Mus musculus Transcriptome or Gene expression

We report that the regulation of glycogen metabolism by catecholamines is critical for Ucp1 expression. Chronic beta-adrenergic activation of adipocytes leads to increased expression of glycogen metabolism genes and glycogen accumulation in cells expressing Ucp1. Adipocyte-specific deletion of the glycogen scaffolding protein targeting to glycogen (PTG) reduces glycogen levels in beige adipocytes, producing a concomitant reduction in Ucp1 expression, and reduced responsiveness to cold or beta-adrenergic-stimulated weight loss in obese animals. Surprisingly, glycogen synthesis and degradation are increased in response to catecholamines, and glycogen turnover is required to produce reactive oxygen species leading to the activation of p38 MAPK, which drives Ucp1 expression. Thus, glycogen plays a key regulatory role in adipocytes, linking glucose metabolism to thermogenesis.