The Skinny on Fat: It’s Good for You
MED research shows cells can help reduce inflammation
Fat may be getting a bad rap. While there’s little doubt that too much fatty tissue is bad for your health, fat cells in a lean body can help decrease inflammation, according to researchers at the School of Medicine. Their study could help clinicians and the rest of us understand the role of fat in fighting or contributing to cardiovascular and autoimmune diseases.
“This study has figured out one of the mechanisms through which fat contributes to many disease processes by controlling inflammation,” says Kenneth Walsh, director of molecular cardiology at MED’s Whitaker Cardiovascular Institute and a senior author of the study.
The study, which appeared in the January 25 issue of The Journal of Clinical Investigation, showed that fat cells produce a protein that helps the immune system clean out the billions of dead cells that accumulate in our bodies. It’s an important function; if dead cells build up, they can cause chronic inflammation, increasing the risk of diabetes, heart disease, and autoimmune diseases such as Crohn’s disease and lupus.
The healthy immune system, in addition to identifying and attacking harmful foreign bodies like viruses and bacteria, routinely cleans up these dead cells, sending macrophages, or “eater cells,” to break down and dispose of the cells, whose numbers increase when the body’s immune system is fighting an infection.
The MED study found that fat cells produce a protein called adiponectin, which helps the macrophages clear out accumulated dead cells.
“We know quite a bit about the process of clearing dead cells — the cellular debris are moved very rapidly,” says Walsh. “What we’ve just learned is that the adiponectin protein functions as a bridging molecule for the macrophages and dead cells in the immune system.”
This process happens only in lean, healthy people, however, Walsh says. Fat cells produce both anti- and pro-inflammatory proteins. “Adiponectin is made at high levels by lean, healthy people, but it’s paradoxical,” he says. “As you become obese, it decreases; the more fat you have, the less adiponectin it makes.”
In animal trials, the researchers found that an excess of body fat caused the suppression of adiponectin and an increase in the production of pro-inflammatory proteins.
In Walsh’s experiments, mice without any adiponectin showed more autoimmune symptoms and an increase in inflammatory antibodies. Conversely, in autoimmune mice — mice whose immune systems essentially attack their own tissues, causing protracted inflammation and, thereafter, tissue degeneration — the anti-inflammatory adiponectin decreased their symptoms and reduced the presence of antibodies by 80 to 90 percent.
The research, says Walsh, could help in the development of new drugs to elevate adiponectin levels and lower the risk of autoimmune and cardiovascular diseases.