We next wanted to identify the nonhepatic tissues responsible for the tesaglitazar induced enhancement in peripheral insulin action, as well as the roles of insulin sensitivity versus responsiveness. For this purpose, in vivo tissue specific glucose utilization rates (R g′) were assessed using the 2-deoxyglucose tracer method. Dependence of R g′ on plasma insulin level was determined by performing studies in the basal fasting state and during glucose clamps performed at physiologic and superphysiological levels of hyperinsulinemia in Lean, Obese, and Tesaglitazar groups. Table 3 summarizes insulin infusion rates and steady state plasma insulin and glucose levels, as well as the GIRs needed to maintain isoglycemia, with results consistent with previous findings and in addition showing that tesaglitazar treatment completely restored insulin's ability to maximally stimulate GIR (responsiveness).
