Fat cells tied to whole-body insulin resistance

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Molecular basis of link between obesity and diabetes has remained unclear

Research done by Barbara Kahn, professor of medicine at Beth Israel Deaconess Medical Center, and colleagues now shows that glucose uptake by fatty tissue is important for maintaining the body’s ability to respond to insulin. Their results also point to a mechanism by which an abnormality in fat cells may trigger insulin resistance and ultimately diabetes. Skeletal muscle is the primary tissue for insulin-stimulated glucose uptake. Yet in obesity and Type II diabetes, expression of the primary insulin-stimulated glucose transporter, GLUT4, is normal in muscle but reduced in fatty tissue. This paradox led Kahn and colleagues to ask what role fatty tissue-expressed GLUT4 may play in the development of insulin resistance. The results clearly show that “fat is important for whole-body insulin action,” said Kahn.