Lipoprotein, very low-density

Very low-density lipoprotein receptor ( VLDLR) and APOE receptor-2 ( APOER2) are two gene family members with redundant functions. They are expressed in neurons of the developing brain and act as cell... 

Abbtvviations apoC-lll, apolipoprotein C-lll apoA-l, apolipoprotein A-l apoA-ll, apolipoprotein A-ll CRP, C-reactive protein VLDL, very low density lipoprotein TG, triglycerides LDL-C, low density lipoprotein cholesterol HDL-C, high density lipoprotein cholesterol. 

Systemic treatment of 13-cis retinoic acid frequently leads to cheilitis and eye irritations (e.g., unspecific cornea inflammation). Also other symptoms such as headache, pruritus, alopecia, pains of joints and bone, and exostosis formation have been reported. Notably, an increase of very low density lipoproteins and triglycerides accompanied by a decrease of the high density lipoproteins has been reported in 10-20% of treated patients. Transiently, liver function markers can increase during oral retinoid therapy. Etretinate causes the side effects of 13-cis retinoid acid at lower doses. In addition to this, generalized edema and centrilobulary toxic liver cell necrosis have been observed. 

Venus Flytrap Module Very Long-chain Acyl-CoA Synthetase Very Low-density Lipoprotein Vesicle... 

Fibric acid derivatives, the third group of antihyperlipi-demic drugs, work in a variety of ways. Clofibrate (Atromid-S), acts to stimulate the liver to increase breakdown of very-low-density lipoproteins (VLDL) to low-density lipoproteins (LDL), decreasing liver synthesis of... 

Figure 15-6. Transport and fate of major lipid substrates and metabolites. (FFA, free fatty acids LPL, lipoprotein lipase MG, monoacylglycerol TG, triacylglycerol VLDL, very low density lipoprotein.)...

Abbreviations HDL, high-density iipoproteins IDL, intermediate-density lipoproteins LDL, low-density lipoproteins VLDL, very low density lipoproteins. 

TRIACYLGLYCEROL IS TRANSPORTED FROM THE INTESTINES IN CHYLOMICRONS FROM THE LIVER IN VERY LOW DENSITY LIPOPROTEINS... 

CHYLOMICRONS VERY LOW DENSITY LIPOPROTEINS ARE RAPIDLY CATABOLIZED... 

Figure 25-2. The formation and secretion of (A) chylomicrons by an intestinal cell and (B) very low density lipoproteins by a hepatic cell. (RER, rough endoplasmic reticulum SER, smooth endoplasmic reticulum G, Golgi apparatus N, nucleus C, chylomicrons VLDL, very low density lipoproteins E, endothelium SD, space of Disse, containing blood plasma.) Apolipoprotein B, synthesized in the RER, is incorporated into lipoproteins in the SER, the main site of synthesis of triacylglycerol. After addition of carbohydrate residues in G, they are released from the cell by reverse pinocytosis. Chylomicrons pass into the lymphatic system. VLDL are secreted into the space of Disse and then into the hepatic sinusoids through fenestrae in the endothelial lining.

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 25-6. The synthesis of very low density lipoprotein (VLDL) in the liver and the possible loci of action of factors causing accumulation of triacylglycerol and a fatty liver. (EFA, essential fatty acids FFA, free fatty acids ...

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.)...

Four major groups of lipoproteins are recognized Chylomicrons transport lipids resulting from digestion and absorption. Very low density lipoproteins (VLDL) transport triacylglycerol from the liver. Low-density lipoproteins (LDL) deliver cholesterol to the tissues, and high-density lipoproteins (HDL) remove cholesterol from the tissues in the process known as reverse cholesterol transport. 

Shelness GS, Sellers JA Very-low-density lipoprotein assembly and secretion. Curr Opin Lipidol 2001 12 151. 

Figure 26-5. Factors affecting cholesterol balance at the cellular level. Reverse cholesterol transport may be initiated by pre 3 HDL binding to the ABC-1 transporter protein via apo A-l. Cholesterol is then moved out of the cell via the transporter, lipidating the HDL, and the larger particles then dissociate from the ABC-1 molecule. (C, cholesterol CE, cholesteryl ester PL, phospholipid ACAT, acyl-CoA cholesterol acyltransferase LCAT, lecithinicholesterol acyltransferase A-l, apolipoprotein A-l LDL, low-density lipoprotein VLDL, very low density lipoprotein.) LDL and HDL are not shown to scale.

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.)...

This approach can be used only for fat-soluble compounds that follow the same lymphatic route to be transported to the liver as carotenoids. The bioavailability of the compound of interest is determined by monitoring the appearance of the compound and its newly formed intestinal metabolites in the postprandial chylomicron fraction of plasma [also called the density < 1.006 kg/L fraction or triglyceride-rich lipoprotein (TRL) fraction because it is generally a mixture of chylomicrons (CMs) and very low density lipoproteins (VLDLs)] as a function of the time after ingestion. 

FIGURE 3.2.1 In vitro digestion/Caco-2 cell model combination approach to assess carotenoid bioavailability. LCM = large chylomicrons. SCM = small chylomicrons. VLDL = very low density lipoproteins. 

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. 

TAG-CH3 and TAG-CH2-, acyl chain terminal-CH3 and bulk (-CH2-)n groups, respectively, of fatty acids (predominantly triacylglycerols) associated with chylomicron- and very low-density lipoprotein (VLDL) Thr, threonine-CHs Val, valine-CHs. The asterisk In spectrum (b) denotes a radiolytically-generated 2.74 p.p.m. 

Jurgens, G., Ashy, A. and Esterbauer, H. (1990). Detection of new epitopes formed upon oxidation of low density lipoprotein, lipoprotein (a) and very low density lipoprotein. Biochem. J. 265, 605-608. 

Antibodies to very low density lipoprotein (VLDL) and LDL have been detected in the serum of patients with RA, but not control groups (Lazarevic et al., 1993). In these studies, 38% of patients with active RA tested positive for anti-VLDL/LDL antibodies whilst these autoantibodies were not detected in patients with psoriatic arthritis, osteoarthritis or healthy subjects. Lipoproteins were found in the dissociated components of circulating immune complexes in the serum of 30% of the RA patients. It was concluded that dyslipoproteinaemia in some RA patients may be due to an autoimmune component of the disease. 

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