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Low density lipoproteins metabolism

Jenkins DJ, Kendall, CW, Vidgen E et al. Effect of soy-based breakfast cereal on blood lipids and oxidized low-density lipoprotein. Metabolism 49, 1496-1500, 2000. [Pg.394]

S.A. Hynds, J. Welsh, J.M. Stewart, A. Jack, M. Soukop, C.S. McArdle, K.C. Caiman, C.P. Packard and J. Sheperd, Low-density lipoprotein metabolism in mice with soft tissue tumors, Biochem. Biophys. Acta 795 (1984) 589-595. [Pg.307]

N2. Nestel, P., Billington, T, Tada, N., Nugent, P., and Fidge, N., Heterogeneity of very-low-density lipoprotein metabolism in hyperlipidemic subjects. Metabolism 32, 810-817... [Pg.287]

McLeod, R.S., LeBlanc, A.M., Langille, M.A., Mitchell, P.L., Currie, D.L. 2004. Conjugated linoleic acids, atherosclerosis, and hepatic very-low-density lipoprotein metabolism. Am. J. Clin. Nutr. 79, 1169S-1174S. [Pg.132]

WAGNER, J.D., SCHWENKE, D.C., GREAVES, K.A., ZHANG, L., ANTHONY, M.S., BLAIR, R.M., SHADOAN, M.K, WILLIAMS, J.K., Soy protein with isoflavones, but not an isoflavone-rich supplement, improves arterial low-density lipoprotein metabolism and atherogenesis, Arterioscler. Thromh. Vase. Biol, 2003, Oct 23 [Epub ahead of print]. [Pg.173]

H. G. Morgan, Cholestyramine promotes receptor-mediated low density lipoprotein metabolism, N. Engl. J. Med. 302 1219 (1980). [Pg.111]

Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP. Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP.
Figure 25-7. Metabolism of adipose tissue. Hormone-sensitive lipase is activated by ACTH, TSH, glucagon, epinephrine, norepinephrine, and vasopressin and inhibited by insulin, prostaglandin E, and nicotinic acid. Details of the formation of glycerol 3-phosphate from intermediates of glycolysis are shown in Figure 24-2. (PPP, pentose phosphate pathway TG, triacylglycerol FFA, free fatty acids VLDL, very low density lipoprotein.)... Figure 25-7. Metabolism of adipose tissue. Hormone-sensitive lipase is activated by ACTH, TSH, glucagon, epinephrine, norepinephrine, and vasopressin and inhibited by insulin, prostaglandin E, and nicotinic acid. Details of the formation of glycerol 3-phosphate from intermediates of glycolysis are shown in Figure 24-2. (PPP, pentose phosphate pathway TG, triacylglycerol FFA, free fatty acids VLDL, very low density lipoprotein.)...
Figure 27-1. Metabolic interrelationships between adipose tissue, the liver, and extrahepatic tissues. In extrahepatic tissues such as heart, metabolic fuels are oxidized in the following order of preference (1) ketone bodies, (2) fatty acids, (3) glucose. (LPL, lipoprotein lipase FFA, free fatty acids VLDL, very low density lipoproteins.)... Figure 27-1. Metabolic interrelationships between adipose tissue, the liver, and extrahepatic tissues. In extrahepatic tissues such as heart, metabolic fuels are oxidized in the following order of preference (1) ketone bodies, (2) fatty acids, (3) glucose. (LPL, lipoprotein lipase FFA, free fatty acids VLDL, very low density lipoproteins.)...
As an example, the low-density lipoprotein (LDL) molecule and its receptor (Chapter 25) are internalized by means of coated pits containing the LDL receptor. These endocytotic vesicles containing LDL and its receptor fuse to lysosomes in the cell. The receptor is released and recycled back to the cell surface membrane, but the apoprotein of LDL is degraded and the choles-teryl esters metabolized. Synthesis of the LDL receptor is regulated by secondary or tertiary consequences of pinocytosis, eg, by metabolic products—such as choles-... [Pg.430]

Liu Y, Jones M, Hingtgen CM, Bu G, Laribee N, Tanzi RE, Moir RD, Nath A, He JJ (2000) Uptake of HIV-1 tat protein mediated by low-density lipoprotein receptor-related protein disrupts the neuronal metabolic balance of the receptor ligands. Nat Med 6 1380-1387... [Pg.371]

