J Nutr Health.  2024 Oct;57(5):469-480. 10.4163/jnh.2024.57.5.469.

Chrysin attenuates diabetic sarcopenia by regulating myogenic transcription factors and reducing muscle degradation in high glucose-exposed C2C12 cells and a type 2 diabetes animal model

• Kim DY
• Kang MK

• KMID: 2561292
• DOI: http://doi.org/10.4163/jnh.2024.57.5.469

Abstract

Purpose
Sarcopenia is defined as the age-related loss of muscle mass and strength. Although the etiology, pathogenesis, and diagnosis of sarcopenia are not completely understood, diabetes has been implicated in the development of frailty and functional impairment associated with sarcopenia. This study examined the relationship between diabetes and sarcopenia and explored the efficacy of chrysin, a natural flavonoid found in honey and propolis, as a preventive agent for diabetic sarcopenia.
Methods
A mouse myoblast cell line (C2C12) was incubated in media containing 5.5 mM glucose or 33 mM glucose (high glucose) with or without 20 μM chrysin for up to seven days. In addition, a type 2 diabetic animal model, db/db mice, was administered chrysin (10 mg/ kg/day) orally for 10 weeks. The protein levels were quantified using western blot analysis with antibodies targeting specific myogenic transcription factors, such as MyoD, myogenin, and Myf5, as well as proteins associated with muscle protein degradation, including Murf1, Atrogin1, and myostatin.
Results
Hyperglycemia downregulated the expression of myogenic transcription factors (MyoD, myogenin, and Myf5) and proteins that regulate muscle degradation (Murf1 and Atrogin1) in C2C12 cells treated with high glucose and db/db mice. The chrysin treatment counteracted these effects, promoting the expression of these factors. These results suggest that chrysin can regulate muscle protein turnover and prevent muscle atrophy in diabetic sarcopenia.
Conclusion
Chrysin has potential as a bioactive ingredient in preventing diabetic sarcopenia.

Keyword

sarcopenia; diabetes; chrysin; muscle atrophy