Very low density lipoprotein production

Nestel P, Connor WE, Reardon MF et al. (1984) Suppression by diets rich in fish oil of very low density lipoprotein production in man. J Clin Invest 74 82-89... 

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.

When the diet contains more fatty acids than are needed immediately as fuel, they are converted to triacylglycerols in the liver and packaged with specific apolipoproteins into very-low-density lipoprotein (VLDL). Excess carbohydrate in the diet can also be converted to triacylglycerols in the liver and exported as VLDLs (Fig. 21-40a). In addition to triacylglycerols, VLDLs contain some cholesterol and cholesteryl esters, as well as apoB-100, apoC-I, apoC-II, apoC-III, and apo-E (Table 21-3). These lipoproteins are transported in the blood from the liver to muscle and adipose tissue, where activation of lipoprotein lipase by apoC-II causes the release of free fatty acids from the VLDL triacylglycerols. Adipocytes take up these fatty acids, reconvert them to triacylglycerols, and store the products in intracellular lipid droplets myocytes, in contrast, primarily oxidize the fatty acids to supply energy. Most VLDL remnants are removed from the circulation by hepatocytes. The uptake, like that for chylomicrons, is... 

D5. Deckelbaum, R. J., Eisenberg, S., Fainaru, M., Barenholz, Y., and Olivecrona, T., In vitro production of human plasma low density lipoprotein-like particles A model for very low density lipoprotein catabolism. /. Biol. Chem. 254, 6079-6087 (1979). 

Liver health. As noted above, a biomarker of choline deficiency is elevated serum ALT levels, which is an indication of liver damage. One of the many functions of the liver is its role in fat metabolism. Without PC, the liver is unable to synthesize lipoproteins. Of particular importance in liver is the synthesis of very low-density lipoproteins (VLDL). With diminished VLDL production, the liver is not able to export lipid. This results in an accumulation of fat in the liver. Lipid accumulation in the liver leads to various stages of liver disease such as liver cell death, fibrosis, cirrhosis, and liver cancer (248-250). The role of choline in liver disease was underscored in the early 1990s when it was determined that patients on extended total parental nutrition (TPN) treatment developed fatty livers (251). At that time, TPN formulas did not include choline. Adding choline (in the form of lecithin) to TPN formulas reversed fatty buildup in these patients, and a... 

The term visceral adipose tissue (VAT) refers to fat cells located within the abdominal cavity and includes omental, mesenteric, retroperitoneal, and perinephric adipose tissue. VAT has been shown to correlate with insuhn resistance and explain much of the variation in insuhn resistance seen in a population of African-Americans. Visceral adipose tissue represents 20% of fat in men and 6% of fat in women. This fat tissue has been shown to have a higher rate of lipolysis than subcutaneous fat, resulting in an increase in free fatty acid production. These fatty acids are released into the portal circulation and drain into the liver, where they stimulate the production of very-low-density lipoproteins and decrease insuhn sensitivity in peripheral tissues. VAT also produces a number of cytokines which cause insulin resistance. These factors drain into the portal circulation and reduce insulin sensitivity in peripheral tissues. ... 

LDL Low-density lipoprotein a product of the degradation of very-low-density lipoproteins (VLDLs) by the action of lipoprotein lipase. LDLs are taken up by a receptor-mediated endocytosis by both peripheral tissues and the liver. It is commonly called the bad cholesterol. ... 

Fig. 1. Simplified schematic summary of the essential pathways for receptor-mediated human lipoprotein metabolism. The liver is the crossing point between the exogenous pathway (left-hand side), which deals with dietary lipids, and the endogenous pathway (right-hand side) that starts with the hepatic synthesis of VLDL. The endogenous metabolic branch starts with the production of chylomicrons (CM) in the intestine, which are converted to chylomicron remnants (CMR). Very-low-density lipoprotein particles (VLDL) are lipolyzed to LDL particles, which bind to the LDL receptor. IDL, intermediate-density lipoproteins LDL, low-density lipoproteins HDL, high-density lipoproteins LCAT, lecithinxholesterol acyltransferase CETP, cholesteryl ester transfer protein A, LDL receptor-related protein (LRPl) and W, LDL receptor. Lipolysis denotes lipoprotein lipase-catalyzed triacylglycerol lipolysis in the capillary bed.

VERY-LOW-DENSITY LIPOPROTEINS VLDL are produced in the liver when triglyceride production is stimulated by an increased flux of free fatty acids or by increased hepatic... 

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