Figure 1 shows the results of the tracer based measurements, whole body glucose disposal (R d), and hepatic glucose output (HGO) plotted against plasma insulin at basal (fasting) and ClampL levels. Tesaglitazar treatment did not correct the elevation in basal HGO or the associated moderate hyperglycemia of the obese Zucker rat. The afore mentioned treatment induced improvement in whole body insulin action involved both enhanced peripheral insulin action (greater increment in R d at lower insulin levels compared to Obese) and hepatic insulin sensitization (Figure 1). Estimated insulin concentrations required to suppress HGO to 50% of the basal level (EC50) were substantially reduced in Tesaglitazar 2.4 ± 0.4 versus Obese 15.4 ± 5.0 nM, P < 0.05. For comparison the EC50 for Lean was 0.65 ± 0.08 nM.
