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Updated 5:30 PM February 1, 2008
 

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Link explored between belly fat, heart disease

Research has shown that people who carry their extra weight around their waist — giving them a "beer belly" or an "apple" shape — have the highest risk of all of heart attacks, strokes and other problems that arise from clogged, hardened arteries.

But the reasons behind this connection between heart disease and belly fat — also known as visceral fat — have eluded scientists. A new study in mice gives the first direct evidence of why the link may exist and offers a look at how it might be broken.

In a paper published in the journal Circulation a team of Cardiovascular Center scientists reports direct evidence of a link between inflammation around the cells of visceral fat deposits, and the artery-hardening process of atherosclerosis.

The researchers also show that a medication often given to people with diabetes can be used to calm that inflammation, and protect against further artery damage.

The research team is led by Dr. Daniel Eitzman, a cardiologist, laboratory scientist and associate professor in the Division of Cardiovascular Medicine at the Medical School and the VA Ann Arbor Healthcare System.

The discovery came partly by chance. He and his colleagues had been studying mice that lack the gene for leptin, a hormone generated by fat cells that plays a role in appetite and metabolism as well as reproduction. In an effort to get these obese mice to produce some leptin, the team developed a technique to transplant clusters of fat cells from normal mice of the same strain, into the leptin-deficient mice.

The result surprised them. "In addition to producing leptin and preventing obesity, the fat transplants became inflamed, attracting immune cells called macrophages," Eitzman explains. "Since the mice were genetically identical except for leptin, this shouldn't have happened. But the inflammation was there, and it was chronic."

The inflammation occurred around individual fat cells, or adipocytes. Further tests showed it was regulated by the same factors that control the inflammation other researchers have seen in the naturally occurring fat deposits of obese mice, specifically a chemokine called MCP-1.

But because the fat was transplanted, the inflammation could be attributed directly to the fat and not to overfeeding of the mice, or the metabolic problems that overfeeding and obesity bring, such as diabetes.

Armed with this discovery, the researchers set out to see what was causing inflammation to occur, and what implications it had. The team included postdoctoral fellow Dr. Miina U+00C3U+0096hman, U-M professor of cardiovascular medicine Daniel Lawrence, and members of the Eitzman and Lawrence laboratory teams.

They especially were interested to see if there might be any link between the inflammation and atherosclerosis — the process by which blood vessels become stiff, narrowed and lined with plaque formations that can trigger the development of blood clots.

This process, which occurs throughout the body, sets the stage for most heart attacks and strokes. Scientists and clinicians now realize that it is based on inflammation — the abnormal reaction of the body's immune system to its own tissue — and in the damage that immune-system cells and molecules can inflict.

Although the scientists caution that it's too early to apply the findings to humans with belly fat, they hope further research will reveal more about how this dangerous link comes about, why it begins, how it can be reversed and how it can be diagnosed at an early stage, perhaps through blood tests.

Until then, the best advice for overweight people who want to reduce their chance of a heart attack or stroke remains the same: Work on losing belly fat and other excess body weight through a balanced, healthy diet and regular exercise.

In addition to Eitzman, Öhman and Lawrence, the team includes former research associate Dr. Yuechen Shen; former undergraduate Chinyere Obimba, now a Harvard Medical School student; former undergraduate and current U-M medical student Andrew P. Wright; and Mark Warnock.

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