Molecular Basis of Insulin-stimulated GLUT4 Vesicle Trafficking

J. Pessin,D. Thurmond,J. Elmendorf,K. Coker,S. Okada

Published 1999 in Journal of Biological Chemistry

ABSTRACT

Among all the diverse actions of insulin, one of the most critical and intensively studied is its regulation of glucose homeostasis. In the postabsorptive state, insulin action in muscle and adipose tissue results in increased glucose uptake from the circulation, thereby maintaining plasma euglycemia and preventing hyperglycemia (1–3). Defects in this pathway result in insulin resistance, a condition in which excessive concentrations of insulin are required to reduce blood glucose levels and often precede the development of frank Type II diabetes (3, 4). Although it has been appreciated for almost two decades that this major action of insulin results from a redistribution of glucose transporter proteins from intracellular storage sites to the plasma membrane (5, 6), the cellular mechanisms responsible for these trafficking events and the defects associated with insulin resistance have remained largely enigmatic.

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