Bell Jill A, Volpi Elena, Fujita Satoshi, Cadenas Jerson G, Sheffield-Moore Melinda, Rasmussen Blake B
Department of Kinesiology, University of Southern California, Los Angeles, CA, USA.
J Nutr. 2006 May;136(5):1249-55. doi: 10.1093/jn/136.5.1249.
Type 2 diabetes (T2DM) subjects failing diet treatment are characterized by hyperinsulinemia and insulin resistance leading to fasting and postprandial hyperglycemia and hyperlipidemia. Energy is essential for allowing the process of protein synthesis to proceed. Additionally, insulin can stimulate protein synthesis in human muscle. The aims of this study were to determine if poorly controlled T2DM affects postabsorptive muscle protein anabolism, and if the muscle anabolic response to hyperinsulinemia with high energy availability is maintained. Control (n = 6) and T2DM subjects (n = 6) were studied in the postabsorptive state and during an isoenergetic high nutritional energy clamp (relative to postabsorptive state). Muscle protein synthesis and breakdown (nmol . min(-1) . 100 g leg muscle(-1)) were assessed using stable isotope methodology, femoral arterio-venous sampling, muscle biopsies, and a three-pool model to calculate protein turnover. Postabsorptive phenylalanine net balance and whole body rate of appearance (Ra) were not different between groups; however, basal muscle protein breakdown was higher in T2DM (94 +/- 9) than in controls (58 +/- 12) (P < 0.05) and muscle protein synthesis tended (P = 0.07) to be elevated in T2DM (66 +/- 14) compared with controls (39 +/- 6). During the clamp, net balance increased, whole body Ra and muscle protein breakdown decreased (P < 0.05), and muscle protein synthesis tended to decrease (P = 0.08) to a similar extent in both groups. We conclude that postabsorptive muscle protein turnover is elevated in poorly controlled T2DM, however, there is no excessive loss of muscle protein because net balance is not different from controls. Moreover, the anabolic response to increased insulin and energy availability is maintained in T2DM.
饮食治疗失败的2型糖尿病（T2DM）患者的特征是高胰岛素血症和胰岛素抵抗，导致空腹及餐后高血糖和高脂血症。能量对于蛋白质合成过程的进行至关重要。此外，胰岛素可刺激人体肌肉中的蛋白质合成。本研究的目的是确定控制不佳的T2DM是否会影响吸收后肌肉蛋白质合成代谢，以及对高能量状态下高胰岛素血症的肌肉合成代谢反应是否得以维持。在吸收后状态以及等能量高营养能量钳夹期间（相对于吸收后状态），对对照组（n = 6）和T2DM患者（n = 6）进行了研究。使用稳定同位素方法、股动静脉采样、肌肉活检和三池模型评估肌肉蛋白质合成和分解（nmol·min⁻¹·100 g腿部肌肉⁻¹），以计算蛋白质周转率。两组之间吸收后苯丙氨酸净平衡和全身出现率（Ra）无差异；然而，T2DM组的基础肌肉蛋白质分解（94±9）高于对照组（58±12）（P < 0.05），与对照组（39±6）相比，T2DM组的肌肉蛋白质合成有升高趋势（P = 0.07）（66±14）。在钳夹期间，两组的净平衡均增加，全身Ra和肌肉蛋白质分解均降低（P < 0.05），肌肉蛋白质合成均有降低趋势（P = 0.08），且降低程度相似。我们得出结论，控制不佳的T2DM患者吸收后肌肉蛋白质周转率升高，然而，由于净平衡与对照组无差异，因此肌肉蛋白质没有过度损失。此外，T2DM患者对胰岛素和能量供应增加的合成代谢反应得以维持。
