Juvenile coho salmon, Oncorhynchus kisutch, were either immersed in thyroxin-containing water (T4; 20 μg/ml) or implanted with cortisol (5 mg), bovine growth hormone (GH; 1.5 μg/g body wt), or ovine prolactin (PRL; 1.5 μg/g body wt), both early and late in smoltification. T4 and cortisol treatment stimulated lipid mobilization in parr. T4-stimulated lipid mobilization was indicated by decreased total lipids, primarily as triacylglycerols, and increased lipolytic enzyme (triacylglycerol lipase) activity in the liver and dark muscle. T4-stimulated lipid mobilization from mesenteric fat was indicated by decreased total tissue mass and by increased lipase activity. Cortisol caused significant reductions in total lipid concentration and triacylglycerol content of the liver and dark muscle; these effects were accompanied by increased lipase activity. Cortisol treatment did not affect mesenteric fat total lipid concentration, total tissue mass, or triacylglycerol content. However, cortisol implantation did enhance mesenteric fat lipase activity. Thyroxin and cortisol treatment failed to elicit alterations in the pattern of tissue lipid mobilization of smolts. GH stimulated lipid mobilization from coho salmon parr. Depletion of liver total lipids was accompanied by increased lipolytic enzyme (triacylglycerol lipase) activity. GH had limited effects on dark muscle and mesenteric fat. In smolts, GH had virtually no effect on lipid mobilization. PRL strongly stimulated lipid mobilization in parr; this effect was evident in all depots studied (liver, dark muscle, mesenteric fat). Decreases in total lipid concentration, or in total tissue mass (mesenteric fat), were accompanied by increased lipase activity and generally resulted in reduced tissue triacylglycerol content. Smolts appeared refractory to PRL treatment. Smolts (characteristically possessing elevated liver lipase activity) that were hypophysectomized exhibited low levels of liver lipase activity. Cortisol replacement restored enzyme activity to approximately the same levels as those observed in sham-operated controls. GH replacement restored lipase activity, but not to the levels observed in sham-operated controls. These results indicate that T4, cortisol, GH, and PRL all stimulate lipid mobilization in developing salmon by enhancement of lipolysis and suggest that T4, cortisol, GH, and PRL are among the factors which contribute to smoltification-associated lipid depletion.