Uncoupling protein-3 (UCP3) is a mitochondria-regulatory protein with potential energy- homeostatic functions. This study explores the role of UCP3 in the regulation of muscle- and energy metabolism. UCP3 is critical for tuning substrate utilization, favoring lipid oxidation, particularly in conditions of high-fat availability. While UCP3 is non-essential for lipid oxidation during energy excess, it proves vital during fasting, indicating an energy-homeostatic trait. Preliminary evidence indicates UCP3′ promotion of glucose uptake and oxidation, at least in conditions of high glucose/low fat availability. However, the dynamics of how fats and glucose differentially influence UCP3 remain undefined. UCP3 exhibits inducible proton transport and uncoupling activity, operating in a dual manner: with no/low activity and an in the presence of activators. Uncoupling may enhance thermogenesis in specific conditions and in the presence of activators such as fatty acids, thyroid hormones, and catecholamines. This energy-dissipative activity adapts to varying energy availability, balancing energy dissipation with fatty acid oxidation to optimize whole-body energy homeostasis: fasting triggers UCP3 upregulation, enhancing lipid utilization while suppressing uncoupling. Additionally, UCP3 upregulation induces glucose and lipid disposal from the bloodstream and decreases tri-/diglyceride storage in muscle. This process improves mitochondrial functionality and insulin signaling, leading to enhanced systemicgluco-metabolic balance and protection from metabolic conditions. Reviewed evidence suggests that UCP3 plays a crucial role in adapting the system to changing energy conditions. However, the precise role of UCP3 in regulating metabolism requires further elucidation.

中文翻译：

---

Muscle-UCP3 在能量代谢调节中的作用

解偶联蛋白 3 (UCP3) 是一种线粒体调节蛋白，具有潜在的能量稳态功能。本研究探讨了 UCP3 在肌肉和能量代谢调节中的作用。 UCP3 对于调节底物利用率、促进脂质氧化至关重要，特别是在高脂肪可用性的条件下。虽然 UCP3 在能量过剩期间对于脂质氧化不是必需的，但事实证明它在禁食期间至关重要，表明其具有能量稳态特征。初步证据表明 UCP3' 促进葡萄糖摄取和氧化，至少在高葡萄糖/低脂肪可用性的条件下是如此。然而，脂肪和葡萄糖如何差异影响 UCP3 的动态仍不清楚。 UCP3 表现出诱导质子传输和解偶联活性，以双重方式运行：无/低活性和在激活剂存在下。在特定条件下以及在存在脂肪酸、甲状腺激素和儿茶酚胺等激活剂的情况下，解偶联可能会增强生热作用。这种能量耗散活动适应不同的能量可用性，平衡能量耗散与脂肪酸氧化，以优化全身能量稳态：禁食触发 UCP3 上调，增强脂质利用率，同时抑制解偶联。此外，UCP3 上调会诱导血液中的葡萄糖和脂质排出，并减少肌肉中甘油三酯/甘油二酯的储存。这一过程改善了线粒体功能和胰岛素信号传导，从而增强了全身葡萄糖代谢平衡并免受代谢状况的影响。审查的证据表明 UCP3 在使系统适应不断变化的能源条件方面发挥着至关重要的作用。然而，UCP3在调节代谢中的确切作用需要进一步阐明。