Fat Cells Can Trigger Heart Diseases

According to the latest research studies it is suggested that the fat cells around coronary arteries may play a key role in heart disease. Researchers from the University of Iowa have found that the cells release chemicals that can trigger inflammation. Which under certain circumstances, they might also stimulate potentially damaging growth of new blood vessels.

The researchers hope to explain why obesity increases the risk of heart disease, presented their findings to the Experimental Biology 2006 conference in San Francisco. They found that the fat cells also called as adipocytes, that lie close to blood vessels in the heart are highly active, releasing many chemicals that influence biological processes within the body. Contrary to the existing thought they do nothing other than to store excess fat tissue. Almost all of the large blood vessels in the body have a layer of fat cells enveloping them.

The research team suspect that the chemicals released by the fat cells surrounding the coronary arteries might play a role in triggering heart disease by contributing to the deterioration of these vessels. The researchers isolated and cultured these cells, known as epicardial adipocytes, and compared them with cells taken from other fat tissue. The tests showed that these epicardial adipocytes tended to release far greater amounts of cytokines that were potentially more harmful and could produce inflammation in response to certain stimuli.

The researchers feel that their studies suggests that when the blood supply is reduced, possibly by a blockage in the blood vessel, the fat cells respond by releasing cytokines, which in turn trigger inflammation and make the problem worse. They also feel that at the same time, the fat cells may also trigger excessive formation of new blood vessels which could raise the risk of cardiovascular disease by raising the risk of fatty deposits haemorrhaging and causing a dangerous blockage.

Lead researcher Dr Lynn Stoll said, that the fat cells surrounding coronary arteries might ultimately prove to be an important link between obesity, type II diabetes, and coronary artery disease, which are all increasing at an epidemic rate. He suggested that on trying to understand better as to how the epicardial adipocytes sense and respond to inflammation and ischemia could lead to new, rational design for therapies on heart disease.

Stating that it is an interesting piece of research, Professor Jeremy Pearson, associate medical director of the British Heart Foundation, said that though it had been recognised for several years that fat cells stored up around the body secrete hormones that affect blood vessel function, this is the first time that researchers have paid careful attention to fat cells lying close to blood vessels in the heart.

He said that Dr Stoll's results strongly suggest that the probability of these cells being important regulators of blood vessel growth and repair might have previously gone unrecognised. He suggested that they should in future investigate some more to try and get a better understanding on the role the cells play in the development of coronary heart disease.

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