Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz-Center for Diabetes Research at the Heinrich Heine University, Medical Faculty, Düsseldorf, Auf'm Hennekamp 65, 40225 Duesseldorf, Germany.
German Center for Diabetes Research (DZD), Partner Düsseldorf, München-Neuherberg, 85764 München, Germany.
Int J Mol Sci. 2022 Apr 26;23(9):4759. doi: 10.3390/ijms23094759.
The discovery of functional brown adipose tissue (BAT) in adult humans and the possibility to recruit beige cells with high thermogenic potential within white adipose tissue (WAT) depots opened the field for new strategies to combat obesity and its associated comorbidities. Exercise training as well as cold exposure and dietary components are associated with the enhanced accumulation of metabolically-active beige adipocytes and BAT activation. Both activated beige and brown adipocytes increase their metabolic rate by utilizing lipids to generate heat via non-shivering thermogenesis, which is dependent on uncoupling protein 1 (UCP1) in the inner mitochondrial membrane. Non-shivering thermogenesis elevates energy expenditure and promotes a negative energy balance, which may ameliorate metabolic complications of obesity and Type 2 Diabetes Mellitus (T2DM) such as insulin resistance (IR) in skeletal muscle and adipose tissue. Despite the recent advances in pharmacological approaches to reduce obesity and IR by inducing non-shivering thermogenesis in BAT and WAT, the administered pharmacological compounds are often associated with unwanted side effects. Therefore, lifestyle interventions such as exercise, cold exposure, and/or specified dietary regimens present promising anchor points for future disease prevention and treatment of obesity and T2DM. The exact mechanisms where exercise, cold exposure, dietary interventions, and pharmacological treatments converge or rather diverge in their specific impact on BAT activation or WAT browning are difficult to determine. In the past, many reviews have demonstrated the mechanistic principles of exercise- and/or cold-induced BAT activation and WAT browning. In this review, we aim to summarize not only the current state of knowledge on the various mechanistic principles of diverse external stimuli on BAT activation and WAT browning, but also present their translational potential in future clinical applications.
棕色脂肪组织(BAT)在成人体内的功能发现,以及在白色脂肪组织(WAT)储存器中募集具有高产热潜能的米色细胞的可能性,为对抗肥胖及其相关合并症开辟了新的策略。运动训练以及寒冷暴露和饮食成分与代谢活跃的米色脂肪细胞和 BAT 激活的增强积累有关。激活的米色和棕色脂肪细胞通过利用脂质通过不颤抖产热来增加其代谢率,这依赖于线粒体内膜中的解偶联蛋白 1(UCP1)。不颤抖产热会增加能量消耗并促进负能平衡,这可能改善肥胖和 2 型糖尿病(T2DM)的代谢并发症,如骨骼肌和脂肪组织中的胰岛素抵抗(IR)。尽管最近在通过诱导 BAT 和 WAT 的不颤抖产热来减少肥胖和 IR 的药理学方法方面取得了进展,但所给予的药理学化合物通常与不良副作用相关。因此,生活方式干预,如运动、寒冷暴露和/或特定饮食方案,为肥胖和 T2DM 的未来疾病预防和治疗提供了有希望的锚点。运动、寒冷暴露、饮食干预和药理学治疗在其对 BAT 激活或 WAT 褐变的特定影响上汇聚或分歧的确切机制很难确定。在过去,许多综述已经证明了运动和/或寒冷诱导的 BAT 激活和 WAT 褐变的机制原则。在这篇综述中,我们不仅旨在总结关于各种外部刺激对 BAT 激活和 WAT 褐变的不同机制原则的最新知识状态,还展示它们在未来临床应用中的转化潜力。