Kobayashi Hisamine, Kato Hiroyuki, Hirabayashi Yuri, Murakami Hitoshi, Suzuki Hiromi
Applied Research Department, AminoScience Laboratories, Ajinomoto Co., Kawasaki, Japan.
J Nutr. 2006 Jan;136(1 Suppl):234S-6S. doi: 10.1093/jn/136.1.234S.
It has been shown that BCAAs, especially leucine, regulate skeletal muscle protein metabolism. However, it remains unclear how BCAAs regulate muscle protein metabolism and lead to anabolism in vivo. We examined muscle protein synthesis rate and breakdown rate simultaneously during BCAA infusion in muscle atrophy models as well as in normal healthy rats. Corticosterone-treated rats and hindlimb-immobilized rats were used as muscle atrophy models. Muscle protein synthesis rate and breakdown rate were measured as phenylalanine kinetics across the hindlimb. In anesthetized normal rats, BCAAs stimulated muscle protein synthesis despite low insulin concentration and did not suppress muscle protein breakdown. In corticosterone-treated rats, BCAAs failed to restore inhibited muscle protein synthesis, but reduced muscle protein breakdown. Immobilization of hindlimb increased muscle protein breakdown within a day. BCAAs did not change muscle protein metabolism, although essential amino acids (EAAs) suppressed muscle protein breakdown in hindlimb-immobilized rats. We also evaluated changes of fractional synthesis rate (FSR) of skeletal muscle protein during infusion of leucine alone or EAAs for 4 h in anesthetized normal rats. FSR showed a transient increase at 15-30 min of leucine infusion and then declined, whereas FSR stayed elevated throughout EAA infusion. We concluded that 1) BCAAs primarily stimulate muscle protein synthesis in normal rats independently of insulin; 2) EAAs are required to maintain the BCAA stimulation of muscle protein synthesis; and 3) The effects of BCAAs on muscle protein metabolism differ between atrophy models.
已有研究表明，支链氨基酸（BCAAs），尤其是亮氨酸，可调节骨骼肌蛋白质代谢。然而，BCAAs如何在体内调节肌肉蛋白质代谢并导致合成代谢仍不清楚。我们在肌肉萎缩模型以及正常健康大鼠中输注BCAAs期间，同时检测了肌肉蛋白质合成速率和分解速率。用皮质酮处理的大鼠和后肢固定的大鼠作为肌肉萎缩模型。通过后肢的苯丙氨酸动力学来测量肌肉蛋白质合成速率和分解速率。在麻醉的正常大鼠中，尽管胰岛素浓度较低，BCAAs仍能刺激肌肉蛋白质合成，且不抑制肌肉蛋白质分解。在皮质酮处理的大鼠中，BCAAs未能恢复受抑制的肌肉蛋白质合成，但降低了肌肉蛋白质分解。后肢固定一天内会增加肌肉蛋白质分解。BCAAs并未改变肌肉蛋白质代谢，尽管必需氨基酸（EAAs）可抑制后肢固定大鼠的肌肉蛋白质分解。我们还评估了在麻醉的正常大鼠中单独输注亮氨酸或EAAs持续4小时期间骨骼肌蛋白质的合成率分数（FSR）变化。输注亮氨酸15 - 30分钟时FSR出现短暂升高，然后下降，而在整个EAA输注过程中FSR一直保持升高。我们得出以下结论：1）在正常大鼠中，BCAAs主要独立于胰岛素刺激肌肉蛋白质合成；2）需要EAAs来维持BCAAs对肌肉蛋白质合成的刺激作用；3）BCAAs对肌肉蛋白质代谢的影响在不同萎缩模型中有所不同。
