No abstract

In a comparison of livers in fish (Sparus auratus and Dicentrarchus labrax) feeding on natural sources of food with livers of artificially fed animals, a much higher C18:1/C22:6 ratio was observed in the latter. Staining livers with oil red O showed extensive steatosis in artificially fed fish, but not in those naturally fed. Juvenile artificially fed fish showed a more extensive steatosis and a higher mortality rate. In steatotic fish fed a natural diet for 2 months, the liver exhibited extensive regeneration and only a few steatotic areas remained. Marine teleosts do not appear to have a proliferative response of peroxisomes and this is likely to contribute to liver lipid accumulation and subsequent steatosis. It is suggested that an excess of C18:1 (or other mono‐unsaturated fatty acids), coupled with a lack of adaptive peroxisomal proliferation, is the primary cause of lipid droplet formation leading to hepatic steatosis.