Wheatley Catherine M, Rattigan Stephen, Richards Stephen M, Barrett Eugene J, Clark Michael G
Department of Biochemistry, Medical School, University of Tasmania, Hobart, Australia, 7001.
Am J Physiol Endocrinol Metab. 2004 Oct;287(4):E804-9. doi: 10.1152/ajpendo.00077.2004. Epub 2004 Jun 22.
Exercise and insulin increase muscle glucose uptake by different mechanisms and also increase capillary recruitment, which is proposed to facilitate access for hormones and nutrients. The genetically obese Zucker rat shows impaired insulin- but not contraction-mediated glucose uptake in muscle. Recently, we have shown the genetically obese Zucker rats to have impaired insulin-mediated capillary recruitment and proposed that this contributes to the insulin resistance of muscle in vivo. Because this might imply a general loss of recruitable capillaries, we now assess responses to contraction in muscles of 18 +/- 3-wk-old lean and obese Zucker rats in vivo. Field stimulation (2 Hz, 0.1 ms) was conducted for 1 h on one leg of anesthetized instrumented rats, and measurements were made of femoral blood flow (FBF), heart rate (HR), blood pressure (BP), hindleg metabolism of 1-methylxanthine (a measure of capillary recruitment), hindleg glucose uptake (HGU), and lower leg muscle glucose uptake by 2-deoxyglucose (R'g). Lean animals (311 +/- 9 g) developed tension at 219 +/- 27 g/g muscle with no change in BP but with significant increases in HR, FBF, HGU, 1-MX metabolism, and R'g (P < 0.05), compared with nonstimulated control leans. Obese animals (469 +/- 7 g) developed tension at 265 +/- 31 g/g muscle with no change in HR or BP but with significant increases in FBF, HGU, 1-MX metabolism, and R'g (P < 0.05) compared with nonstimulated control obese rats. Muscle contraction of lean animals led to a greater increase in lower leg R'g, similar responses in HGU and 1-MX, and a smaller increase in FBF than in obese animals. A tight correlation between FBF and capillary recruitment was noted for all data (P < 0.001). It is concluded that contraction-mediated muscle capillary recruitment and glucose uptake are essentially normal in the obese Zucker rat and that control of FBF and capillary recruitment in exercise is closely linked.
运动和胰岛素通过不同机制增加肌肉对葡萄糖的摄取,并且还会增加毛细血管的募集,这被认为有助于激素和营养物质的进入。遗传性肥胖的 Zucker 大鼠表现出胰岛素介导的肌肉葡萄糖摄取受损,但收缩介导的葡萄糖摄取未受损。最近,我们发现遗传性肥胖的 Zucker 大鼠存在胰岛素介导的毛细血管募集受损的情况,并提出这是导致体内肌肉胰岛素抵抗的原因之一。由于这可能意味着可募集毛细血管的普遍减少,我们现在评估 18±3 周龄的瘦 Zucker 大鼠和肥胖 Zucker 大鼠肌肉对收缩的反应。对麻醉的有仪器监测的大鼠的一条腿进行 1 小时的场刺激(2Hz,0.1ms),并测量股血流量(FBF)、心率(HR)、血压(BP)、后肢 1-甲基黄嘌呤的代谢(毛细血管募集的指标)、后肢葡萄糖摄取(HGU)以及通过 2-脱氧葡萄糖测量的小腿肌肉葡萄糖摄取(R'g)。与未刺激的对照瘦鼠相比,瘦鼠(311±9g)肌肉张力在 219±27g/g 时升高,血压无变化,但心率、FBF、HGU、1-MX 代谢和 R'g 显著增加(P<0.05)。肥胖大鼠(469±7g)肌肉张力在 (265±31g/g)时升高,心率和血压无变化,但与未刺激的对照肥胖大鼠相比,FBF、HGU、1-MX 代谢和 R'g 显著增加(P<0.05)。与肥胖动物相比,瘦动物的肌肉收缩导致小腿 R'g 的增加更大,HGU 和 1-MX 的反应相似,FBF 的增加较小。所有数据中均观察到 FBF 与毛细血管募集之间存在紧密相关性(P<0.001)。结论是,收缩介导的肌肉毛细血管募集和葡萄糖摄取在肥胖 Zucker 大鼠中基本正常,并且运动中 FBF 和毛细血管募集的控制密切相关。