Adipocytes increase energy expenditure in response to prolonged sympathetic activation via persistent expression of uncoupling protein 1 (UCP1)^1,2. Here we report that the regulation of glycogen metabolism by catecholamines is critical for UCP1 expression. Chronic β-adrenergic activation leads to increased glycogen accumulation in adipocytes expressing UCP1. Adipocyte-specific deletion of a scaffolding protein, protein targeting to glycogen (PTG), reduces glycogen levels in beige adipocytes, attenuating UCP1 expression and responsiveness to cold or β-adrenergic receptor-stimulated weight loss in obese mice. Unexpectedly, we observed that glycogen synthesis and degradation are increased in response to catecholamines, and that glycogen turnover is required to produce reactive oxygen species leading to the activation of p38 MAPK, which drives UCP1 expression. Thus, glycogen has a key regulatory role in adipocytes, linking glucose metabolism to thermogenesis.

^{脂肪细胞通过持续表达解偶联蛋白 1 (UCP1) 1,2}来响应延长的交感神经激活，从而增加能量消耗. 在这里，我们报告儿茶酚胺对糖原代谢的调节对于 UCP1 表达至关重要。慢性 β-肾上腺素能激活导致表达 UCP1 的脂肪细胞中糖原积累增加。脂肪细胞特异性缺失支架蛋白，糖原靶向蛋白 (PTG)，降低米色脂肪细胞中的糖原水平，减弱肥胖小鼠的 UCP1 表达和对寒冷或 β-肾上腺素能受体刺激的体重减轻的反应。出乎意料的是，我们观察到糖原合成和降解随着儿茶酚胺的增加而增加，并且需要糖原周转来产生活性氧，从而激活 p38 MAPK，从而驱动 UCP1 表达。因此，糖原在脂肪细胞中具有关键的调节作用，将葡萄糖代谢与产热联系起来。