We get fat and cholesterol from the food we eat. They are then broken down in the gut and reassembled into complex lipid molecules, which are packed into very large, fat-laden lipoproteins called chylomicrons.
The chylomicrons ultimately enter the blood stream where they lose most of their triglycerides as fatty acids to the cells of the body.
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Some of these are taken up by the muscles as fuel while the rest are laid down as fatty (adipose) tissue in the body. The fats in this adipose tissue act as energy reserves – all too often never utilised.
Most of the cholesterol in the diet stays in the chylomicrons and is taken up by the liver where it mixes with new cholesterol which is made by the liver itself. Chylomicrons only remain in the bloodstream for a short while.
The liver is where fats are broken down and made. Not only does the liver make cholesterol, it also makes fatty acids, triglycerides and phospholipids for export to the rest of the body.
The fats made in the liver are assembled together with apolipoproteins to make a new, fat-rich lipoprotein called VLDL – very-low-density lipoproteins.
Again, the VLDLs lose most of their triglycerides as fatty acids to muscle and adipose tissue. But, instead of excess being taken up by the liver, they convert in the plasma (the liquid, non-cellular part of the blood) into a new form of lipoprotein called LDL or low-density lipoprotein.
This LDL is very rich in cholesterol and is known as the "bad" form of cholesterol. It is these particles which, in excess, can lead to atherosclerosis and coronary artery disease.
LDL remains in the blood stream for around three days before being removed by the liver.
The mechanism whereby LDL is removed by the liver is important. LDL is linked to a protein called apoB. This recognises a specific receptor on the liver cell – the apoB-receptor. This allows LDL to “dock” on this receptor and so be taken up by the liver.
This is important because if this receptor is faulty, as happens with familial hypercholesterolaemia, then the LDL is not taken up. When this happens, an excess of LDL circulates in the blood stream, clogging up the arteries and leading to coronary artery disease.
There is another lipoprotein in this story – HDL or high-density lipoprotein. This is secreted by the liver and also formed from VLDL and chylomicrons.
HDL has the ability to pick up excess free cholesterol from peripheral (non-liver) cells, including those accumulating in the arterial wall which predispose to coronary artery disease.
HDL returns the excess cholesterol directly to the liver. HDL also carries important protective antioxidant enzymes and other molecules which lessen the risk of coronary artery disease.
All these properties make HDL an effective anti-coronary disease agent. The cholesterol measured in HDL is thus called "good" cholesterol.
This means that not only are your levels of cholesterol and triglycerides important, but also the levels of LDL and HDL.
High levels of LDL and low levels of HDL mean that you have a greater risk of coronary artery disease, and vice versa.
(The Heart and Stroke Foundation/Health24)