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Subcutaneous white adipose tissue independently regulates burn-induced hypermetabolism via immune-adipose crosstalk
Cell Reports ( IF 7.5 ) Pub Date : 2023-12-20 , DOI: 10.1016/j.celrep.2023.113584 Carly M Knuth 1 , Dalia Barayan 1 , Ju Hee Lee 2 , Christopher Auger 3 , Lauar de Brito Monteiro 4 , Zachary Ricciuti 5 , Dea Metko 5 , Lisa Wells 5 , Hoon-Ki Sung 2 , Robert A Screaton 6 , Marc G Jeschke 7
Cell Reports ( IF 7.5 ) Pub Date : 2023-12-20 , DOI: 10.1016/j.celrep.2023.113584 Carly M Knuth 1 , Dalia Barayan 1 , Ju Hee Lee 2 , Christopher Auger 3 , Lauar de Brito Monteiro 4 , Zachary Ricciuti 5 , Dea Metko 5 , Lisa Wells 5 , Hoon-Ki Sung 2 , Robert A Screaton 6 , Marc G Jeschke 7
Affiliation
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Severe burns induce a chronic hypermetabolic state that persists well past wound closure, indicating that additional internal mechanisms must be involved. Adipose tissue is suggested to be a central regulator in perpetuating hypermetabolism, although this has not been directly tested. Here, we show that thermogenic adipose tissues are activated in parallel to increases in hypermetabolism independent of cold stress. Using an adipose tissue transplantation model, we discover that burn-derived subcutaneous white adipose tissue alone is sufficient to invoke a hypermetabolic response in a healthy recipient mouse. Concomitantly, transplantation of healthy adipose tissue alleviates metabolic dysfunction in a burn recipient. We further show that the nicotinic acetylcholine receptor signaling pathway may mediate an immune-adipose crosstalk to regulate adipose tissue remodeling post-injury. Targeting this pathway could lead to innovative therapeutic interventions to counteract hypermetabolic pathologies.
中文翻译：
皮下白色脂肪组织通过免疫脂肪串扰独立调节烧伤引起的代谢亢进
严重烧伤会诱发慢性高代谢状态，这种状态在伤口闭合后仍持续存在，表明必须涉及其他内部机制。脂肪组织被认为是维持高代谢的核心调节器，尽管这尚未经过直接测试。在这里，我们发现生热脂肪组织被激活的同时，代谢亢进的增加与冷应激无关。使用脂肪组织移植模型，我们发现仅烧伤来源的皮下白色脂肪组织就足以引起健康受体小鼠的高代谢反应。与此同时，健康脂肪组织的移植可以减轻烧伤患者的代谢功能障碍。我们进一步表明烟碱乙酰胆碱受体信号通路可能介导免疫脂肪串扰以调节损伤后脂肪组织重塑。针对这一途径可能会导致创新的治疗干预措施来对抗代谢亢进的病理学。
更新日期：2023-12-20
中文翻译：
皮下白色脂肪组织通过免疫脂肪串扰独立调节烧伤引起的代谢亢进
严重烧伤会诱发慢性高代谢状态，这种状态在伤口闭合后仍持续存在，表明必须涉及其他内部机制。脂肪组织被认为是维持高代谢的核心调节器，尽管这尚未经过直接测试。在这里，我们发现生热脂肪组织被激活的同时，代谢亢进的增加与冷应激无关。使用脂肪组织移植模型，我们发现仅烧伤来源的皮下白色脂肪组织就足以引起健康受体小鼠的高代谢反应。与此同时，健康脂肪组织的移植可以减轻烧伤患者的代谢功能障碍。我们进一步表明烟碱乙酰胆碱受体信号通路可能介导免疫脂肪串扰以调节损伤后脂肪组织重塑。针对这一途径可能会导致创新的治疗干预措施来对抗代谢亢进的病理学。
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