Iozzo Patricia, Takala Teemu, Oikonen Vesa, Bergman Jörgen, Grönroos Tove, Ferrannini Ele, Nuutila Pirjo, Knuuti Juhani
Institute of Clinical Physiology, National Research Council (CNR), Via Moruzzi 1, 56100 Pisa, Italy.
Diabetes Care. 2004 Sep;27(9):2172-7. doi: 10.2337/diacare.27.9.2172.
Fat metabolism is increasingly implicated in the pathogenesis of type 2 diabetes. Endurance training has been shown to prevent hepatic steatosis and to alter skeletal muscle fat metabolism, and regional free fatty acid (FFA) uptake adaptations were suggested as a mechanism. Thus, we tested whether endurance training modifies the uptake of plasma FFAs occurring in the liver and in skeletal muscle during anabolic, i.e., hyperinsulinemic, conditions.
Trained and untrained healthy male subjects underwent positron emission tomography scanning of the liver and thigh regions, with the FFA analog 14(R,S)-[(18)F]fluoro-6-thia-heptadecanoic acid, during euglycemic hyperinsulinemia. Tracer influx rate constants in skeletal muscle (MK(i)) and liver (LK(i)) were multiplied by plasma FFA levels to obtain FFA uptake for skeletal muscle (MFU) and liver (LFU), respectively.
Athletes showed increased Vo(2max) (P < 0.0001), insulin-mediated glucose disposal (M value, 61 +/- 4 vs. 46 +/- 3 micromol. min(-1). kg(-1), P = 0.01), and plasma lactate levels during the clamp and lower percentage of body fat mass (P = 0.002). MK(i) was 25% higher in athletes than in sedentary men (P = 0.03). In all subjects, MK(i) and MFU were positively correlated with the M value (r = 0.56, P = 0.02, and r = 0.51, P = 0.03, respectively) and with plasma lactate levels (r = 0.63, P = 0.006, and r = 0.63, P = 0.005, respectively). LK(i) was significantly reduced by 20% in the athletes (P = 0.04). By multiple regression, LFU was inversely correlated with the two fitness categories (P = 0.008), and it was lower in athletes. Linear fitting of liver data showed time consistency, indicating no release of FFAs as a mechanism for the reduced liver retention in athletes.
We conclude that endurance training promotes insulin-mediated glucose and FFA disposal in skeletal muscle, while lowering hepatic FFA uptake. Such changes may result in a divergent pattern of fat accumulation in the two organs.
脂肪代谢在2型糖尿病发病机制中的作用日益受到关注。耐力训练已被证明可预防肝脏脂肪变性并改变骨骼肌脂肪代谢，区域游离脂肪酸（FFA）摄取适应性被认为是一种机制。因此，我们测试了耐力训练是否会改变合成代谢状态（即高胰岛素血症状态）下肝脏和骨骼肌中血浆FFA的摄取情况。
受过训练和未受过训练的健康男性受试者在正常血糖高胰岛素血症期间，使用FFA类似物14（R，S）-[(18)F]氟-6-硫代十七烷酸对肝脏和大腿区域进行正电子发射断层扫描。将骨骼肌（MK(i)）和肝脏（LK(i)）中的示踪剂流入速率常数乘以血浆FFA水平，分别得到骨骼肌（MFU）和肝脏（LFU）的FFA摄取量。
运动员的最大摄氧量（Vo(2max)）增加（P < 0.0001），胰岛素介导的葡萄糖处置（M值，61 +/- 4对46 +/- 3微摩尔·分钟(-1)·千克(-1)，P = 0.01），钳夹期间血浆乳酸水平升高，体脂百分比降低（P = 0.002）。运动员的MK(i)比久坐男性高25%（P = 0.03）。在所有受试者中，MK(i)和MFU与M值（分别为r = 0.56，P = 0.02和r = 0.51，P = 0.03）以及血浆乳酸水平（分别为r = 0.63，P = 0.006和r = 0.63，P = 0.005）呈正相关。运动员的LK(i)显著降低了20%（P = 0.04）。通过多元回归分析，LFU与两种健康状况类别呈负相关（P = 0.008），且在运动员中较低。肝脏数据的线性拟合显示出时间一致性，表明FFA没有释放，这是运动员肝脏中FFA保留减少的机制。
我们得出结论，耐力训练可促进胰岛素介导的骨骼肌葡萄糖和FFA处置，同时降低肝脏FFA摄取。这些变化可能导致两个器官中脂肪堆积模式不同。
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