Metabolism of chylomicrons

 

Once dietetic lipids have been hydrolyzed and absorbed, the fatty acids are reesterified to other lipid products in the intestinal cells, to form new neutral fats, new cholesterol esters, new phospholipids and other lipids.

 

These new molecules, formed inside the intestinal cell, should be transported to different tissues through the polar environment of blood, so it is necessary to assamble, inside the intestinal cells,  these lipidic molecules with amphipatic apolipoproteins, to form Chylomicrons.

  

These chylomicrons, very rich in triacylglycerols, already contain apoproteins A  and apoB-48, an apoprotein that is exclusive of chylomicrons (Apo B-48 belongs to the same family that Apo B-100, but does not show the domain that is necessary to bind to the B-100 receptor). These chylomicrons do not contain yet Apo C-II, and they are called “nascent chylomicrons” 

 

Nascent chylomicrons are secreted by the intestinal cells and are transported via the limphatic system to the blood, where they will pick Apoprotein C-II and Apo E.  

Apolipoproteina C-II, as part of chylomicrons, activates Lipoprotein Lipase, an enzyme attached to the lumenal surface of the endothelial cells of capillaries. This enzyme catalyzes the hydrolysis of the triacylglycerols in the chylomicrons. 

 

 

 

Released fatty acids and glycerol from the hydrolized acylglycerols are uptaked by adipose cells, muscle and other tissues near the capillaries. Glycerol is also used heavily by the liver and kidneys and can continue glycolysis. Hydrolysis of chylomicron’s neutral fat provokes also the release of Apo A and Apo C-II and the shrink in size of chylomicrons, that become now “chylomicron remnant”, with lipids core that have a high proportion of cholesterol.

 

Chylomicron remnants  will be taken up by liver cells.

   

The hepatic uptake of chylomicrons remnants is based on a receptor-mediated endocytosis, that involves the recognition of chylomicron remnant ApoE by receptors on the surface of liver cells. It  should be noted that throughout this process, chylomicrons have acted as a means of transportating the component of lipids in diet, from the intestinal cells to peripheral tissues as adipose and muscular tissues, including the heart, whose activity depends heavily (up to 80 % in certain physiological conditions) on the oxidation of fatty acids.

 

Chylomicron metabolic process allows the understanding of the causes and characteristics of Hiperlipoproteinemia Tipe I, familial hyperchylomicronemia or familial lipoprotein lipase deficiency, whose main feature is an increase of  chylomicron concentration and a very slow plasma clearence of them. The genetically identified causes of this disease are the deficit of Liporptein Lipase, the production of an abnormal LPL, or the deficit of Apo C-II  (in that case, LPL would not be activated. Clinical features are abdominal pain afer the ingestion of fat-rich meals,  xanthomas, acute pancreatitis, hepatic steatosis, as result of an excess of fatty deposit in various tissues.

 

Related links

 

http://en.wikipedia.org/wiki/Chylomicrons

 

http://themedicalbiochemistrypage.org/lipoproteins.html#uptake

 

http://themedicalbiochemistrypage.org/lipoproteins.html#chylomicrons

 

Related Posts:

 

Structure and Classification of Lipoproteins

 

Metabolism of VLDL and Formation of IDL

 

Apolipoproteins