FIGURE 3.2.2 Metabolic pathways of carotenoids such as p-carotene. CM = chylomicrons. VLDL = very low-density lipoproteins. LDL = low-density lipoproteins. HDL = high-density lipoproteins. BCO = p-carotene 15,15 -oxygenase. BCO2 = p-carotene 9, 10 -oxygenase. LPL = lipoprotein lipase. RBP = retinol binding protein. SR-BI = scavenger receptor class B, type I. [Pg.162]

FIGURE 9. Endogenous lipoprotein metabolism. In liver cells, cholesterol and triglycerides are packaged into VLDL particles and exported into blood where VLDL is converted to IDL. Intermediate-density lipoprotein can be either cleared by hepatic LDL receptors or further metabolized to LDL. LDL can be cleared by hepatic LDL receptors or can enter the arterial wall, contributing to atherosclerosis. Acetyl CoA, acetyl coenzyme A Apo, apolipoprotein C, cholesterol CE, cholesterol ester FA, fatty acid HL, hepatic lipase HMG CoA, 3-hydroxy-3-methyglutaryl coenzyme A IDL, intermediate-density lipoprotein LCAT, lecithin-cholesterol acyltransferase LDL, low-density lipoprotein LPL, lipoprotein lipase VLDL, very low-density lipoprotein. [Pg.178]

Metformin also has been shown to produce beneficial effects on serum lipid levels and thus has become a first-line agent for type 2 DM patients with metabolic syndrome. Triglyceride and low-density lipoprotein (LDL) cholesterol levels often are reduced by 8% to 15%, whereas high-density lipoprotein (HDL) cholesterol improves by approximately 2%. A modest weight loss of 2 to 3 kg (4.4—6.6 lb) also has been reported with metformin therapy. Metformin often is used in combination with a sulfonylurea or a thiazolidinedione for synergistic effects. [Pg.656]

Aro, A., Tuomilehto, J., Kostiainen, E., Uusitalo, U., Pietinen, P., Boiled coffee increases serum low density lipoprotein concentration, Metabolism, 36, 1027, 1987... [Pg.326]

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]

The hemolymphal transport of carotenoids by lipophorin has been elucidated and documented (Law and Wells 1989, Tsuchida et al. 1998, Arrese et al. 2001, Canavoso et al. 2001), as has plasma transport by mammalian lipoproteins (Paker 1996, Yeum and Russell 2002). Lipophorin serves as a shuttle that moves carotenoids from one tissue to another without itself entering the cells, in stark contrast to the vertebrate low-density lipoprotein (LDL) (Brown and Goldstein 1986), which is endocytosed and metabolized in the cell. Here, we focus on the recent biochemical and genetic studies of the intracellular CBP of the silkworm, which mainly transports lutein. We hope this review provides insights into the studies of CBPs in other organisms. [Pg.512]

Further research on serum cholesterol revealed that is exists in two forms, high and low density lipoprotein. The high density lipoprotein appears to consist of cholesterol that is being moved to the liver for metabolism while low density lipoprotein appears to be cholesterol that is likely to block arteries. This has led to the labelling of high density lipoprotein as good cholesterol and of low density lipoprotein as bad cholesterol. [Pg.43]

Hoogerbrugge N, Zillikens MC, Jansen H, Meeter K, Deckers J W, Birkenhager JC (1998) Estrogen replacement decreases the level of antibodies against oxidized low-density lipoprotein in postmenopausal women with coronary heart disease. Metabolism 47 675-680... [Pg.241]

Details of plasma lipoproteins and their metabolism are given in Section 5.5. Most of the cholesterol in the blood is carried as part of low density lipoprotein (LDL) or high density lipoprotein (HDL), whereas most triglyceride, in the fasting state, is carried by very low density lipoprotein (VLDL). The relative concentrations of these lipoproteins constitute the lipid profile and determine CVD risk. Diabetics are more likely to show an unhealthy profile with elevated concentrations of LDL and triglyceride but reduced HDL concentration. This pattern can be partly explained by enhanced fatty acid liberation from adipocytes as a consequence of insulin resistance in that tissue and due to reduced removal from the circulation of triglycerides, which is also insulin dependent. [Pg.123]

Jenkins, D.J. A., Kendall, C.W.C., Garsetti, M., et al. (2000). Effects of soy protein food on low density lipoprotein oxidation and ex vivo sex hormone receptor activity -a controlled cross over trial, Metabolism, 49, 537-543. [Pg.106]


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See also in sourсe #XX -- [ Pg.2 , Pg.9 , Pg.210 ]

See also in sourсe #XX -- [ Pg.236 , Pg.237 , Pg.238 ]

See also in sourсe #XX -- [ Pg.200 , Pg.223 ]




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