A disordered thermostat pg. 6
These studies are helping researchers determine how glucose gets into the muscle cell, and what may be going on when tissues become resistant to insulin, says David H. Wasserman, Ph.D., director the federally funded Mouse Metabolic Phenotyping Center at Vanderbilt. The center, one of four in the country, helps develop new mouse models of diabetes to further research in the disease.
The adipocyte fatty-acid-binding protein (aP2) is produced by adipocytes (fat cells), which contribute to insulin resistance, and also by macrophages, inflammatory cells that play a crucial role in atherosclerosis.
The researchers studied apoE-deficient mice, a widely used mouse model of high cholesterol and atherosclerosis. Mice that lacked aP2 were dramatically protected from atherosclerosis, even though they remained insulin resistant, suggesting that the expression of aP2 by macrophages promotes atherosclerosis.
This finding was confirmed in the following way: apoE-deficient mice lacking expression of aP2 only in macrophages were similarly protected from developing atherosclerosis. Earlier studies found that obese mice lacking aP2 expression in adipose tissue showed increased insulin sensitivity. Thus, aP2, which links two major features of the metabolic syndrome, is a potential drug target for preventing both atherosclerosis and insulin resistance.