Qvisth Veronica, Hagström-Toft Eva, Moberg Erik, Sjöberg Stefan, Bolinder Jan
Department of Medicine, Karolinska University Hospital-Huddinge, Karolinska Institutet, Stockholm, Sweden.
Am J Physiol Endocrinol Metab. 2007 Mar;292(3):E709-14. doi: 10.1152/ajpendo.00104.2006. Epub 2006 Oct 31.
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 11 healthy nonobese and 11 insulin-resistant obese women. A combination of microdialysis, to measure interstitial lactate, and the 133Xe clearance technique, to determine local blood flow, were 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 in lactate remained unchanged in both tissues during hyperinsulinemia. The lactate release (micromol100 g-1min-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, 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 women. It is concluded that AT and SM are both significant sources of lactate release postabsorptively, and AT is at least 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.
为研究正常状态下局部组织乳酸生成及其在胰岛素抵抗时可能出现的紊乱情况，对11名健康非肥胖女性和11名胰岛素抵抗肥胖女性在吸收后状态及高胰岛素正常血糖钳夹期间，比较了脂肪组织（AT）和骨骼肌（SM）的乳酸释放速率。采用微透析（测量间质乳酸）和133Xe清除技术（测定局部血流）相结合的方法。在对照组中，高胰岛素血症期间，SM的局部血流增加40%（P<0.05），AT的局部血流保持不变，而AT中乳酸的间质-血浆差值增加一倍（P<0.005），SM中的该差值未受影响。在肥胖女性中，高胰岛素血症期间，两个组织的血流和乳酸的间质-血浆差值均保持不变。吸收后状态下，对照组中SM的乳酸释放（微摩尔·100克-1·分钟-1）为1.17±0.22，AT为0.43±0.11（P<0.01），肥胖女性中SM为0.86±0.23，AT为0.83±0.25。胰岛素输注期间，对照组中SM的乳酸释放增加至1.92±0.26（P<0.005），AT增加至1.14±0.22（P<0.005），而肥胖女性中的乳酸释放保持不变。结论是，吸收后状态下AT和SM都是乳酸释放的重要来源，且AT对胰岛素的反应至少与SM一样。胰岛素抵抗肥胖女性的AT和SM中，胰岛素刺激乳酸释放的能力受损，涉及组织乳酸代谢和局部血流的胰岛素调节缺陷。
