Fatty acid β-oxidation in fish: a review

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.