Lipoproteins are multicomponent complexes of proteins and lipids that are involved in the transport of cholesterol and triglycerides in the blood. Cholesterol and triglyc-erides do not circulate freely in the plasma because lipids, on their own, would be unable to remain in suspension. The association of the protein with the lipid-containing core makes the complex sufficiently hydrophilic to remain suspended in the plasma. Lipoproteins serve a variety of functions in cellular mem-branes and in the transport and metabolism of lipids. Lipoprotein precursors are produced in the liver. The lipid component is produced in the sER; the protein component is produced in the rER of the hepatocytes. The lipoprotein complexes pass to the Golgi, where secretory vesicles containing electron-dense lipoprotein particles bud off and are then released at the cell surface bordering the perisinu-soidal space to reach the bloodstream. Several hormones, such as estrogen and thyroid hormones, regulate the se-cretion of lipoproteins. In general, four classes of lipoproteins have been de-fined by their characteristic density, molecular weight, size, and chemical composition: chylomicrons, VLDLs, LDLs, and HDLs. These lipoproteins differ in chemical composi-tion and can be isolated from plasma according to their flotation properties, from largest and least dense to small-est and most dense. Chylomicrons, the lightest of all lipoproteins, are made only in the small intestine. Their main function is to transport the large amount of absorbed fat to the bloodstream. VLDLs are denser and smaller than chylomicrons; they are synthesized predominately in the liver and to a lesser extent in the small intestine. VLDLs are rich in triglycerides. Their function is to transport most of the triglycerides from the liver to other organs. Liver VLDLs are associated with circulating apolipoprotein B-100, also synthesized in the liver, which aids in secretion of VLDLs. In congenital liver disease, such as abetalipoproteinemia, and to a lesser degree in acute and chronic disorders, the liver is unable to produce apolipoprotein B-100, leading to blockage in the secretion of VLDLs. In liver biopsy specimens from these individuals, large lipid droplets occupy most of the hepato-cyte cytoplasm. LDLs and HDLs are produced in the plasma; however, small amounts of these fractions are produced by the liver. LDLs are denser than VLDLs, and HDLs are denser than LDLs. The function of LDLs is to transport cholesterol es-ters from the liver to the peripheral organs. The HDLs are involved in the transport of cholesterol from the peripheral tissues to the liver. High levels of LDL are directly corre-lated with increased risk of cardiovascular disease; high levels of HDL or low levels of LDL are associated with decreased risk.
 FOLDER 18.1 Clinical Correlation: Lipoproteins conversion takes place in the kidney to 1,25-hydroxycholecalciferol, which is 10 times more active than vitamin D3.
Vitamin D is essential for development and growth of the skeletal system and teeth. Deficiency of vitamin D is associated with rickets and disorders of bone mineralization.
 vitamin K, which is important in hepatic synthesis of prothrombin and several other clotting factors. Like vitamin D, it is derived from two sources: dietary vitamin K and synthesis in the small intestine by intestinal bacterial flora. Vitamin K is transported to the liver with chylomicrons, where it is rapidly absorbed, partially used, and then partially secreted with the VLDL fraction. Vitamin K deficiency is associated with hypoprothrombinemia and bleeding disorders.