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Apolipoprotein apo

Lipid profile alteration. Hot water extract of the seed, administered orally to adults at a dose of five cups per day, produced weak activity on apolipoprotein (apo) B HDL-C and apo A-l . [Pg.175]

Gallbladder effect. Seed oil, administered orally to 11 young normocholesterolemic males at a dose of 100 g/day, was active. The subjects received 3 weeks of a low-fat diet followed by 3 weeks of a diet enriched with 100 g/daily of olive oil. Mean total cholesterol, total apolipoprotein (apo) B, low-density lipoprotein (LDL) cholesterol, and triglycerides decreased significantly after the olive oil diet. High-density lipoprotein (HDL) cholesterol, apo A-1, cholesterol saturation of bile, and gallbladder volumes were unchanged . [Pg.385]

Apoliprotein. Any of the protein constituents of lipoproteins, grouped by function in four classes A, B, C, and E (the former apolipoprotein [apo] D is now apo A-111). Apoptosis. Fragmentation of a cell into membrane-bound particles that are eliminated by phagocytosis. Programmed cell death. [Pg.564]

Atherosclerosis is the leading cause of death for both genders in the USA and other Western countries. Lipoproteins that contain apolipoprotein (apo) B-100 convey lipids into the artery wall. These are low-density (LDL), intermediate-density (IDL), very-low-density (VLDL), and lipoprotein(a) (Lp[a]). [Pg.776]

Apolipoproteins ( apo designates the protein in its lipid-free form) combine with lipids to form several classes of lipoprotein particles, spherical complexes with hydrophobic lipids in the core and hydrophilic amino acid side chains at the surface (Fig. 21-39a). Different combinations of lipids and proteins produce particles of different densities, ranging from chylomicrons to high-density lipoproteins. These particles can be separated by ultracentrifugation (Table 21-2) and visualized by electron microscopy (Fig. 21-39b). [Pg.821]

Bohnet K, Pillot T, Visvikis S, Sabolovic N, Siest G 1. Apolipoprotein (apo) E genotype and apoE concentration determine binding of normal very low density lipoproteins to HepG2 cell surface receptors. J Lipid Res 1996 37 1316-1324. [Pg.206]

Paul-Hayase H, Rosseneu M, Robinson D, Van Bervliet JP, Deslypere JP, Humphries SE. Polymorphisms in the apolipoprotein (apo) AI-CIII-AIV gene cluster Detection of genetic variation determining plasma apo AI, apo CIII and apo AIV concentrations. Hum Genet. 1992, 88 439 446. [Pg.166]

Figure 14.6. The role of apolipoprotein (Apo)E4 in the genesis of plaque and neurofibrillary tangle formation. Note that ApoE3 may have a protective effect against the activation of the microglia and the production of pro-inflammatory cytokines (such as interleukin-1). Figure 14.6. The role of apolipoprotein (Apo)E4 in the genesis of plaque and neurofibrillary tangle formation. Note that ApoE3 may have a protective effect against the activation of the microglia and the production of pro-inflammatory cytokines (such as interleukin-1).
B46. Brewer, H. B., Jr., Shulman, R., Herbert, P., Ronan, R., and Wehrly, K., The complete amino acid sequence of alanine apolipoprotein (apo C-III), an apolipoprotein from human plasma very low density lipoproteins. J. Biol. Chem. 249, 4975-4984 (1974). [Pg.271]

U5. Utermann, G., Jaescbke, M., and Menzel, J., Familial hyperlipoproteinemia type III Deficiency of a specific apolipoprotein (apo E-III) in the very-low-density lipoproteins. FEBS Lett. 56, 352-355 (1975). [Pg.296]

Subsequently, Qureshi (169) extended his investigations to TRF (Palm Vitee) from palm oil in both animal and human models. In a double-blind crossover study involving 20 hypercholesterolaemic human subjects (serum cholesterol >294 mg/dL), Palm Vitee supplementation was found to cause a significant drop in serum TC and LDL-C. The LDL-associated apolipoprotein Apo B was also decreased by 9-11%. Moreover, Palm Vitee supplementation resulted in a significant decrease (25%) in serum thromboxane and platelet factor PF4 by 16%. Similar cholesterol-lowering effects of Palm Vitee have also been indicated in genetically hypercholesterolemic swine (170). [Pg.1053]

Apolipoprotein (apo) A-I expression was demonstrated in porcine brain capillaries, suggesting an independent lipid metabolism inthebrain(151). Apo A-Iisthe major protein component of HDLs, which are responsible for reverse cholesterol transport from various tissues to the liver via the SR-BI receptor. Further research indicated that apo A-I was effluxed by porcine BCEC, whereas aortic endothelial cells did not. In addition, apo A-I-inducing compounds, such as cholesterol,... [Pg.646]

After its absorption into the intestinal mucosal cell, cholesterol, together with triglycerides, phospholipids, and a number of specific apoproteins, is assembled into a large lipoprotein called the chylomicron (see later section on lipoprotein metabolism, exogenous pathway). One apoprotein component known as apolipoprotein (apo) B-48 is vital to the formation of chylomicrons, and in people with a rare deficiency of apo B-48 synthesis, chylomicron formation, and consequently cholesterol and fat absorption, is severely impaired. Chylomicrons enter the lymphatics, which empty into the thoracic duct and eventually enter the systemic venous circulation at the junction of the left subclavian vein and left internal jugular vein. [Pg.905]

It remains to be established whether manipulation of HDL levels will in itself alter the development of CHD. The components of HDL are derived from different sources. " " HDL (or its precursors) is produced by both the liver and intestine. The structural composition of HDL is regulated by LCAT and lipoprotein lipase. There is also non-enzymatic transfer of apolipoprotein (apo) C between HDL and VLDL, exchange of free... [Pg.199]

The principal functions of the lipoprotein classes are determined by their apolipoprotein (apo) and lipid components. The CM are synthesized in the intestines for the transport of dietary triacylglycerols to various tissues (Chapter 19). VLDL are synthesized in the liver for the export of endogenous triacylglycerols (Chapter 19), while LDL arise from the metabolic transformation of VLDL in circulation (Chapter 20). The function of LDL is to deliver CE to peripheral tissues and to the liver. HDL are synthesized and assembled in the liver and intestine or are formed from metabolic transformations of other lipoproteins in circulation, and from cellular lipids at the cell membranes (see Chapter 20). HDL remove excess cholesterol from cells and transport it to liver and steroidogenic tissues for metabolism and excretion. [Pg.487]

The apolipoproteins found in plasma are classified into two broad types the nonexchangeable and the exchangeable (or soluble) apolipoproteins. Apo BlOO and apo B48,... [Pg.490]


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