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 shouldnt 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. The team included postdoctoral fellow Miina hman, M.D., Ph.D., U-M professor Daniel Lawrence, Ph.D., and members of the Eitzman and Lawrence laboratory teams.
They were especially interested to see if there might be any link between the inflammation and atherosclerosis the formal name for 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 inflammatio
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| Contact: Kara Gavin kegavin@umich.edu 734-764-2220 University of Michigan Health System Source:Eurekalert |