In type 2 diabetes, heart muscle is insulin resistant. Protein kinase B (PKB)/Akt) acts as a mediator of the metabolic effects of insulin, including translocation of the insulin sensitive glucose transporter, GLUT4, in a manner dependent on phosphatidylinositol-3-kinase (PI-3-K).¹ We have previously described dysregulation of PKB/Akt in hearts from a rat model of type 2 diabetes, the Zucker fa/fa rat.²

Exercise or contraction of heart muscle does not activate PKB/Akt or PI-3-K but can induce GLUT4 translocation and glucose uptake.³ However, exercise alleviates peripheral insulin resistance at a currently unknown, post-receptor level. To better understand the mechanism whereby this may be accomplished, we investigated whether chronic exercise will induce beneficial changes in the regulation of PKB/Akt that translates into improved myocardial insulin stimulated glucose uptake.

METHODS

To accomplish this, we subjected Zucker fa/fa rats (20 weeks old at the beginning of training) and a control group of age matched Wistar rats, to an exercise training programme, and documented changes in glucose uptake, myocardial GLUT4, and PKB/Akt expression and phosphorylation, in …