Lipoproteins determination

Laboratory and Exercise Evaluation Laboratory evaluations performed at each two-week visit included plasma total cholesterol, LDL-C, HDL-C, VLDL-C, and plasma total triglycerides.23 The lipoprotein determinations, LDL-C, HDL-C, and VLDL-C were not performed at Week 16. White blood cell counts, calcium, and serum glutamic oxaloacetic-transaminase (SGOT) were done before and after feeding LBG products. Weight was recorded at each visit. 

Shi, W., Haberland, M., lien, M.-L., Shih, D. and Lusis, A. Endothelial responses to oxidized lipoproteins determine genetic susceptibility to atherosclerosis in mice. COrM/aJjgg 102, 75-81, 2000. 

Table I Lipid contents in serum lipoproteins determined by HPLC method...

Quality Control. The study procedures were carried out according to the WHO guidelines. Established internal quality controlly procedures were used in the laboratory to ensure high levels of precision and accuracy for the lipid and lipoprotein determination. External quality controls were performed by the WHO Lipid Reference Labmatory, Europe (Dr. Grafnetter, Prague), and in cooperation with the reference laboratory of Boehringer Co., Mannheim. 

Proteins embedded in the shell of lipoproteins. They serve as scaffold for assembly of the lipoprotein particle in the endoplasmic reticulum. In addition, they control metabolism of lipoproteins in the circulation by interaction with enzymes such as lipases. Finally, apolipoproteins determine cellular uptake of the particles by interaction with specific lipoprotein receptors expressed on the surface of target cells. 

The effect of a statin is usually determined by measuring fasting plasma lipids and lipoproteins after 4-6 weeks of treatment. Liver enzymes and eventually creatine kinase (in case of myositis liver enzymes are usually also elevated) are measured simultaneously to exclude side effects related to liver and muscles. After the treatment goal has been reached, blood sampling is usually performed 1-2 times a year. 

VAN HET HOF K H, DE BOER B C, TIJBURG L B, LUCIUS B R, ZIJP I, WEST C E, HAUTVAST J G and WESTRATE J A (2000) Carotenoid bioavailability in humans from tomatoes processed in different ways determined from the carotenoid response in the triglyceride-rich lipoprotein fraction of plasma after a single consumption and in plasma after 4 days of consumption. JNutr 130(5) 1189-96. 

This approach can be used only for fat-soluble compounds that follow the same lymphatic route to be transported to the liver as carotenoids. The bioavailability of the compound of interest is determined by monitoring the appearance of the compound and its newly formed intestinal metabolites in the postprandial chylomicron fraction of plasma [also called the density < 1.006 kg/L fraction or triglyceride-rich lipoprotein (TRL) fraction because it is generally a mixture of chylomicrons (CMs) and very low density lipoproteins (VLDLs)] as a function of the time after ingestion. 

In contrast with the hydrocarbon carotenes primarily located in the cores of the CM particles, xanthophylls are present at the surfaces of the CM particles, making their exchanges with other plasma lipoproteins easier." Therefore, if some exchanges occur between lipoproteins, AUC (or absorption) values of the newly absorbed compound in the TRL fraction will be underestimated. Based on all these considerations, the present approach is more appropriate to determine the relative bioavailability of a compound derived from various treatments within one snbject and/or within one study. 

Characterisation of PemB as a lipoprotein and determination of its cellular localisation... 

Probucol, another di-r-butyl phenol, is an anti-atherosclerotic agent that can suppress the oxidation of low-density lipoprotein (LDL) in addition to lowering cholesterol levels. The antioxidant activity of probucol was measured, using EPR, with oxidation of methyl linoleate that was encapsulated in liposomal membranes or dissolved in hexane. Probucol suppressed ffee-radical-mediated oxidation. Its antioxidant activity was 17-fold less than that of tocopherol. This difference was less in liposomes than in hexane solution. Probucol suppressed the oxidation of LDL as efficiently as tocopherol. This work implies that physical factors as well as chemical reactivity are important in determining overall lipid peroxidation inhibition activity (Gotoh et al., 1992). 

