Lipoproteins derivatives

Helisten H, Hockerstedt A, Wahala K et al. Accumulation of high-density lipoprotein-derived estradiol-17(3 fatty acid esters in low-density lipoprotein particles. J. Clin. Endocrinol Metab. 86, 1294-1300, 2001. 

Plasma lipoproteins can be divided into six major classes (see Fig. 5.2.1). Four of these classes derive from the liver and are present in the plasma of fasted subjects very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). The other two classes of lipoproteins derive from the intestine and are found in the plasma of nor-molipidemic individuals only after a fatty meal (postprandially) chylomicrons and chylomicron remnants. 

Sarria, A. J., Panini, S. R., and Evans, R. M. (1992). A functional role for vimentin intermediate filaments in the metabolism of lipoprotein-derived cholesterol in human SW-13 cells./. Biol. Chem. 267, 19455-19463. 

Glycosphingolipid (GSLs) Contenta of Human Plasma and Plasma Lipoproteins Derived from a Representative Normal Male and Female Subject and... 

Srivastava S, Conklin DJ, Liu S, Prakash N, Boor PJ, Srivastava SK and Bhatnagar A, Identification of biochemical pathways for the metabolism of oxidized low-density lipoprotein derived aldehyde-4-hydroxy trans-2-nonenal in vascular smooth muscle cells. Atherosclerosis 158(2) 339-50,2001. 

Cholesterol accumulation in lesional macrophages intracellular trafficking of lipoprotein-derived cholesterol... 

The trafficking of lipoprotein-derived cholesterol from lysosomes has been a major area of focus in the field of intracellular cholesterol metabolism, and many of the cellular and molecular events are not known (Chapter 17). By analyzing cells with mutations in cholesterol transport, investigators have identified roles for two proteins, called NPCl and NPC2 (HEl), in lysosomal and/or endosomal cholesterol transport (E.J. Blanchette-Mackie, 2000 P. Lobel, 2000). In addition, the lipid lysobisphosphatidic acid and certain GTPases called Rab proteins may also play roles in these processes (J. Gruenberg, 1999 E. Ikonen, 2006). The mechanisms by which these molecules are involved in cholesterol transport, however, are poorly understood [14]. 

Rinninger, F., Kaiser, T., Windier, E., Greten, H., Fruchart, J.C., and Castro, G., 1998. Selective uptake of cholesteryl esters from high-density lipoprotein-derived LpA-I and LpA-I A-II particles by hepatic cells in culture. Biochi-mica et Biophysica Acta. 1393 277-291. 

It is of considerable interest that human erythrocyte phosphoglycerides have a similar distribution of plasmalogens and fatty acids to that of platelets (Farquhar, 1962). Although the fatty add composition of PS in the red cell resembles that of the platelet, there is about twice as much PS in the erythrocyte. This may account for the marked clot-promoting effects of lipids and lipoproteins derived from red cells after damage or hemolysis (O Brien, 1959a Shinowara, 1951, 1957, 1961). 

Intestinally derived triglyceride-rich lipoprotein. Lipoprotein Metabolism... 

Cells in the atheroma derived from both macrophages and smooth muscle cells that have accumulated modified low-density lipoproteins. Their cytoplasm laden with lipid causes the foamy appearance on microscopy... 

Fibric acid derivatives, the third group of antihyperlipi-demic drugs, work in a variety of ways. Clofibrate (Atromid-S), acts to stimulate the liver to increase breakdown of very-low-density lipoproteins (VLDL) to low-density lipoproteins (LDL), decreasing liver synthesis of... 

VLDL is the precursor of IDL, which is then converted to LDL. Only one molecule of apo B-lOO is present in each of these lipoprotein particles, and this is conserved during the transformations. Thus, each LDL particle is derived from only one VLDL particle (Figure 25-4). Two possible fates await IDL. It can be taken up by the liver directly via the LDL (apo B-lOO, E) receptor, or it is converted to LDL. In humans, a relatively large proportion forms LDL, accounting for the increased concentrations of LDL in humans compared with many other mammals. 

As has already been stated, the carotenoids are lipophilic and are therefore absorbed and transported in association with the lipoprotein particles. In theory, this fortuitous juxtaposition of lipid and carotenoid should confer protection on the lipid through the antioxidant properties of the carotenoid. No doubt some antioxidant protection is afforded by the presence of the carotenoids derived from the diet. However, with one or two exceptions, human supplementation studies have not supported a role for higher dose carotenoid supplements in reducing the susceptibility of the low-density lipoproteins to oxidation, either ex vivo or in vivo (Wright et al, 2002 Hininger et al, 2001 Iwamoto et al, 2000). 

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. 

Using human hepatoma-derived cell lines Kong et al. [268] showed that berberine increased mRNA and protein as well as the function of hepatic linear low density lipoprotein receptor (LDLR). It does not stimulate the transcription of LDLR, as the LDLR promoter activity was not increased by this compound. Post-transcriptional regulation appears to be the main working mechanism underlying the effect of this alkaloid on LDLR expression. It was proposed that berberine can be used as a monotherapy to treat hypercholes-terolemic patients [268]. Very recently it was observed [269] that berberine reduces cholesterol and Upid accumulations in plasma as well as Uver. 

O Leary, V.J., Darley-Usmar, V.M., Russell, L.J. and Stone, D. (1992). Pro-oxidant efiects of lipoxygenase derived peroxides on the copper initiated oxidation of low density lipoprotein. Biochem. J. 282, 631-634. 

Chin et al. (1992) have su ested that oxidized LDL and high-density lipoprotein (HDL) inactivate endothelial cell-derived NO. NO inactivation was due to the oxidized lipids within the lipoprotein particles and was thought to be explained by a chemical reaction between the lipoproteins and NO. Other investigators have shown that relaxation of vascular smooth muscle by acetylcholine or bradykinin (endothelium-dependent vasodilators) is inhibited by LDL (Andrews etal., 1987). The role of NO in the modification of LDL is discussed in full detail in Chapter 2. 

Chin, J.H., Azhar, S. and Hoffman, B.B. (1992). Inactivation of endothelial derived relaxing factor by oxidized lipoproteins. 

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