脂肪酸β-氧化是动物脂肪酸分解代谢的主要途径，在动物生理活动的能量供应和代谢内稳态的维持方面具有举足轻重的作用。在哺乳动物中，关于脂肪酸β-氧化的研究已有大量报道，但是在鱼类中，脂肪酸β-氧化研究相对较少。随着水产养殖业对提高饲料脂肪分解供能和降低鱼体脂肪的要求日益迫切，鱼类脂肪酸β-氧化反应及其组成和调控体系越来越受到学界和产业界的关注。为此，本文从鱼类脂肪酸β-氧化体系组成和关键酶系、β-氧化的组织和底物特异性、β-氧化体系调控因子以及鱼类脂肪酸β-氧化的影响因素等几个方面全面综述了鱼类脂肪酸β-氧化的研究进展，并比较了鱼类脂肪酸β-氧化反应及其组成和调控体系在鱼类与哺乳动物之间，乃至不同鱼种之间的异同，以期为人们更深入地理解鱼类脂代谢与调控体系并开展相关应用研究提供有价值的参考资料。

Beta-oxidation is a main pathway of fatty acid catabolism. Although this pathway has been studied for almost half a century in mammals, lots of metabolic details and the related regulatory mechanisms are still unknown in fish. With the rapid development of aquaculture industry, more and more attention is being paid to fish fatty acid β-oxidation, not only because it could help to promote dietary lipid utilization as an alternative energy source for protein, but also it could help to alleviate the severe fat accumulation in farmed fish. In this review paper, we systemically review the research progress of fatty acid β-oxidation in fish. As in mammals, fish fatty acid β-oxidation occurs in mitochondria and peroxisome. In most of fishes, mitochondrial β-oxidation is the main contributor of total fatty acid β-oxidation. Nevertheless, the activity of fatty acid β-oxidation differs from different fish tissues, and in general, the activity of peroxisomal fatty acid β-oxidation in liver is much higher than that in other tissues. Moreover, mitochondrial and peroxisomal β-oxidation has different substrate preference. Peroxisome prefers to oxidize the fatty acids containing more than 18 carbons, while mitochondria prefer to oxidize the fatty acids containing no more than 18 carbons. In fish fatty acid β-oxidation, carnitine palmitoyl transferase (CPT-1) is the speed-limited enzyme and plays key roles in transferring fatty acid from cellular matrix into mitochondria. Fish fatty acid β-oxidation could be regulated by hormone, nuclear receptors (for example peroxisome proliferator-activated receptor, PPAR) and microRNA, and so on. Recently, the mechanisms of PPARα activation and related metabolic regulation have been revealed in Nile tilapia. The activated PPARα could stimulate proliferation of mitochondria and activity of mitochondrial fatty acid β-oxidation, and cause decrease of liver lipid content. In fish, fatty acid β-oxidation is also affected by physiological factors (such as age and body weight), nutritional status (fed and fasting), dietary factors (dietary lipid sources and levers, and some dietary additives, such as L-carnitine) and some environmental pollutants. Among them, dietary lipid content and sources could significantly affect efficiency of fatty acid β-oxidation. In fact, the impaired fatty acid β-oxidation is an important cause or consequence of high energy diet-induced metabolic diseases in fish. Recently, more and more dietary additives, which target on fatty acid β-oxidation, have been widely used. Among these dietary additives, L-carnitine has been intensively studied and the related studies show that L-carnitine could improve fatty acid β-oxidation through increasing transferring efficiency of fatty acids as substrate from cellular matrix into mitochondria for further fatty acid β-oxidation. Moreover, some vitamins, such as V_C and V_D have also been demonstrated to play positive roles through regulating fatty acid β-oxidation-related enzymes or genes. All in all, fatty acid β-oxidation is essential in fish metabolism and energy homeostasis, and more studies are necessary in future fish nutrition studies.

国家重点研发计划（2018YFD0900400）；国家自然科学基金（31830102）