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Apolipoproteins distribution

Hermier, D., Forgez, P. Chapmaa MJ. (1985). A density gradient study of the lipoprotein and apolipoprotein distribution in the chicken. Callus domeslicus. Biochim. Biophys. Acta, 836, 105-18. [Pg.244]

Seet, W.T., Mary Anne, T.J., Yen, T.S. (2004) Apolipoprotein E genotyping in the Malay, Chinese and Indian ethnic groups in Malaysa—a study on the distribution of the different apoE alleles and genotypes. Clin. Chim. Acta, 340, 201-205. [Pg.348]

Saunders, A.M., Schmader, K., Breitner, J.C.S., et al. (1993) Apolipoprotein E epsilon-4 allele distributions in late-onset Alzheimer s disease and in other amyloid-forming diseases. Lancet, 342, 710-711. [Pg.349]

R.M. Cohen, T.A. Podruchny, A.L.W. Bokde, R.E. Carson, P. Herscovitch, D.A. Kiesewetter, W.C. Eckelman, T. Sunderland, Higher in vivo muscarinic-2 receptor distribution volumes In ageing subjects with an apolipoprotein E-s4 allele. Synapse... [Pg.82]

Lipoproteins have hydrophobic core regions containing cholesteryl esters and triglycerides surrounded by unesterified cholesterol, phospholipids, and apoproteins. Certain lipoproteins contain very high-molecular-weight proteins that exist in two forms B-48, formed in the intestine and found in chylomicrons and their remnants and B-lOO, synthesized in liver and found in VLDL, VLDL remnants(IDL),LDL (formed from VLDL), and Lp(a) lipoproteins. HDL consist of at least 15 discrete molecular species. All species contain apolipoprotein A-I (apoA-I). Fifty-three other proteins are known to be distributed variously among the HDL species. [Pg.777]

Fig. 5.2.1 The major metabolic pathways of the lipoprotein metabolism are shown. Chylomicrons (Chylo) are secreted from the intestine and are metabolized by lipoprotein lipase (LPL) before the remnants are taken up by the liver. The liver secretes very-low-density lipoproteins (VLDL) to distribute lipids to the periphery. These VLDL are hydrolyzed by LPL and hepatic lipase (HL) to result in intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), respectively, which then is cleared from the blood by the LDL receptor (LDLR). The liver and the intestine secrete apolipoprotein AI, which forms pre-jS-high-density lipoproteins (pre-jl-HDL) in blood. These pre-/ -HDL accept phospholipids and cholesterol from hepatic and peripheral cells through the activity of the ATP binding cassette transporter Al. Subsequent cholesterol esterification by lecithinxholesterol acyltransferase (LCAT) and transfer of phospholipids by phospholipid transfer protein (PLTP) transform the nascent discoidal high-density lipoproteins (HDL disc) into a spherical particle and increase the size to HDL2. For the elimination of cholesterol from HDL, two possible pathways exist (1) direct hepatic uptake of lipids through scavenger receptor B1 (SR-BI) and HL, and (2) cholesteryl ester transfer protein (CfiTP)-mediated transfer of cholesterol-esters from HDL2 to chylomicrons, and VLDL and hepatic uptake of the lipids via the LDLR pathway... Fig. 5.2.1 The major metabolic pathways of the lipoprotein metabolism are shown. Chylomicrons (Chylo) are secreted from the intestine and are metabolized by lipoprotein lipase (LPL) before the remnants are taken up by the liver. The liver secretes very-low-density lipoproteins (VLDL) to distribute lipids to the periphery. These VLDL are hydrolyzed by LPL and hepatic lipase (HL) to result in intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), respectively, which then is cleared from the blood by the LDL receptor (LDLR). The liver and the intestine secrete apolipoprotein AI, which forms pre-jS-high-density lipoproteins (pre-jl-HDL) in blood. These pre-/ -HDL accept phospholipids and cholesterol from hepatic and peripheral cells through the activity of the ATP binding cassette transporter Al. Subsequent cholesterol esterification by lecithinxholesterol acyltransferase (LCAT) and transfer of phospholipids by phospholipid transfer protein (PLTP) transform the nascent discoidal high-density lipoproteins (HDL disc) into a spherical particle and increase the size to HDL2. For the elimination of cholesterol from HDL, two possible pathways exist (1) direct hepatic uptake of lipids through scavenger receptor B1 (SR-BI) and HL, and (2) cholesteryl ester transfer protein (CfiTP)-mediated transfer of cholesterol-esters from HDL2 to chylomicrons, and VLDL and hepatic uptake of the lipids via the LDLR pathway...
Polybrominated Biphenyls. The mechanism by which PBBs enter the blood stream from the lungs, skin, or gastrointestinal tract is not known and little information is available on how PBBs are distributed in the body. The available data indicate that the absorption mechanism is likely passive diffusion. Results from studies of Michigan subjects showed that in the blood stream, 80% of the PBBs was bound to protein and 20% was associated with lipids (Greaves et al. 1984). Of the fraction bound to protein, 73% was bound to apolipoprotein B and the remaining percent was bound to apolipoprotein A. In an in vitro model, shown to be representative of environmentally contaminated blood, the distribution of PBBs among plasma, erythrocytes, mononucleocytes, and polymorphonucleocytes was 89 9 <1 <1, respectively (Roboz et al. 1985). [Pg.220]

