棕色脂肪组织 (BAT) 的基线量和刺激白色脂肪组织 (WAT) 褐变的能力都可以为重症监护环境中的患者提供保护作用。危重疾病与线粒体体积和功能减少有关，导致活性氧产生增加、对三磷酸腺苷的需求增加、脂肪代谢转变为解偶联以及导致多器官衰竭的细胞器冬眠。增加胰岛素抵抗、减少脂肪酸氧化以及对碳水化合物代谢的依赖。 WAT 的褐变可以对抗许多这些不利影响。 BAT 的存在以及与褐变相关的变化可能有助于消除氧化应激，增加代谢物的消耗和利用，并减少促炎作用。线粒体数量增加，巨噬细胞更多地浸润到脂肪组织中。巨噬细胞表达从 M1 表型转变为 M2 表型，这种作用进一步抑制炎症，增加胰岛素敏感性，并改善组织愈合和重塑。在慢性代谢亢进的疾病状态（例如烧伤或癌症恶病质）中，这些反应的任何益处可能会丧失，其中这些生理效应的持续存在可能会变得有害，导致体重过度减轻、脂肪消耗和去脂体重损失。本文讨论了脂肪组织的可塑性以及其生理学的变化是否为重症监护病房提供临床优势。本文受版权保护。保留所有权利。本文受版权保护。版权所有。

Both the baseline amount of brown adipose tissue (BAT) and the capacity to stimulate browning of white adipose tissue (WAT) may provide a protective effect to the patient in a critical care setting. Critical illness is associated with reduced mitochondrial volume and function resulting in increased production of reactive oxygen species, greater demand for adenosine triphosphate, a switch to uncoupled fat metabolism, and hibernation of the organelle which contribute to multiple organ failure. Increasing insulin resistance, decreasing fatty acid oxidation, and dependence on carbohydrate metabolism results. Browning of WAT may oppose many of these adverse effects. The presence of BAT and the changes associated with browning may help dissipate oxidative stress, increase consumption and utilization of metabolites, and reduce pro-inflammatory actions. The number of mitochondria increases and there is greater infiltration of macrophages into adipose tissue. A shift occurs in macrophage expression from the M1 to M2 phenotype, an effect which further dampens inflammation, increases insulin sensitivity, and improves tissue healing and remodeling. Any benefit from these responses may be lost in disease states of chronic hypermetabolism (such as burns or cancer cachexia) where the persistence of these physiologic effects may become detrimental contributing to excessive weight loss, adipose wasting, and loss of lean body mass. This paper discusses the plasticity of adipose tissue and whether shifts in its physiology provide clinical advantages in the intensive care unit. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.