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Lipoprotein table

Lipoproteins (Table 5.2) are macromolecular aggregates with varying proportions of triglycerides and cholesterol (with some phosphoacylglycerols) and apoproteins. The apoproteins act as recognition flags for receptor binding, for example apo B and apo E,... [Pg.163]

Antilipemics lower lipid levels (Table 19.4). Lipids are composed of cholesterol, triglycerides, and phospholipids, which are bound to lipoproteins (Table 19.5) that transport lipids throughout the body. There are three classifications of lipoproteins ... [Pg.311]

The major classes of lipoproteins (Table 30-1) and some of their properties... [Pg.276]

See also Lipoproteins, Table 18.1, Familial Hypercholesterolemia, Atherogenesis, Coated Pits... [Pg.1673]

When most lipids circulate in the body, they do so in the form of lipoprotein complexes. Simple, unesterified fatty acids are merely bound to serum albumin and other proteins in blood plasma, but phospholipids, triacylglycerols, cholesterol, and cholesterol esters are all transported in the form of lipoproteins. At various sites in the body, lipoproteins interact with specific receptors and enzymes that transfer or modify their lipid cargoes. It is now customary to classify lipoproteins according to their densities (Table 25.1). The densities are... [Pg.840]

Low-density Lipoprotein Receptor Gene Family. Table 1 Human diseases of the LDL receptor gene family... [Pg.706]

Figure 25-5. Metabolism of high-density lipoprotein (HDL) in reverse cholesteroi transport. (LCAT, lecithinxholesterol acyltransferase C, cholesterol CE, cholesteryl ester PL, phospholipid A-l, apolipoprotein A-l SR-Bl, scavenger receptor B1 ABC-1, ATP binding cassette transporter 1.) Prep-HDL, HDLj, HDL3—see Table 25-1. Surplus surface constituents from the action of lipoprotein lipase on chylomicrons and VLDL are another source of preP-HDL. Hepatic lipase activity is increased by androgens and decreased by estrogens, which may account for higher concentrations of plasma HDLj in women. Figure 25-5. Metabolism of high-density lipoprotein (HDL) in reverse cholesteroi transport. (LCAT, lecithinxholesterol acyltransferase C, cholesterol CE, cholesteryl ester PL, phospholipid A-l, apolipoprotein A-l SR-Bl, scavenger receptor B1 ABC-1, ATP binding cassette transporter 1.) Prep-HDL, HDLj, HDL3—see Table 25-1. Surplus surface constituents from the action of lipoprotein lipase on chylomicrons and VLDL are another source of preP-HDL. Hepatic lipase activity is increased by androgens and decreased by estrogens, which may account for higher concentrations of plasma HDLj in women.
Inherited defects in lipoprotein metabofism lead to the primary condition of either hypo- or hyperlipoproteinemia (Table 26-1). In addition, diseases such as diabetes mellitus, hypothyroidism, kidney disease (nephrotic syndrome), and atherosclerosis are associated with secondary abnormal hpoprotein patterns that are very similar to one or another of the primary inherited conditions. Virtually all of the primary conditions are due to a defect at a stage in hpoprotein formation, transport, or destruction (see Figures 25—, 26-5, and 26-6). Not all of the abnormafities are harmful. [Pg.229]

Table 50-2 summarizes the functions of many of the plasma proteins. The remainder of the material in this chapter presents basic information regarding selected plasma proteins albumin, haptoglobin, transferrin, ceruloplasmin, aj-antitrypsin, aj i roglobulin, the immunoglobulins, and the complement system. The lipoproteins are discussed in Chapter 25. [Pg.583]

Table 14.4 Serum ASAT, ALAT, creatinine, serum lipoproteins and oxidation kinetics before and after four week consumption of study breads ... Table 14.4 Serum ASAT, ALAT, creatinine, serum lipoproteins and oxidation kinetics before and after four week consumption of study breads ...
In individuals who do not have established CHD or CHD risk equivalent, the next step is to count major risk factors for CHD as presented in Table 9-4. These risk factors are considered independent predictors of CHD. High-density lipoprotein cholesterol of greater than or equal to 60 mg/dL (1.55 mmol/L) is considered a negative risk factor and means 1 risk factor can be subtracted from the total count.3... [Pg.183]