Each class of lipoprotein has a specific function, determined by its point of synthesis, lipid composition, and apolipoprotein content. At least nine different apolipoproteins are found in the lipoproteins of human plasma (Table 21-3), distinguishable by their size, their reactions with specific antibodies, and their characteristic distribution in the lipoprotein classes. These protein components act as signals, targeting lipoproteins to specific tissues or activating enzymes that act on the lipoproteins. [Pg.821]

Similarly, apolipoprotein E expression increases in neurotoxicity mediated by KA (Table 6.3) (Boschert et al., 1999). Apolipoprotein E is a major lipoprotein in the brain. It is involved in the transport, distribution, and other aspects of cholesterol homeostasis. Apolipoprotein E also plays a dominant role in the mobilization and redistribution of brain lipids in repair, growth, and maintenance of nerve cells (Mahley, 1988). The secretion of apolipoproteins E and D may be differentially regulated in cultured astrocytes. In cell culture systems this depends upon the extracellular lipid milieu (Patel et al., 1995). During neurotoxicity mediated by KA, apolipoprotein E levels increase moderately in astrocytes and apolipoprotein E mRNA increases very strongly in clusters of CA1 and CA3 pyramidal neurons. Based on hybridization in situ and immunohistochemical studies, expression of apolipoprotein E in neurons may be a part of a rescue program to counteract neurodegeneration mediated by KA (Boschert et al., 1999). [Pg.116]

In Chapter 14, it was explained that the lipid composition of LCM (cf. Section 12.1) is similar to the lipid composition of both chylomicron remnant particles (cf. Section 14.2.1) and LDL particles (cf. Section 14.1). Based upon this molecular similarity, it was proposed that i.v. injected LCM could readily bind (as do chylomicron remnants) to apolipoprotein E in the bloodstream (cf. Section 14.2.1). Both the LDL receptor (a.k.a. apo B,E receptor ) and the LRP (cf. Section 14.2.1) have a high affinity for apo E (ref. 666), and both receptors play an essential role in the receptor-mediated endocytosis of chylomicron remnants (ref. 650,665,709). Accordingly, these two endocytic pathways have been proposed (together with scavenger receptor-mediated endocytosis) to influence LCM distribution in vivo in certain pathological states (cf. above). [Pg.255]

Yamagata Z, Asada T, Kinoshita A, Zhang Y, Asaka A. Distribution of apolipoprotein E gene polymorphisms in Japanese patients with Alzheimer s disease and in Japanese centenarians. Hum Hered 1997 47 22-26. [Pg.205]

Weinberg RB. Apolipoprotein A-IV-2 allele Association of its worldwide distribution with adult persistence of lactase and speculation on its function and origin. Genet Epidemiol. 1999, 17 285-297. [Pg.168]

Sepehrnia B, Kamboh MI, Adams-Campbell LL, Nwankwo M, Ferrell RE. Genetic studies of human apolipoproteins. VII. Population distribution of polymorphisms of apolipoproteins A-I, A-II, A-IV, C-II, E, and H in Nigeria. Am J Hum Genet. 1988, 43 847-853. [Pg.168]

When infants were fed the same amount of palmitic acid, significantly lower values of high-density lipoprotein-cholesterol and of apolipoprotein A and significantly higher levels of apoB were found in infants when the same amount of palmitic acid was fed in TAGs in the i 2-position than in the i l(3)-position (69). This illustrates that lipoprotein metabolism can be affected by fatty acid distribution in TAGs. [Pg.1906]

The lipids of the diet include TGs, phospholipids, cholesteryl esters, cholesterol, and the fat-soluble vitamins. These nutrients require special types of biochemical machinery to facilitate their assimilation and distribution within the body. The biochemical apparatus used includes bile salts, apolipoproteins, serum albumin, and vitamin-binding proteins. Apolipoproteins are the primary subject of this section. The term apolipoprotein is used when referring only to the protein, whereas the term lipoprotein refers to the complex of apolipoprotein and lipid. [Pg.332]

Modified from Bachorilc PS, Lovejoy KL, CarroU MD, Johnson CL. Apolipoprotein B and AI distributions in the United States, 1988-1991 results of the National Health and Nutrition Examination Survey III (NHANES III), Clin Chem 1997 43 2364-78. [Pg.926]

Absorption, distribution, metabolism, elimination 5 -adenylyl /1-y-imidodiphosphate Aminohexanoic acid Adenosine monophosphate Apolipoprotein D... [Pg.259]


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See also in sourсe #XX -- [ Pg.214 ]




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