Hypoxia tolerance in fish depends on catabolic preference between lipids and carbohydrates
Qiang Ma, 华东师范大学生命科学学院水生动物营养与环境健康实验室, 上海 200241, 中国, Yuan Luo, Jia Zhong, Samwel Mchele Limbu, Lingyu Li, Liqiao Chen, Fang Qiao, Mei‐Ling Zhang, Qiang Lin, Zhen‐Yu Du, 中国水产科学研究院黄海水产研究所, 山东 青岛 266071, 中国, 中国科学院南海海洋研究所中国科学院热带海洋生物资源与生态重点实验室, 广东 广州 510301, 中国, 达累斯萨拉姆大学水产科学与渔业技术学院, 达累斯萨拉姆 60091, 坦桑尼亚
Abstract
Hypoxia is a common environmental stress factor in aquatic organisms, which varies among fish species. However, the mechanisms underlying the ability of fish species to tolerate hypoxia are not well known. Here, we showed that hypoxia response in different fish species was affected by lipid catabolism and preference for lipid or carbohydrate energy sources. Activation of biochemical lipid catabolism through peroxisome proliferator-activated receptor alpha (Pparα) or increasing mitochondrial fat oxidation in tilapia decreased tolerance to acute hypoxia by increasing oxygen consumption and oxidative damage and reducing carbohydrate catabolism as an energy source. Conversely, lipid catabolism inhibition by suppressing entry of lipids into mitochondria in tilapia or individually knocking out three key genes of lipid catabolism in zebrafish increased tolerance to acute hypoxia by decreasing oxygen consumption and oxidative damage and promoting carbohydrate catabolism. However, anaerobic glycolysis suppression eliminated lipid catabolism inhibition-promoted hypoxia tolerance in adipose triglyceride lipase (<i>atgl</i>) mutant zebrafish. Using 14 fish species with different trophic levels and taxonomic status, the fish preferentially using lipids for energy were more intolerant to acute hypoxia than those preferentially using carbohydrates. Our study shows that hypoxia tolerance in fish depends on catabolic preference for lipids or carbohydrates, which can be modified by regulating lipid catabolism.