Hypoxia-tolerant animals use metabolic suppression as an essential strategy to survive low oxygen. Ectotherms can alter membrane lipid composition in response to changes in environmental temperature, but it is currently unknown whether chronic hypoxia can also elicit membrane restructuring. The goal of this study was to investigate a possible physiological link between membrane remodelling and metabolic suppression in goldfish exposed to prolonged hypoxia (4 weeks at 10% air saturation). We have tested the hypothesis that chronic hypoxia would modulate membrane lipid composition in ways that are consistent with known mechanisms of ion pump inhibition. Because homeoviscous membrane restructuring could interfere with the response to hypoxia, measurements were made at 2 temperatures. Results show that hypoxic goldfish suppress metabolic rate by 74% (at 13 °C) and 63% (at 20 °C). This study is the first to reveal that cold-acclimated animals undergo extensive, tissue-specific restructuring of membrane lipids as they reach minimal metabolic rates. However, hypoxia does not affect membrane composition in fish acclimated to 20 °C. The strong membrane response of cold-acclimated fish involves increases in cholesterol abundance (in white muscle and gills) and in fatty acid saturation, mainly caused by a reduction in %22:6 (docosahexaenoic acid in gills and liver). Major ion pumps like Na⁺/K⁺-ATPase are known to be inhibited by cholesterol and activated by 22:6. Because ion pumping by membrane-bound ATPases accounts for a large fraction of basal cellular energy use, we propose that the membrane responses reported here could be a novel mechanism to promote metabolic suppression in cold-acclimated animals.

耐缺氧的动物​​利用代谢抑制作为低氧生存的基本策略。体温可以响应于环境温度的变化而改变膜脂质的组成，但是目前尚不清楚慢性低氧是否也会引起膜重构。这项研究的目的是研究长时间缺氧（在空气饱和度为10％的情况下4周）的金鱼的膜重塑与代谢抑制之间的可能生理联系。我们已经检验了以下假设：慢性缺氧会以与已知的离子泵抑制机制相一致的方式调节膜脂质的组成。由于体内粘性膜的重组可能会干扰对缺氧的反应，因此在2个温度下进行了测量。结果表明，低氧金鱼将代谢率抑制了74％（在13°C时）和63％（在20°C时）。这项研究首次揭示了冷适应的动物由于达到最小的代谢率而经历了广泛的，组织特异性的膜脂重组。但是，低氧不会影响适应20°C的鱼的膜成分。冷驯化鱼的强烈膜反应涉及胆固醇丰度（白肌肉和腮）和脂肪酸饱和度的增加，这主要是由％22：6（腮和肝脏中的二十二碳六烯酸）减少引起的。像Na这样的主要离子泵 缺氧不会影响适应20°C的鱼的膜成分。冷驯化鱼的强烈膜反应涉及胆固醇丰度（白肌肉和腮）和脂肪酸饱和度的增加，这主要是由％22：6（腮和肝脏中的二十二碳六烯酸）减少引起的。像Na这样的主要离子泵 缺氧不会影响适应20°C的鱼的膜成分。冷驯化鱼的强膜反应涉及胆固醇丰度（白肌肉和腮中）和脂肪酸饱和度的增加，这主要是由％22：6（腮和肝脏中的二十二碳六烯酸）减少引起的。像Na这样的主要离子泵已知⁺ / K ⁺ -ATPase被胆固醇抑制并被22：6激活。因为通过膜结合的ATPase进行的离子泵作用占基础细胞能量使用的很大一部分，所以我们认为这里报道的膜反应可能是促进冷驯化动物代谢抑制的新机制。