New study finds fat cell particles may indicate increased heart disease risk

A new study suggests that particles released from fat cells could determine a patient’s risk of developing cardiovascular disease, according to a Milken Institute School of Public Health release.

Matthew Barberio, an assistant professor of exercise and nutrition studies and the study’s lead author, collaborated with researchers from Children’s National Medical Center and the Winthrop Hospital at New York University, the release states. The team found that the presence of the particles, called extracellular vesicles, can prevent macrophages, a type of white blood cell, from eliminating excess cholesterol buildup in blood vessels, according to the release.

The excess cholesterol overloads white blood cells and, over time, settles in the walls of blood vessels and hardens into a plaque, according to the study, which was published Monday in the Journal of Translational Medicine. The plaque may then restrict blood flow through the vessels and increase the likelihood of heart attack and stroke, the release states.

“We were surprised to find that EVs could hobble the macrophage cholesterol outflow system in adolescents of any weight,” Barberio said in the release. “It’s still an open question whether young people who are healthy can tolerate obesity – or whether there are specific differences in fat tissue composition that up kids’ risk for heart disease.”

The researchers collected belly fat samples during abdominal surgeries from 93 children aged 12 to 19 who were lean, overweight and obese for the study, according to the release. They found that seven small sequences of ribonucleic acid, the messenger molecule responsible for protein synthesis in the body, inhibit white blood cells from eliminating cholesterol – building upon previous researchers’ findings that obesity alters RNA found in fat cells.

The research team will use the results of the study to find ways to reduce the risk of cardiovascular disease in children and adults, according to the release.

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