美国宾夕法尼亚大学Zoltan Arany研究团队取得一项新突破。他们的研究开发出了小鼠急性运动时营养通量的定量分析。相关论文于2024年10月15日发表在《细胞—代谢》杂志上。

课题组使用体内稳态同位素标记输注法，来定量空腹、进食和疲惫状态下的雌性小鼠在运动过程中燃料流动和氧化，取得了若干新发现。运动显著促进了来自肝糖原、乳酸和甘油的葡萄糖流动，这一过程与人类不同。尽管伴随低血糖，几个器官在疲惫的小鼠中对葡萄糖的节省过程却遭到了破坏。蛋白质水解显著增加，也与人类不同。

脂肪酸氧化在禁食运动中占主导地位。酮的产生和氧化迅速上升，似乎是由糖异生诱导的突变应激引起的肝脏瓶颈所驱动的。在不直接参与肌肉收缩的器官中，包括胰腺和褐色脂肪，可以观察到燃料消耗的改变。

在运动过程中，尽管会消耗能量，但几个徒劳的循环却出人意料地持续存在。总之，该研究团队提供了一个全面、综合、整体和定量的代谢分析，揭示了在完整生物体内运动期间的代谢过程。

附：英文原文

Title: Quantification of nutrient fluxes during acute exercise in mice

Author: Jessie Axsom, Tara TeSlaa, Won Dong Lee, Qingwei Chu, Alexis Cowan, Marc R. Bornstein, Michael D. Neinast, Caroline R. Bartman, Megan C. Blair, Kristina Li, Chelsea Thorsheim, Joshua D. Rabinowitz, Zoltan Arany

Issue&Volume: 2024-10-15

Abstract: Despite the known metabolic benefits of exercise, an integrated metabolic understanding of exercise is lacking. Here, we use in vivo steady-state isotope-labeled infusions to quantify fuel flux and oxidation during exercise in fasted, fed, and exhausted female mice, revealing several novel findings. Exercise strongly promoted glucose fluxes from liver glycogen, lactate, and glycerol, distinct from humans. Several organs spared glucose, a process that broke down in exhausted mice despite concomitant hypoglycemia. Proteolysis increased markedly, also divergent from humans. Fatty acid oxidation dominated during fasted exercise. Ketone production and oxidation rose rapidly, seemingly driven by a hepatic bottleneck caused by gluconeogenesis-induced cataplerotic stress. Altered fuel consumption was observed in organs not directly involved in muscle contraction, including the pancreas and brown fat. Several futile cycles surprisingly persisted during exercise, despite their energy cost. In sum, we provide a comprehensive, integrated, holistic, and quantitative accounting of metabolism during exercise in an intact organism.

DOI: 10.1016/j.cmet.2024.09.010

Source: https://www.cell.com/cell-metabolism/abstract/S1550-4131(24)00374-7