Effects of Partially DefattedHermetia illucensMeal in Rainbow Trout Diet on Hepatic Methionine Metabolism

Simple Summary For sustainable aquaculture development, fish meal from the sea in aquafeed should be replaced with other sustainable materials such as insect larvae. The authors fed black soldier fly maggot meal to rainbow trout and examined the expression of three genes and two metabolites involved in turn-over of methionine that is an essential amino acid in fish. According to the increase in the maggot content in the aquafeed, gene expression was modulated to maintain an optimal level of methionine metabolites. Dietary replacement of up to 50% of fish meal with the maggot meal was acceptable, implying future development of a new aquafeed for sustainable aquaculture. This study investigated, for the first time, the effects of replacement of fishmeal (FM) with insect meal fromHermetia illucens(HI) on the transcript levels of three genes involved in methionine (Met) metabolism in rainbow trout (Oncorhynchus mykiss) liver. Two target genes-betaine-homocysteine S-methyltransferase (BHMT) and S-adenosylhomocysteine hydrolase (SAHH)-are involved in Met resynthesis and the third one-cystathionine beta synthase (CBS)-is involved in net Met loss (taurine synthesis). We also investigated the levels of two Met metabolites involved in the maintenance of methyl groups and homocysteine homeostasis in the hepatic tissue: S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH). Three diets were formulated, an FM-based diet (HI0) and two diets in which 25% (HI25) and 50% (HI50) of FM was replaced with HI larvae meal. A 78-day feeding trial involved 360 rainbow trout with 178.9 +/- 9.81 g initial average weight. Dietary replacement of up to 50% of FM with HI larvae meal, without any Met supplementation, did not negatively affect rainbow trout growth parameters and hepatic Met metabolism. In particular, Met availability from the insect-based diets directly modulated the transcript levels of two out of three target genes (CBS,SAHH) to maintain an optimal level of one-carbon metabolic substrates, i.e., the SAM:SAH ratio in the hepatic tissue.