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Scientists have known that immune cells are responsible for most of the inflammatory chemicals that are released within fat tissue--but they haven't known why. Now a study published by Agricultural Research Service-funded scientists shows that white blood cells, called macrophages, appear to rush to dead fat cells to mop them up, the same way they surround a splinter lodged in skin.
The study, authored by physician Andrew Greenberg, cell biologist Martin Obin and colleagues, was published in the Journal of Lipid Research. Both scientists are with the Obesity and Metabolism Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, Mass.
The researchers found that as people gain weight, fat cells gradually enlarge and eventually break down and die. When obesity continues over a period of time, a cycle occurs in which new fat cells form to store the added fat, then peak in size and finally die. The study showed that more than 90 percent of the macrophages in the fatty tissue of obese mice and humans are located around these dead fat cells. In addition, as the fat cells get bigger, the prevalence of macrophages increases proportionally.
Because fat doesn't dissolve in the blood, the authors theorize that the immune system is essentially sequestering the dead fat cells and gorging on the leftover lipids and cellular debris. During that process, the macrophages could emit potentially dangerous amounts of inflammatory chemicals.
In a scenario of molecular rescue gone awry, the new findings may explain how enlarged fat cells, as found in obesity, promote obesity-related complications such as insulin resistance, diabetes or heart disease.
Read more about this research in the March 2006 issue of Agricultural Research magazine.
ARS is the U.S. Department of Agriculture's chief scientific research agency.