(P03-038-23) Umbelliferone Mitigates Muscle Protein Degradation and Regulates Expression Myogenic Transcription Factors in High Glucose-Exposed Myoblast and Diabetic Sarcopenia

Objectives: Sarcopenia is defined as the loss of muscle mass and strength that occurs with aging. Although the etiology, pathogenesis, and diagnosis of sarcopenia are obscure, diabetes has been reported to play a role in the pathogenesis of frailty and functional impairment in sarcopenia. This study attempted to investigate the relationship between diabetes and sarcopenia and to explore the efficacy of umbelliferone, a natural product of the coumarin family with diverse bioactive properties found in carrot and coriander, as a preventive agent for diabetic sarcopenia.

Methods: In this study, a mouse myoblast cell line (C2C12) was incubated in media containing 5.5 mM glucose and 33 mM glucose (high glucose) in the absence and presence of 1-20 μM umbiliferone for up to 7 days. The level of proteins was quantified using western blot analysis, which involved the use of antibodies of specific myogenic transcription factors such as MyoD, myogenin, and Myf-5, as well as proteins associated with muscle protein degradation, including MuRF1, Atrogin-1 and Myostatin.

Results: Hyperglycemia downregulated the induction of myogenic transcription factors including MyoD, miogenin, and Myf-5, as well as the expression of MuRF1, Atrogin-1, and Myostatin, which are known to inhibit muscle protein degradation in C2C12 cells treated with 33mM high glucose. This study confirmed the ability of Umbiliferone to amplify their expressions. These results showed that Umbelliferone was able to modulate muscle protein turnover and prevent muscle atrophy in the C2C12 cell line.

Conclusions: These findings suggest the potential use of umbiliferone as a physiologically active ingredient in suppressing diabetic sarcopenia.

Funding Sources: This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea government (2021R1 I1A0104231612 and 2017R1A6A3A04011473).