The weight of research into the biomechanisms of fat tissue continues to grow. It just isn't sensible to be overweight - at least if long-term health and longevity happen to be on your list of goals. Here's the latest update on one of the ways in which excess fat tissue slowly destroys you from the inside:
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 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.
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.
“There appeared to be an interaction between the macrophages causing the inflammation in the visceral fat, and the process of atherosclerosis,” says Eitzman, who notes that blood vessels far from the site of the fat transplant developed increased atherosclerosis.
All that excess fat hanging around over the years generates atherosclerosis, which then kills you:
Most commonly, soft plaque suddenly ruptures, [causing] the formation of a thrombus that will rapidly slow or stop blood flow, that is, within 5 minutes, leading to death of the tissues fed by the artery. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis is a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, etc.
According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).
This is one of the many reasons why people who keep in shape and stick to the health basics tend to live longer, healthier lives.