Murray Andrew J, Montgomery Hugh E
Department of Physiology, Development & Neuroscience, University of Cambridge, Cambridge, UK.
Bioessays. 2014 Aug;36(8):721-9. doi: 10.1002/bies.201400042. Epub 2014 Jun 11.
At extreme altitude (>5,000 - 5,500 m), sustained hypoxia threatens human function and survival, and is associated with marked involuntary weight loss (cachexia). This seems to be a coordinated response: appetite and protein synthesis are suppressed, and muscle catabolism promoted. We hypothesise that, rather than simply being pathophysiological dysregulation, this cachexia is protective. Ketone bodies, synthesised during relative starvation, protect tissues such as the brain from reduced oxygen availability by mechanisms including the reduced generation of reactive oxygen species, improved mitochondrial efficiency and activation of the ATP-sensitive potassium (KATP ) channel. Amino acids released from skeletal muscle also protect cells from hypoxia, and may interact synergistically with ketones to offer added protection. We thus propose that weight loss in hypoxia is an adaptive response: the amino acids and ketone bodies made available act not only as metabolic substrates, but as metabolic modulators, protecting cells from the hypoxic challenge.
在极高海拔地区(>5000 - 5500米),持续性缺氧会威胁人体机能和生存,并与显著的非自愿体重减轻(恶病质)相关。这似乎是一种协调反应:食欲和蛋白质合成受到抑制,肌肉分解代谢增强。我们推测,这种恶病质并非简单的病理生理失调,而是具有保护作用。在相对饥饿期间合成的酮体,通过包括减少活性氧生成、提高线粒体效率和激活三磷酸腺苷敏感性钾(KATP)通道等机制,保护大脑等组织免受氧供应减少的影响。骨骼肌释放的氨基酸也能保护细胞免受缺氧影响,并且可能与酮体协同作用,提供额外保护。因此,我们提出缺氧导致的体重减轻是一种适应性反应:产生的氨基酸和酮体不仅作为代谢底物,还作为代谢调节剂,保护细胞免受缺氧挑战。