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.
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.