Umami taste receptor suppresses cancer cachexia by regulating skeletal muscle atrophy in vivo and in vitro
- Author:
Sumin LEE
1
;
Yoonha CHOI
;
Yerin KIM
;
Yeon Kyung CHA
;
Tai Hyun PARK
;
Yuri KIM
Author Information
- Publication Type:Original Research
- From:Nutrition Research and Practice 2024;18(4):451-463
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 in vivo and in vitro models.MATERIALS/METHODS: The Lewis lung carcinoma-induced cancer cachexia model was used in vivo and in vitro, 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:Results showed that TAS1R1 was significantly downregulated in vivo and in vitro under the muscle wasting condition. Moreover, overexpression of TAS1R1 in vitro in the human primary cell model protected the cells from muscle atrophy, and knockdown of TAS1R1 using siRNA exacerbated muscle atrophy.
CONCLUSION: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.