Fatty acids play an important role as a risk factor for cardiovascular diseases, that is by forming plaques within the arteria. Low density lipoproteins (LDL) are seen as the most important risk factor. In the clinical chemistry laboratory, both LDLs and HDLs (high density lipids, considered as an anti-atherogenic factor) are determined. 

Lipoproteins. A lipoprotein is an endogenous macromolecule consisting of an inner apolar core of cholesteryl esters and triglycerides surrounded by a monolayer of phospholipid embedded with cholesterol and apoproteins. The functions of lipoproteins are to transport lipids and to mediate lipid metabolism. There are four main types of lipoproteins (classified based on their flotation rates in salt solutions) chylomicrons, very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). These differ in size, molecular weight, and density and have different lipid, protein, and apoprotein compositions (Table 11). The apoproteins are important determinants in the metabolism of lipoproteins—they serve as ligands for lipoprotein receptors and as mediators in lipoproteins interconversion by enzymes. 

Pittenauer, E. Quintela, J. C. Schmid, E. R. Allmaier, G. Paulus, G. de Pedro, M. A. Characterization of Braun s lipoprotein and determination of its attachment sites to peptidoglycan by 252-Cf-PD and MALDI time-of-flight mass spectrometry. /. Am. Soc. Mass Spectrom. 1995, 6, 892-905. 

So far, we have focused mainly on the potential pathways of carotenoid uptake by the RPE from the choroidal blood supply. As mentioned earlier, POS contain lutein and zeaxanthin, and their distal tips are phagocytosed by the RPE. Therefore POS is another source of xanthophylls in the RPE and this pathway of carotenoid delivery and their further fate can be easily tested in cultured RPE. It has been shown that exposure of RPE cells in vitro to HDL stimulates efflux of phospholipids from phagocytosed POS out of the cell (Ishida et al., 2006). Thus it is of interest to determine whether that transport may potentially include xanthophylls and whether other types of lipoproteins may... 

Lipoprotein (a) is an independent risk factor for coronary artery disease [68]. It consists of two components an LDL particle and apolipoprotein (a) which are linked by a disulfide bridge. Apo(a) reveals a genetically determined size polymorphism, resulting from a variable number of plasminogen kringle IV-type repeats [69]. Statins either do not affect Lp(a) or may even increase Lp(a) [70, 71]. In a study of 51 FH patients, treated with 40 mgd 1 pravastatin, it has been shown that the increase in Lp(a) was greatest in patients with the low molecular-weight apo(a) phenotypes [70]. 

It is commonly known that lipids, carbohydrates, and glycolipids are present in the Golgi apparatus (27). The determination of the components that react with the ZIO mixture was carried out by removing each component from tissues before incubation in the ZIO mixture. After lipid extraction by acetone (14), chloroform-methanol (15), or propylene oxide (27), no osmium-zinc precipitates could be detected in structures that normally reacted with ZIO. Blumcke et al. (15) summarized the nature of the lipids that react with the ZIO mixture as follows lipids and lipoproteins of cell membranes, neutral fat droplets (41), and lipid globules of type II pneumocytes and alveolar macrophages were, however, not as electron dense as the normally reactive lamellae containing highly unsaturated fatty acids. 

Lp(a) exhibits a genetic size polymorphism (MW 350-840 kDa) controlled by at least seven autosomal alleles. At the same time, these alleles are also involved in determining the plasma concentrations of the lipoprotein. 

So, according to Emancipator (E8), a meal has a clinically significant influence on the Lp(a) level, as measured by ELISA methods (the effect decreases 2 h after the meal). Whether this is caused by a different distribution of apo(a) and Lp(a) over other lipoproteins, in which antigenic determinants are covered, is not clear. 

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