Although the expression of apolipoprotein genes in the developing embryo and larva has been thoroughly characterized, the lipoprotein profile at these stages is less well defined. Most work on fish lipoproteins has focused on adults, likely due to the difficulty of obtaining adequate blood samples from larvae (19). Secretion of very low-density lipoprotein (VLDL) particles from the yolk has been demonstrated by electron microscopy (20, 21). The YSL also expresses apoA-I and apoA-II, which are found in HDL (high-density lipoprotein) particles and chylomicrons but not LDL (low-density lipoprotein) or VLDL (13, 14). ApoB, which is a component of chylomicrons, LDL, and VLDL, has a vital role in the export of yolk lipids. Microsomal triglyceride (TG) transfer protein (MTP) packages TGs into ApoB-containing lipoproteins. ApoB is degraded if it is not associated with lipid so, in the absence of MTP function, ApoB is not functional (22). In mtp−/− mutant zebrafish larvae, lipids are trapped in the yolk (characterized by retention of yolk volume, an increase in yolk opacity, and a reduction in neutral lipid in the body) and larvae do not survive beyond 5 days (23). Additionally, unlike their wild-type siblings, mtp−/− embryos retain fluorescent fatty acid injected into the yolk and do not export it or its fluorescent products to the circulation (18). The ability of mtp−/− larvae to grow and survive to 5 dpf suggests that some lipid must be transported out of the yolk in order for membranes to be synthesized, possibly through the synthesis of HDL-like particles that contain ApoA-I and do not require MTP for their assembly.