Lee Sumin, Choi Yoonha, Kim Yerin, Cha Yeon Kyung, Park Tai Hyun, Kim Yuri
Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea.
Interdisciplinary Program in Bioengineering, Seoul National University, Seoul 08826, Korea.
Nutr Res Pract. 2024 Aug;18(4):451-463. doi: 10.4162/nrp.2024.18.4.451. Epub 2024 May 23.
BACKGROUND/OBJECTIVES: The umami taste receptor (TAS1R1/TAS1R3) is endogenously expressed in skeletal muscle and is involved in myogenesis; however, there is a lack of evidence about whether the expression of the umami taste receptor is involved in muscular diseases. This study aimed to elucidate the effects of the umami taste receptor and its mechanism on muscle wasting in cancer cachexia using and models.
MATERIALS/METHODS: The Lewis lung carcinoma-induced cancer cachexia model was used and , and the expressions of umami taste receptor and muscle atrophy-related markers, muscle atrophy F-box protein, and muscle RING-finger protein-1 were analyzed.
Results showed that TAS1R1 was significantly downregulated and under the muscle wasting condition. Moreover, overexpression of TAS1R1 in the human primary cell model protected the cells from muscle atrophy, and knockdown of TAS1R1 using siRNA exacerbated muscle atrophy.
Taken together, the umami taste receptor exerts protective effects on muscle-wasting conditions by restoring dysregulated muscle atrophy in cancer cachexia. In conclusion, this result provided evidence that the umami taste receptor exerts a therapeutic anti-cancer cachexia effect by restoring muscle atrophy.
背景/目的：鲜味味觉受体（TAS1R1/TAS1R3）在骨骼肌中内源性表达并参与肌生成；然而，关于鲜味味觉受体的表达是否参与肌肉疾病，目前缺乏证据。本研究旨在使用[具体模型1]和[具体模型2]阐明鲜味味觉受体对癌症恶病质中肌肉萎缩的影响及其机制。
材料/方法：使用Lewis肺癌诱导的癌症恶病质模型[具体动物模型1]和[具体动物模型2]，分析鲜味味觉受体和肌肉萎缩相关标志物、肌肉萎缩F盒蛋白以及肌肉环状指蛋白-1的表达。
结果显示，在肌肉萎缩条件下，TAS1R1在[具体动物模型1]和[具体动物模型2]中显著下调。此外，在人原代细胞模型中过表达TAS1R1可保护细胞免受肌肉萎缩，而使用小干扰RNA敲低TAS1R1会加剧肌肉萎缩。
综上所述，鲜味味觉受体通过恢复癌症恶病质中失调的肌肉萎缩，对肌肉萎缩状况发挥保护作用。总之，该结果提供了证据，表明鲜味味觉受体通过恢复肌肉萎缩发挥治疗癌症恶病质的作用。
