chylomicron

Chylomicron retention disease is a disorder of fat absorption.

In the liver, chylomicron particles release triglycerides and some cholesterol.

As a consequence, chylomicron remnants are left over and are taken up by the liver.

Low levels of plasma chylomicron are also characteristic.

There are three stages in the chylomicron's "life cycle":

The liver receives many lipids from the systemic circulation and metabolizes chylomicron remnants.

The hydrolyzed chylomicrons are now called chylomicron remnants.

In one experiment, 43% of the chylomicron triglyceride fatty acids was of endogenous origin.

The triglycerides are coated with cholesterol and protein (protein coat) into a compound called a chylomicron.

This interaction causes the endocytosis of the chylomicron remnants, which are subsequently hydrolyzed within lysosomes.

Apolipoprotein E, a main apoprotein of the chylomicron, also studied for its involvement in Alzheimer's Disease risk.

It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids.

Cholesterol that is not used by muscles remains in more cholesterol-rich chylomicron remnants, which are taken up from here to the bloodstream by the liver.

In contrast, chylomicron cholesterol ester formation showed marked specificity for oleic acid, relative to the other three fatty acids.

These eddies create abnormal fluid velocity gradients which push blood elements such as cholesterol or chylomicron bodies to the endothelium.

In the first, and most predominant, it is esterified with a fatty acid to form a retinyl ester, and packaged into a chylomicron.

Apo A-IV is secreted into circulation on the surface of newly synthesized chylomicron particles.

A third form, chylomicron retention disease (CRD), is associated with SARA2.

Double-blind controlled study on the effects of dietary diacylglycerol on postprandial serum and chylomicron triacylglycerol responses in healthy humans.

The chylomicron enters a lymphatic capillary and enters into the bloodstream first at the left subclavian vein (having bypassed the liver).

Within the villi, the chylomicron enters a lymphatic capillary called a lacteal, which merges into larger lymphatic vessels.

LRP5 knockout in mice led to increased plasma cholesterol levels on a high-fat diet because of the decreased hepatic clearance of chylomicron remnants.

The chyle or chylomicron lipid so obtained was chromatographed on silicic acid columns to separate cholesterol esters and glycerides (the latter being 98.2% triglycerides).

Eventually, enough lipid has been lost and additional apolipoproteins gained, that the resulting particle (now referred to as a chylomicron remnant) can be taken up by the liver.

APOB48 and APOE are important to identify the chylomicron remnant in the liver for endocytosis and breakdown.