Monier S, Le Cam A, Le Marchand-Brustel Y
Diabetes. 1983 May;32(5):392-7. doi: 10.2337/diab.32.5.392.
The effects of insulin and insulin-like growth factor I (IFG-I) on protein synthesis were compared in muscle isolated from lean and goldthioglucose (GTG)-obese mice. Two types of skeletal muscles, the red soleus and the white extensor digitorum longus (EDL) muscles, were studied. In muscles from lean mice, 6.7 nM insulin and 50 nM IGF-I caused a similar maximal stimulation of tyrosine incorporation in total proteins (40% increase). However, the potency of IGF-I was only 5-10% that of insulin both in soleus and in EDL muscles (EC50 approximately equal to 6 nM for IGF-I and 0.5 nM for insulin). Basal rate of protein synthesis was identical in muscles from GTG-obese and lean mice. Similarly, a comparable increase in the rate of protein synthesis was obtained using maximally effective concentrations of insulin and IGF-I in both lean and GTG-obese animals. SDS-polyacrylamide gel electrophoresis analysis of proteins labeled with 35S-methionine confirmed that, in muscles from lean and GTG-obese animals, insulin and IGF-I increased overall protein synthesis in a similar manner. These results suggest that the protein synthesis machinery is not impaired in GTG-induced obesity, which is therefore not associated with resistance to insulin for its effect on protein metabolism.
在从瘦小鼠和金硫葡糖（GTG）诱导的肥胖小鼠分离出的肌肉中，比较了胰岛素和胰岛素样生长因子I（IGF-I）对蛋白质合成的影响。研究了两种类型的骨骼肌，即红色比目鱼肌和白色趾长伸肌（EDL）。在瘦小鼠的肌肉中，6.7 nM胰岛素和50 nM IGF-I对总蛋白中酪氨酸掺入的刺激作用相似，达到最大刺激（增加40%）。然而，在比目鱼肌和EDL肌肉中，IGF-I的效力仅为胰岛素的5%-10%（IGF-I的EC50约为6 nM，胰岛素的EC50约为0.5 nM）。GTG诱导的肥胖小鼠和瘦小鼠肌肉中的蛋白质合成基础速率相同。同样，在瘦小鼠和GTG诱导的肥胖小鼠中，使用最大有效浓度的胰岛素和IGF-I均可使蛋白质合成速率得到相当程度的提高。对用35S-甲硫氨酸标记的蛋白质进行的SDS-聚丙烯酰胺凝胶电泳分析证实，在瘦小鼠和GTG诱导的肥胖小鼠的肌肉中，胰岛素和IGF-I以相似的方式增加了整体蛋白质合成。这些结果表明，在GTG诱导的肥胖中，蛋白质合成机制未受损，因此GTG诱导的肥胖与胰岛素对蛋白质代谢的作用产生抵抗无关。
