Saturated lipids are more effective than others in juvenile California yellowtail feeds—Understanding and harnessing LC-PUFA sparing for fish oil replacement

Diet-to-tissue transfer of long-chain polyunsaturated fatty acids (LC-PUFAs) is more efficient when diets contain saturated fatty acid (SFA) or monounsaturated fatty acid (MUFA)-rich alternative lipids. This mechanism, the omega-3 or LC-PUFA “sparing effect”, encourages more efficient metabolism of the limited LC-PUFAs available in terms of their important physiological functions and tissue retention, and the likelihood of successful fish oil sparing (i.e. complete fish oil replacement maintaining growth and tissue fatty acid profile). However, it is still unclear whether dietary SFAs and MUFAs are equivalent or interact synergistically or antagonistically in this context. Accordingly, we compared production performance and tissue fatty acid composition of California Yellowtail fed diets containing fish oil (rich in LC-PUFAs) or soybean oil (rich in C18 PUFAs), partially hydrogenated soybean oil (rich in MUFAs), fully hydrogenated soybean oil (rich in SFAs), or blends of these soybean oils. After 10 weeks, production performance was not affected by dietary lipid source or fatty acid composition, and tissue fatty acid profiles generally mimicked dietary fatty acid composition. However, tissues of fish fed SFA-rich lipids exhibited the greatest similarity to those fed fish oil, and fillets of fish fed fully hydrogenated soybean oil had significantly higher levels of LC-PUFAs (43.9 g LC-PUFA /100 g fatty acid methyl esters; FAMEs) than those fed any of the other diets (22.5–36.9 g LC-PUFA /100 g FAMEs), including the LC-PUFA-rich fish oil-based feed (39.8 g LC-PUFA /100 g FAMEs). Power regression analyses demonstrated a stronger positive relationship between dietary SFAs with fillet LC-PUFA deposition (r2 = 0.73) than dietary MUFAs (r2 = 0.09), whereas dietary C18 PUFAs were observed to have a negative relationship with fillet LC-PUFA content (r2 = 0.85). These trends were also observed in liver and eye tissues, and to a lesser extent in brain tissue. Multiple linear regression analyses demonstrated a stronger relationship between dietary levels of PUFAs and SFAs and tissue fatty acid profile composition, including LC-PUFA content, than dietary levels of PUFAs and MUFAs. Fillet lipid content varied significantly, with the FISH and C18 PUFA SOY diets displaying the highest levels. The same pattern was observed for liver lipid content, but not significantly. Our findings suggest that SFAs are the primary drivers of LC-PUFA sparing, whereas MUFAs exert a weaker independent sparing effect and appear to diminish the sparing effect of dietary SFAs when MUFAs were also present.