Effects of defatted yellow mealworm (Tenebrio molitor) on growth performance, intestine, and liver health of turbot (Scophthalmus maximus)

Abstract

Yellow mealworm Tenebrio molitor is an emerging feed ingredient with several key advantages. However, research on the T. molitor as a fishmeal substitute reported discrepancies in feasibility in different fish species, with a particular need for T. molitor products to be widely evaluated. In this research, an eight-week feeding trial was conducted to evaluate the effect of T. molitor on turbot Scophthalmus maximus mainly from the perspective of growth performance and health status of the intestine and liver. Turbot with an initial weight of approximately 150 g were randomly assigned six isonitrogenous and isolipidic diets, including fishmeal-based control diet or diets with gradually increasing level of defatted T. molitor meal (TM) to replace 15 % (TM15), 30 %, 45 %, 60 % and 75 % of fishmeal compared to the control diet. Weight gain of turbot increased significantly at the 30 % replacement level (P < 0.05). However, TM in 45 %, 60 % and 75 % of fishmeal replacement level impaired overall growth performance. There was no obvious impairment in the assayed levels of TM towards the intestine from the view of structure, activities of brush border enzymes, antioxidant conditions, or immunity of proximal, middle and distal segments. However, the amount of goblet cells was significantly decreased by TM (P < 0.05). Similarly, TM in the assayed levels did not induce any negative effects on the antioxidant and immune status of the liver. But TM45, TM60 and TM75 diets induced weight loss in the liver and smaller hepatocytes, accompanied by a decrease of liver lipid content as well as decreases in levels of triglyceride and cholesterol in plasma. In conclusion, the optimal dietary level of TM for turbot was 24.5 %, corresponding to a 30 % substitution of fishmeal from the control group. Dietary TM can improve the antioxidant and immune function of the intestine and liver, but excess TM will disturb lipid metabolisms.