Boosting brown adipose tissue (BAT) development is of great interest because of its therapeutic potential for obesity and its related metabolic disorders. A new study identifies a key miRNA switch that controls the development of adult skeletal muscle precursor cells called satellite cells into brown fat (Cell Metab. 17, 210–224 ).

Although brown adipocytes were known to originate from myogenic progenitor cells, satellite cells were thought to be committed toward muscle development. Hang Yin et al. now show that satellite cells from mice are multipotent and can differentiate into brown adipocytes or myogenic cells. The authors then identified miR-133 as a key determinant of the differentiation pathway adopted by satellite cells. They found that this miRNA targets and inhibits Prdm16, a transcription factor responsible for activating brown fat genes and repressing white adipose tissue– and muscle-specific transcriptional programs.

Using antisense oligonucleotides, the authors targeted miR-133 in activated satellite cells in vivo and showed that this stimulated the development of metabolically active brown adipocytes during muscle regeneration. In mice on a high-fat diet, similar treatment with anti–miR-133 oligonucleotides after muscle injury resulted in reduced weight gain and an improvement in metabolic symptoms. Although it remains to be determined whether miR-133 has targets other than BAT development in muscle, these results suggest that targeting this miRNA in satellite cells might hold therapeutic promise for reducing obesity.