) and B-100 within plasma lipoprotein(a)

Xuezhikang Decreases Serum Lipoprotein(a) and C-reactive Protein Concentrations in Patients with Coronary Heart Disease

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

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