Researchers at the University of Central Florida recently identified a small protein that is crucial for the release of very low density lipoprotein (VLDL) — more commonly known as bad cholesterol — from the liver. The factor is controlled by myristic acid, a food component present in different kinds of fats, and researchers hypothesize that eating too much fatty foods can disrupt the cholesterol balance and lead to heart disease.
The study describing the findings is titled “Silencing of Small Valosin-containing Protein-interacting Protein (SVIP) Reduces Very Low Density Lipoprotein (VLDL) Secretion from Rat Hepatocytes by Disrupting Its Endoplasmic Reticulum (ER)-to-Golgi Trafficking,” and was published in The Journal of Biological Chemistry.
VLDLs are a type of molecules transporting cholesterol and other forms of fat around the body. Once in the blood, it is converted to the equally bad cholesterol LDL, which many might recognize as the villain in heart disease. Dr. Shadab Siddiqi and his research team have been trying to find ways to prevent heart disease by controlling the release of VLDL from the liver. Low density lipoproteins are believed to contribute to heart disease by increasing blood cholesterol levels, building up as plaque in blood vessels.
Cholesterol release from the liver is a fine balance. If the liver secretes too much VLDL, scientists believe the body might be at increased risk for heart disease. However, if too little is released, the cholesterol remains in place, leading to fatty liver — a strong risk factor for cancer.
Siddiqi’s earlier research mapped the molecular processes that led to the release of VLDL from the liver. Now he discovered a protein, called SVIP (small valosin-containing protein-interacting protein), that controls the release of VLDL.
The protein, it turns out, reacts to a component found in most vegetable and animal fats, myristic acid. Adding the fatty acid to liver cells in a lab dish increased the release of VLDL, while preventing myristic acid binding to SVIP prevented cholesterol release. The effect seemed to be specific to myristic acid, since other dietary fats had no impact on the release of VLDL.
“These findings suggest that our diet modulates the complex molecular processes that have profound effects on our health and lifespan,” Siddiqi said in a press release. “The challenge will be in creating a therapy that does not impact the liver’s many other functions.”
The idea that our diet and, as a consequence, high blood cholesterol levels, cause heart disease, a paradigm held for the last decades, has recently been questioned in several studies, among them a recent large study analyzing previously published data on the link. The study found no relationship — and even a reverse relationship — between the two.
Further research on the possible link between heart disease and high cholesterol levels is therefore needed.