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.

Beta cells are blue in this image of mouse pancreatic islets that have been transplanted beneath the capsule, or outer layer of the kidney. Endothelial cells that line blood vessels are shown in green. Some of them grow into the islets from the underlying kidney. Other endothelial cells, found within the islets and transplanted with them, continue to grow and are shown in red.
Courtesy of Marcela Brissova and Alvin C. Powers, Vanderbilt Division of Endocrinology.
Animal studies also are shedding light on the complications of the metabolic syndrome. Two years ago, for example, Drs. MacRae Linton and Sergio Fazio at Vanderbilt and their colleague, Gokan Hotamisligil at Harvard found that they could protect mice from atherosclerosis, the build up of fatty deposits in blood vessels, by eliminating a protein linked to insulin resistance.

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.

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