'Ultra-bad' LDL cholesterol discovery helps explain heart disease risk
Scientists have discovered an especially bad form of so called bad LDL cholesterol that promotes coronary artery disease.
The cholesterol, according to the scientists, is very sticky, making the fatty substance more prone to clump and stick to the walls of the arteries.
The 'ultrabad' cholesterol, called MGmin-low-density lipoprotein (LDL), differs from other LDL cholesterol as the result of a process called glycation.
Glycation occurs when a molecule binds with fructose or glucose. The researchers added sugar groups to LDL cholesterol in the lab. The result was smaller, more dense molecules that change shape, making them stick to the artery walls to produce narrowing and poor blood flow.
LDL study explains danger for heart disease
Understanding the ‘ultra-bad’, ‘sticky’ type of LDL also helps researchers understand why the drug metformin used to treat diabetes lowers the chances of coronary artery plaque development.
The drug may prevent LDL cholesterol from changing from “normal” to MGmin-LDL.
Dr Shannon Amoils, Research Advisor at the British Heart Foundation, said, "We've known for a long time that people with diabetes are at greater risk of heart attack and stroke. There is still more work to be done to untangle why this is the case, but this study is an important step in the right direction.”
The authors say the finding could also explain why elderly are at higher risk for heart disease from the ‘ultra-bad’ type of LDL cholesterol.
More studies are needed to understand all of the factors that lead to heart disease. The researchers found watched LDL cholesterol particles in the lab to see how they interact with sugars, change shape and become sticky.
MGmin-low-density lipoprotein (LDL) could be a key player that leads to heart disease. The study helps researchers understand it’s the shape and density of bad cholesterol in the body that causes damage and heart disease. The lab findings show how bad cholesterol changes into ‘ultra-bad’ particles.
'Glycation of LDL by Methylglyoxal Increases Arterial Atherogenicity'