To study the local tissue lactate production in the normal state and its possible disturbances in insulin resistance, rates of lactate release from adipose tissue (AT) and skeletal muscle (SM) were compared postabsorptively and during a hyperinsulinemic euglycemic clamp in eleven healthy non-obese and eleven insulin resistant obese women. A combination of microdialysis, to measure interstitial lactate and the ¹³³Xe-clearance technique, to determine local blood flow, was used. In the controls, local blood flow increased by 40% in SM (p<0.05) and remained unchanged in AT, whereas the interstitial-plasma difference in lactate doubled in AT (p< 0.005) and was unaffected in SM during hyperinsulinemia. In the obese, blood flow and interstitial-plasma difference were unchanged during hyperinsulinemia. The lactate release (umol · 100g^-1 · min ^-1) was 1.17 ± 0.22 in SM and 0.43 ± 0.11 in AT among the controls (p<0.01) and 0.86 ± 0.23 in SM and 0.83 ± 0.25 in AT among the obese women in the postabsorptive state. During insulin-infusion, the lactate release in the controls increased to 1.92 ± 0.26 in SM (p <0.005) and to 1.14 ± 0.22 in AT (p<0.005) but remained unchanged in the obese. It is concluded that, AT and SM are both significant sources of lactate release. postabsorptively and AT is as responsive to insulin as SM. The ability to increase lactate release in response to insulin is impaired in AT and SM in insulin resistant obese women, involving defective insulin regulation of both tissue lactate metabolism and local blood flow.