The Missing Link Between Belly Fat and Heart Disease?

By now, everyone knows that overweight people have a higher risk of heart attacks, strokes and other problems that arise from clogged, hardened arteries. And people who carry their extra weight around their waist – giving them a “beer belly” or an “apple” shape - have the highest risk of all.

But despite the impact on human health, the reasons behind this connection between heart disease and belly fat – also known as visceral fat - have eluded scientists. Now, a new study in mice gives the first direct evidence of why this link might exist – and a tantalizing look at how it might be broken.

In a paper that will be published online today in the journal Circulation before print publication in February, a team of University of Michigan 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.

Although the scientists caution that it’s far too early to apply their findings to humans with belly fat, they hope that further research in animals and people will reveal more about how this dangerous link comes about, why it begins, how it can be reversed, and perhaps how it can be diagnosed at an early stage 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 your belly fat, and your other excess body weight, through a balanced, healthy diet and regular exercise.

The research team is led by Daniel Eitzman, M.D., a cardiologist, laboratory scientist and associate professor in the Division of Cardiovascular Medicine at the U-M 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 regulate the inflammation that other researchers have seen in the naturally occurring fat deposits of obese mice – specifically a chemokine called MCP-1.