VLDL metabolism is very similar to Chylomicrons metabolism. As described in a former post, the main lipid found in VLDL is also triacylglycerol, but in this case triacylglycerols come from excess fatty acids on diet or an increase in the hepatic synthesis of fatty acids as a consequence of excess carbohydrates in diet. Fats coming from the hepatocytes uptake of Chylomicrons remnants are also a source of triacylglycerols for VLDL.
Additionally to triacylglycerols, VLDL contains around 35 % of free and esterified cholesterol, 35 % of phospholipids, and various apoproteins, including ApoB-100.
VLDL, in the same way than Chylomicrons, acquires in the blood stream Apo C-II and Apo E. The functions of these apoproteins in VLDL are similar to their functions in Chylomicrons: Apo C-II activates Lipoprotein Lipase and as a consequence, VLDL triacylglycerols are hydrolyzed, so the proportion of cholesterol increases. The VLDL remnant is called IDL, or Intermediate Density Lipoprotein.
Intermediate Density Lipoproteins (IDL) have two metabolic fates: to be uptaken by hepatocytes in an Apo-E mediated process, or to continue losing TAG and become Low Density Lipoprotein (LDL), which contain around 50 % of cholesterol.
Since it is necessary that the hepatocytes recognize ApoE in Chylomicrons remnants and in VLDL in order to take up these lipoproteins from the blood, the deficit of Apo E or the genetic expression of an abnormal ApoE, provokes hyperlipidemia characterized by hypercholesterolemia and hypertriglyceridemia, as a consequence of high levels of Chylomicrons and VLDL remnants, that can result in xanthomatosis and premature coronary or peripheral vascular disease. This kind of Hyperlipidemia, which results from the deficit or abnormal ApoE, is called Hyperlipoproteinemia Type III, Apolipoprotein E Deficiency or Familial Disbetalipoproteinemia.
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OMIM- Apolipoprotein E; APOE
Type III Hyperlipidemia