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Lipid uptake

Genes involved in the uptake and degradation of tocopherols - Genes implicated with lipid uptake and. Mi / °f J - Protein kinase C (PKC) - Cyclooxygenase - 5-Lipoxygenase - Cytokine release (IL-1P)... [Pg.1297]

Merkel M, Eckel RH, Goldberg IJ (2002) Lipoprotein lipase genetics, lipid uptake, and regulation. J Lipid Res 43 1997-2006... [Pg.547]

The protein moieties of lipoproteins are recognized by receptors on cell surfaces. In lipid uptake from the intestine, chylomicrons, which contain apolipoprotein C-II (apoC-ID, move from the intestinal mucosa into the lymphatic system, and then enter the blood, which carries them to muscle and adipose tissue (Fig. 17-1, step... [Pg.632]

Moffat, D. and Kusel, J.R. (1992) Fluorescent lipid uptake and transport in adult Schistosoma mansoni. Parasitology 1 05, 81-89. [Pg.406]

Liu B. and Krieger M. (2002) Highly purified scavenger receptor class B, type I reconstituted into phosphatidylcholine/cholesterol liposomes mediates high affinity high density lipoprotein binding and selective lipid uptake. J. Biol. Chem. 277, 34125-34135. [Pg.438]

A poorly understood aspect of lipophorin metabolism is tissue-specific delivery of lipids. At present mechanistic details are lacking, but some properties of the system are apparent. Lipid seems to be transferred from lipophorin to tissue only in those cases in which the tissue can carry out some additional reaction with the lipid, e.g., in the fat body DG is converted to TG, and in the epidermis hydrocarbon is secreted onto the outer surface of cuticle. In other cases there may be intracellular lipidbinding proteins that, by binding the lipid, drive lipid uptake into the tissue. These or other processes would drive the equilibrium of lipid transfer in favor of the tissue, irrespective of the mechanism by which lipid delivery occurs. [Pg.408]

F Bellemare, J Noel, C Malo. Characteristics of exogenous lipid uptake by renal and intestinal brush border membrane vesicles. Biochem Cell Biol 73 171—179,1995. [Pg.268]

Fig. 4 The lipid influx/efflux rheostat model maintains lipid uptake and export mechanisms in a balance. ATP synthase is regulated by apoA-I or apoE leading to enhanced conversion of ATP to ADP. The absence of apoA-I would lead to enhanced sinking in phagocytosis since actin can bind ATP, polymerize, and form F-actin which is essential for type 11 phagocytosis. Hence apoA-I could lead to increased influx. On the other hand, apoA-I binds to ABCAl leading to enhanced lipid efflux. Dysfunction of this equilibrium may lead to severe disturbances of cellular lipid traffic. This is obvious in Tangier disease patients where ABCAl is inoperative and apoA-/-dependent cholesterol is absent. Cholesterol influx, however, is enhanced due to apoA-Z-dependent stimulation of ATP synthase B leading to cholesteryl ester formation and enhanced foam cell formation... Fig. 4 The lipid influx/efflux rheostat model maintains lipid uptake and export mechanisms in a balance. ATP synthase is regulated by apoA-I or apoE leading to enhanced conversion of ATP to ADP. The absence of apoA-I would lead to enhanced sinking in phagocytosis since actin can bind ATP, polymerize, and form F-actin which is essential for type 11 phagocytosis. Hence apoA-I could lead to increased influx. On the other hand, apoA-I binds to ABCAl leading to enhanced lipid efflux. Dysfunction of this equilibrium may lead to severe disturbances of cellular lipid traffic. This is obvious in Tangier disease patients where ABCAl is inoperative and apoA-/-dependent cholesterol is absent. Cholesterol influx, however, is enhanced due to apoA-Z-dependent stimulation of ATP synthase B leading to cholesteryl ester formation and enhanced foam cell formation...
From quantitative structure-activity relationships, the bioconcentration factors (BCFs) for 2-butoxyethanol and 2-butoxyethanol acetate in fathead minnows Pimephales promelas) have been estimated to be 2 and 9, respectively (ASTER 1995a, 1995b). Therefore, bioconcentration of either compound in aquatic organisms is not important. No information was located that would suggest that either compound biomagnifies in the food chain. This is not surprising, considering that the low values (see Tables 3-3 and 3-4) indicate low probability of lipid uptake. [Pg.327]

The most commonly employed in vitro technique for study of lipid uptake into the cell is the use of segments of small intestine in the form of biopsies, disks, slices or everted sacs. Thomson and O Brien [53] found that although the rate of lipid uptake was not the same for different types of in vitro preparations, they all gave similar results as far as the qualitative role of bile salts for lipid uptake was concerned. [Pg.411]

A detailed investigation of the effect of micellar solubilization on the transport of lipids has been made by Westergaard and Dietschy [59]. They studied in vitro uptake of lipids into rabbit intestinal disks by varying the proportions of lipid and bile salts in mixed micelles in 3 different ways. Either lipid concentration was increased with bile salts kept at a constant level, lipid concentration was unchanged while bile salt concentration was varied, or both lipid and bile salt concentration was increased with the molar ratio kept constant. Theoretical calculations of how the mass of the lipid probe was distributed between the aqueous and the micellar compartment showed that there was a good correlation between calculated aqueous monomer concentration and experimentally obtained values for lipid uptake. The rate of uptake is thus proportional to the aqueous monomer concentration of a particular lipid. The conclusion drawn was that diffusion of the lipid molecules in monomeric form through the aqueous phase is an obligatory step before uptake into the plasma membrane, and that the role of bile salt is therefore to overcome the resistance of the unstirred water layer by micellar solubilization. [Pg.415]

By comparing the relative rate of uptake of two different lipid probe molecules, another piece of evidence for a monomeric mechanism in lipid uptake by membranes has been found. Hoffman [70] and Hoffman and Yeoh [71] have determined the relationship between micellar concentration and uptake by rat small intestine in vitro for oleic acid and a monoglyceride analog, a 1-monoether. They found that the rate of uptake for both of the two micellar solutes was linearly dependent on the micellar concentration, but that the ratio of rate of uptake was different from the molar ratio of the two lipids in the micellar phase. Oleic acid was absorbed more rapidly than the monoether, probably due to a higher monomer concentration in the... [Pg.415]

Export by ABC proteins endocytosis/exocytosis as part of lipoproteins import by selective lipid uptake from lipoproteins... [Pg.745]

NPCl) protein 753 receptor SR-Bl 763 receptor-mediated endocytosis 760 reverse cholesterol transport 771 selective lipid uptake 760 SRE-binding protein (SREBP) 764 statin 773... [Pg.774]

While most of the known functions of apolipoproteins are associated with their lipid-bound states, lipid-free or lipid-poor exchangeable apolipoproteins do exist in plasma and interstitial fluid, and have important metabolic roles in lipid uptake from cells, transfers between lipoproteins, structural remodeling of lipoproteins, and apolipoprotein catabolism. [Pg.495]

Moore, K.J., Freeman, M.W. 2006. Scavenger receptors in atherosclerosis beyond lipid uptake. Arterioscler. Thromb. Vase. Biol. 26 1702-1711. [Pg.578]

M.W. 2005. Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice. J. Clin. Invest. 115 2192-2201. [Pg.604]


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See also in sourсe #XX -- [ Pg.40 , Pg.197 , Pg.198 , Pg.202 ]

See also in sourсe #XX -- [ Pg.197 , Pg.198 , Pg.202 ]




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Lipid uptake mixed micelles, from

Membrane lipid uptake

Membrane vesicle lipid uptake

Mixed micelles lipid uptake

Selective lipid uptake

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