The researchers fed high-fat diet to a group of animals for 12 weeks and saw an increased amount of key proteins that stimulate white blood cells bound to red blood cells.
Researchers have discovered the negative impact a high-fat diet has on red blood cells and how these cells, in turn, promote the development of cardiovascular disease.
“Obesity caused by chronic consumption of a high-calorie, high-fat diet is a worldwide epidemic, representing one of the greatest threats to global health,” said principal investigator Vladimir Bogdanov, associate professor at University of Cincinnati College of Medicine in the US. “We explored how a high fat-diet causes red blood cell dysfunction in this study,” Bogdanov said.
The researchers fed high-fat diet to a group of animals for 12 weeks and saw an increased amount of key proteins that stimulate white blood cells bound to red blood cells. These white blood cells, also known as macrophages, are a type of white blood cell that “eats” cellular debris, foreign substances, microbes, cancer cells and anything else that does not have the types of proteins specific to the surface of healthy body cells on its surface. They also play a crucial role in clogging of arteries, or atherosclerosis.
“In red blood cells from animal models fed a high-fat diet, there was an increase in cholesterol found in the cell membrane and phosphatidylserine levels, promoting inflammatory reactions. Phosphatidylserine is a phospholipid membrane component which plays a key role in the cycle of cells,” Bogdanov explained.
When red blood cells from the animals being fed the high-fat diet were injected into a control group, eating a normal diet, there was a three-fold increase in their spleens’ uptake of red blood cells. The spleen is involved in the removal of blood cells, as well as systemic inflammation. “All of these findings show that the dysfunction of red blood cells, corresponding with dysfunction of the lining of blood vessels, occurs very early in diet-induced obesity and may play a part in the formation of atherosclerosis,” Bogdanov noted.
The findings appeared in the journal Circulation.
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