Molecular Basis of Insulin Action and Insulin Resistance in Peripheral Tissues

To understand the molecular basis of insulin resistance (whether primary or secondary) in muscle and fat cells, it is imperative to gain knowledge of the normal mechanisms of insulin action. In these tissues, insulin stimulates glucose uptake by rapidly mobilizing preexisting glucose transporters (primarily the GLUT4 isoform) from an intracellular storage organelle (or vesicle) to the plasma membrane (5,6). This is achieved by a series of signals elicited from the receptor, which are detected in an unknown fashion by the intracellular organelle. The latter is then free to find and interact with docking sites on the plasma membrane (7) that will ultimately enable fusion of the two membranes to provide functional glucose transporters. Detailed knowledge has emerged on the signals emanating from the receptor that are essential for GLUT4 translocation and the nature of the proteins engaged in vesicle docking and fusion with the plasma membrane.

The signaling events involved in the insulin-mediated GLUT4 translocation include autophosphorylation of the insulin receptor, tyrosine phosphorylation of docking proteins known as insulin receptor substrates (IRS 1 -4), their subsequent binding to the enzyme phosphatidylinositol 3-kinase (PI 3-kinase), and the resultant activation of PI 3-kinase to produce phosphorylated phospho-inositides. How these signals then translate into translocation of the GLUT4 vesicle is the subject of vigorous study. A serine/threonine kinase identified

Insulin Recepf—


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