Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes
Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes
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DOI：
10.1007/s00125-003-1265-7
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发表时间：
2004-01-01
期刊：
影响因子：
8.2
通讯作者：
Hawley, JA
中科院分区：
文献类型：
--
作者：
Bruce, CR;Kriketos, AD;Hawley, JA
目的/假设。我们确定运动训练对2型糖尿病患者胰岛素敏感性和肌肉脂质（甘油三酯[TG（m）]和长链脂肪酰辅酶A [LCACoA]浓度）的影响。7名2型糖尿病患者和6名年龄、BMI、%体脂和VO（2）峰值匹配的健康对照者参加了每周3天的训练计划，为期8周。在120分钟的正常血-高胰岛素钳夹期间，在训练前和训练后测定胰岛素敏感性，并在每次钳夹之前和之后获得肌肉活检。氧化酶活性[柠檬酸合酶（CS），β-羟基-酰基-CoA（β-HAD）]和TG（m）在训练前和训练后从基础肌肉样品中测定，而总LCACoA含量在胰岛素刺激前后，训练前和训练后获得的样品中测定。训练诱导的VO（2）峰值的增加（接近20%，p < 0.01）在两组中相似。与对照组相比，糖尿病患者训练前后胰岛素敏感性均较低（接近60%; p < 0.05），但训练后两组胰岛素敏感性均较对照组增加（接近30%; p < 0.01）。2型糖尿病患者的TG（m）在训练前升高（1.70%; p < 0.05），但在训练后恢复到对照组的水平。两组之间的基础LCACoA含量相似，并且未因训练而改变。胰岛素刺激对LCACoA含量没有可检测的影响。CS和P-HAD活性在两组对训练的反应中增加到相同的程度（p < 0.001）。我们的结论是，短期运动训练后观察到的胰岛素敏感性增强与2型糖尿病患者TG（m）含量显着降低有关。然而，尽管TG（m）正常化至健康个体中观察到的水平，但糖尿病患者的胰岛素抵抗并未完全逆转。
Aim/hypothesis. We determined the effect of exercise training on insulin sensitivity and muscle lipids (triglyceride [TG(m)] and long-chain fatty acyl CoA [LCACoA] concentration) in patients with Type 2 diabetes.Methods. Seven patients with Type 2 diabetes and six healthy control subjects who were matched for age, BMI, % body fat and VO(2)peak participated in a 3 days per week training program for 8 weeks. Insulin sensitivity was determined pre- and post-training during a 120 min euglycaemic-hyperinsulinaemic clamp and muscle biopsies were obtained before and after each clamp. Oxidative enzyme activities [citrate synthase (CS), beta-hydroxy-acyl-CoA (beta-HAD)] and TG(m) were determined from basal muscle samples pre- and post training, while total LCACoA content was measured in samples obtained before and after insulin-stimulation, pre- and post training.Results. The training-induced increase in VO(2)peak (similar to20%, p < 0.01) was similar in both groups. Compared with control subjects, insulin sensitivity was lower in the diabetic patients before and after training (similar to 60%; p < 0.05), but was increased to the same extent in both groups with training (similar to30%; p < 0.01). TG(m) was increased in patients with Type 2 diabetes (1.70%; p < 0.05) before, but was normalized to levels observed in control subjects after training. Basal LCACoA content was similar between groups and was unaltered by training. Insulin-stimulation had no detectable effect on LCACoA content. CS and P-HAD activity were increased to the same extent in both groups in response to training (p < 0.001).Conclusion/interpretation. We conclude that the enhanced insulin sensitivity observed after short-term exercise training was associated with a marked decrease in TG(m) content in patients with Type 2 diabetes. However, despite the normalization of TG(m) to levels observed in healthy individuals, insulin resistance was not completely reversed in the diabetic patients.