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Lipoprotein lipase distribution

Hohe, K. A., Dimick, P. S. and Kilara, A. 1985. Milk lipoprotein lipase distribution in the major fractions of bovine milk. J. Dairy Sci. 68, 1067-1073. [Pg.572]

Both intact carotenoids and their apolar metabolites (retinyl esters) are secreted into the lymphatic system associated with CMs. In the blood circulation, CM particles undergo lipolysis, catalyzed by a lipoprotein lipase, resulting in the formation of CM remnants that are quickly taken up by the liver. In the liver, the remnant-associated carotenoid can be either (1) metabolized into vitamin A and other metabolites, (2) stored, (3) secreted with the bile, or (4) repackaged and released with VLDL particles. In the bloodstream, VLDLs are transformed to LDLs, and then HDLs by delipidation and the carotenoids associated with the lipoprotein particles are finally distributed to extrahepatic tissues (Figure 3.2.2). Time-course studies focusing on carotenoid appearances in different lipoprotein fractions after ingestion showed that CM carotenoid levels peak early (4 to 8 hr) whereas LDL and HDL carotenoid levels reach peaks later (16 to 24 hr). [Pg.163]

Sandholzer, C., Feussner, G., Brunzell, J., and Utermann, G., Distribution of apolipopro-tein(a) in the plasma from patients with lipoprotein lipase deficiency and with type III hyperlipoproteinemia. J. Clin. Invest. 90, 1958-1965 (1992). [Pg.129]

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...
Paradis E., Clavel S., Julien P., Murthy M. R. V., de Bilbao F., Arsenijevic D., Giannakopoulos P., Vallet P., and Richard D. (2004). Lipoprotein lipase and endothelial lipase expression in mouse brain regional distribution and selective induction following kainic acid-induced lesion and focal cerebral ischemia. Neurobiol. Dis. 15 312-325. [Pg.134]

Anderson, M. 1982a. Factors affecting the distribution of lipoprotein lipase activity between serum and casein micelles in bovine milk. J. Dairy Res. 49, 51-59. [Pg.531]

Bachman, K.C., Wilcox, C.J. 1990b. Effect of blood and high density lipoprotein preparations upon lipase distribution and spontaneous lipolysis in bovine milk. J. Dairy Sci. 73, 3393-3401. [Pg.532]

Sundheim, G., Bengtsson-Olivecrona, G. 1987d. Hydrolysis of bovine and caprine milk fat globules by lipoprotein lipase. Effects of heparin and of skim milk on lipase distribution and on lipolysis. J. Dairy Sci. 70, 2467-2475. [Pg.554]

Camps, L., Relna, M., Llobeia, Bengtsson-Olivecrona, G Olivecrona, T, and Vilaro, S. fl99l). Lipoprotein lipase in lungs, spleen, and liver Synthesis and distribution./. Lipid to. 32,1877-1888. [Pg.371]

Chylomicrons are synthesized in the intestine and transport dietary triglycerides and cholesterol. While circulating, the core triglycerides in these particles are hydrolyzed by lipoprotein lipase, which results in the production of a cholesterol-enriched remnant particle. When synthesized and initially released by the intestine, chylomicrons contain essentially no apoE, but as they circulate and are processed to remnants, the particles acquire apoE from other lipoprotein classes. This results in a shift of the distribution of apoE in plasma to the triglyceride-rich remnants in the absorptive state (Blum, 1982). [Pg.265]

Castanospermine is able to suppress the processing and secretion of lipoprotein lipase (249-251). Incubation of aortic endothelial cells with the alkaloid altered the distribution of scavenger receptors for low-density lipoproteins, a finding that has significance in the fight against coronary heart diseases involving the deposition of cholesterol on arterial walls (252,253). [Pg.141]

Wu, G., G. Olivecrona, and T. Olivecrona. 2003. The distribution of lipoprotein lipase in rat adipose tissue. Journal of Biological Chemistry 278 11925-11930. [Pg.199]

Fat emulsions must have a small particle size (200-500 nm), which requires the use of high-pressure homogenisers. It is essential to store the emulsion at various temperatures and investigate any increase in fatty acid composition that causes lipoprotein lipase reactions. Also, an increase in droplet size increased the toxicity of the emulsion. Addition of drugs and nutrients to fat emulsions can also cause instability and/or cracking of the emulsion. Following the administration of fat emulsions to the body, it will be distributed rapidly throughout the circulation and then cleared. [Pg.481]

Within twenty seconds of injecting heparin into the femoral artery of a rabbit, blood samples of the femoral vein contained lipolytic activity. As this time is no greater than that required for the heparin to traverse the capillary bed of the hind Umb, this result indicates that the enzyme is readily accessible to heparin in the circulating blood (Robinson and Harris 1959). The enzyme is also found in the perfusate, when a heparin-serum albumin solution is perfused through an isolated hind limb. These findings led to the conclusion that the clearing factor is not present in the blood but is released into it by excessive doses of heparin. It is located in the capillary epithelium or on cell surfaces and its normal fimction is to act at these sites to facihtate transport of fat across the barriers. In accord with this concept is the distribution of lipoprotein lipase in the extrahepatic tissues, where an unmterrupted capillary epithelium exists and a special mechanism for fat transport is required. [Pg.59]


See other pages where Lipoprotein lipase distribution is mentioned: [Pg.118]    [Pg.249]    [Pg.1085]    [Pg.2007]    [Pg.25]    [Pg.390]    [Pg.43]    [Pg.108]    [Pg.537]    [Pg.102]    [Pg.205]    [Pg.536]    [Pg.205]    [Pg.478]    [Pg.99]    [Pg.514]    [Pg.1446]   


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