Beyond enabling movement, muscle tissue acts as a critical endocrine organ that secretes various factors, known as myokines, therefore influencing systemic metabolic balance. in a recent study published in Life Metabolism, Dr. Zhuoxian Meng’s team at Zhejiang University School of Medicine uncovered a novel mechanism by which the chromatin remodeler Brg1/Brm-associated factor 60c (Baf60c) regulates fat tissue thermogenesis and overall energy metabolism through its control of the muscle-derived myokine, Musclin.

While previous studies have established the essential role of Baf60c in muscle differentiation and glucose metabolism, its potential role in controlling muscle-secreted factors and facilitating inter-organ metabolic communication remains unclear. The present study demonstrates for the first time that Baf60c negatively regulates Musclin gene expression at the chromatin level through interaction with the transcription factor myocyte enhancer factor 2c (Mef2c) (Figure 1).

Musclin is a myokine known to suppress thermogenesis in beige fat cells, thus reducing overall energy expenditure. Using muscle-specific Baf60c knockout and overexpression mouse models, the researchers demonstrated that loss of Baf60c in muscle increases Musclin production, which inhibits adipose tissue thermogenesis, elevates blood glucose levels, and raises the risk of obesity. In contrast, enhancing Baf60c expression suppresses Musclin, stimulates fat-burning in adipose tissue, and improves systemic glucose metabolism.

Taken together, this study not only deepens our understanding of the metabolic communication network between muscle and adipose tissue but also identifies a potential therapeutic target for obesity and metabolic disorders. For further details, access the original study at:
DOI:10.1093/lifemeta/loaf015.