Lipoproteins. A lipoprotein is an endogenous macromolecule consisting of an inner apolar core of cholesteryl esters and triglycerides surrounded by a monolayer of phospholipid embedded with cholesterol and apoproteins. The functions of lipoproteins are to transport lipids and to mediate lipid metabolism. There are four main types of lipoproteins (classified based on their flotation rates in salt solutions) chylomicrons, very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). These differ in size, molecular weight, and density and have different lipid, protein, and apoprotein compositions (Table 11). The apoproteins are important determinants in the metabolism of lipoproteins—they serve as ligands for lipoprotein receptors and as mediators in lipoproteins interconversion by enzymes. [Pg.557]

Table 11 Physicochemical Properties and Composition of Human Lipoproteins... [Pg.558]

The effect of drug therapy on lipids and lipoproteins is shown in Table 9-5. [Pg.116]

Recommended drugs of choice for each lipoprotein phenotype are given in Table 9-6. [Pg.116]

TABLE 9-6 Lipoprotein Phenotype and Recommended Drug Treatment ... [Pg.117]

As indicated in Table 1, statins, which block cholesterol biosynthesis by inhibition of hepatic HMGCoA reductase, have been used extensively to reduce LDL-C levels. At most therapeutic doses, statins marginally increase HDL levels by 5-10% [3,16]. The HDL elevation observed with statins has been highly variable and not easily extrapolated from the effects on LDL. A recent study (STELLAR) demonstrated increased HDL elevation with the use of rosuvastatin compared to simvastatin, pravastatin or atorvastatin (10% vs. 2-6%) [16,24], Although the mechanism of HDL elevation by statins is not clearly understood, it is proposed that statins enhance hepatic apoA-I synthesis [25] and decrease apoB-containing lipoproteins [26]. A number of clinical trials have demonstrated that statins reduce the risk of major coronary events. However, it is not clear if the statin-induced rise in HDL levels is an independent contributor to the reduced risk of coronary events. The observed small increase in HDL and adverse side effect profile related to liver function abnormalities and muscle toxicity limits the use of statins as monotherapy for HDL elevation [27],... [Pg.179]

Table II gives the distribution of lipoproteins in the various density classes from these animals. Since the total amounts of... Table II gives the distribution of lipoproteins in the various density classes from these animals. Since the total amounts of...
Table II. Percentage Distribution of Lipoproteins fed Various Proteins from Rabbits... Table II. Percentage Distribution of Lipoproteins fed Various Proteins from Rabbits...

See other pages where Lipoprotein table is mentioned: [Pg.842]    [Pg.1314]    [Pg.112]    [Pg.199]    [Pg.433]    [Pg.105]    [Pg.2421]    [Pg.64]    [Pg.197]    [Pg.842]    [Pg.1314]    [Pg.112]    [Pg.199]    [Pg.433]    [Pg.105]    [Pg.2421]    [Pg.64]    [Pg.197]    [Pg.361]    [Pg.1090]    [Pg.1091]    [Pg.942]    [Pg.22]    [Pg.205]    [Pg.206]    [Pg.607]    [Pg.349]    [Pg.176]    [Pg.177]    [Pg.179]    [Pg.182]    [Pg.1531]    [Pg.372]    [Pg.716]    [Pg.1284]    [Pg.180]    [Pg.162]    [Pg.421]    [Pg.422]   
See also in sourсe #XX -- [ Pg.1183 ]

See also in sourсe #XX -- [ Pg.979 ]




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High density lipoproteins composition of, table

Intermediate density lipoproteins (IDL composition of, table

Lipoprotein classes of, table

Low density lipoprotein composition of, table

Serum lipoprotein, table

Very low density lipoprotein composition of, table

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