神経筋電気刺激療法とグルタミン投与の併用がcolon 26がんモデルマウスにおける筋萎縮に及ぼす影響

抄録

The depressed protein synthetic response, a phenomenon termed as anabolic resistance, has been shown to be involved in muscle wasting induced by cancer cachexia. Moreover, a positive relationship between protein synthetic rate and intracellular glutamine (GLN) concentration has been found in skeletal muscles. We here investigated the effects of neuromuscular electrical stimulation (ES) and GLN administration on muscle wasting and GLN metabolism in colon 26 (C-26) tumor bearing mice. CD2F1 mice were divided into 8 groups; control (CNT), CNT+ES, CNT+GLN, CNT+ES+GLN, C-26, C-26+ES, C-26+GLN, C-26+ES+GLN. Cancer cachexia was induced by a subcutaneous injection of C-26 cells and was developed for four weeks. ES was performed to the left plantar flexor muscles every other day and GLN (1 g/kg) was daily intraperitoneally administered starting one day following C-26 injection. Tumor-free body mass and fast-twitch gastrocnemius (Gas) muscle weight were lower in the C-26 group than in the CNT group (-19% and -17%, respectively). Niether ES training nor GLN administration, alone or in combination, ameliorated the loss of Gas muscle weight in the C-26 mice. ES training in combination with GLN administration inhibited the increased GLN synthetase (GS) expression in the C-26 muscles. Thus, it is unlikely that GLN plays a critical role in muscle protein metabolism and thereby can be targeted as a tentative treatment of cancer cachexia.