Development of a drug for diabetes using human genome information

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Evidence suggesting that polygenetic factors contribute to the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) is accumulating, but the nature of the genetic defect is unknown. The common form of NIDDM is a heterogeneous disorder in which at least two major defects contribute to the pathophysiology of the phenotype : insulin deficiency and insulin resistance. Insulin stimulates the disposal of blood glucose into skeletal muscles and adipose tissues by the translocation of glucose transporter type4 (GLUT4) from intracellular pools to the plasma membrane, and consequently the concentration of blood glucose levels decreases rapidly in vivo. Failure of this action of insulin seems to be one of the major causes of Type2 diabetes. Phosphatidylinositol 3-kinase (PI 3-kinase) and AKT play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknownDur aim is to elucidate the new signalling factors after Akt and to develop the drug to stimulate the insulin signalling. we analyzed the proteins which bind to the PH domain of Akt2 using proteome analysis and found some factors which may participate the insulin signalling