A feeding experiment was conducted to evaluate the supplemental effect of bile salts to a defatted soybean meal-based non-fish meal diet for rainbow trout Oncorhynchus mykiss. A fish meal-based diet (FM) and two non-fish meal diets with and without bovine bile salts (SC + B and SC, respectively) were fed to fish (13 g initial weight) for 10 weeks. Fish fed diet SC showed inferior growth and feed efficiency, while bile salt supplementation improved the parameters to the same levels as fish fed diet FM. Crude fat and starch digestibility of diet SC-fed fish decreased after the 10-week feeding trial compared to the data obtained with fish that had no experience of the diet. Total biliary bile salt content and intestinal maltase activity of fish fed diet SC were the lowest among treatments, while these parameters were improved by bile salt supplementation. Morphological changes occurred in the distal intestine and liver of the diet SC group, although the histological features of fish fed diet SC + B were similar to those of fish fed diet FM. These results suggest that bile salt supplementation to a soybean meal-based diet improves the nutrient utilization by normalizing digestive processes in rainbow trout.
Modified uridine containing taurine, 5-taurinomethyluridine (τm5U), is found at the anticodon first position of mitochondrial (mt-)transfer RNAs (tRNAs). Previously, we reported that τm5U is absent in mt-tRNAs with pathogenic mutations associated with mitochondrial diseases. However, biogenesis and physiological role of τm5U remained elusive. Here, we elucidated τm5U biogenesis by confirming that 5,10-methylene-tetrahydrofolate and taurine are metabolic substrates for τm5U formation catalyzed by MTO1 and GTPBP3. GTPBP3-knockout cells exhibited respiratory defects and reduced mitochondrial translation. Very little τm5U34 was detected in patient’s cells with the GTPBP3 mutation, demonstrating that lack of τm5U results in pathological consequences. Taurine starvation resulted in downregulation of τm5U frequency in cultured cells and animal tissues (cat liver and flatfish). Strikingly, 5-carboxymethylaminomethyluridine (cmnm5U), in which the taurine moiety of τm5U is replaced with glycine, was detected in mt-tRNAs from taurine-depleted cells. These results indicate that tRNA modifications are dynamically regulated via sensing of intracellular metabolites under physiological condition.
To elucidate the hemolytic suppression roles of taurine and the necessity of dietary taurine supplementation in yellowtail Seriola quinqueradiata fed a diet without fishmeal, juvenile fish with an initial body weight of 250 g were fed for 40 weeks in floating net cages on soybean protein diets supplemented with 0, 3.0, 4.5 and 6.0% taurine. Taurine concentration of the experimental diets were 0.03, 33.9, 52.8 and 71.6 mg/g, respectively. On the 21st week, fish fed the taurine unsupplemented diet had inferior growth and feed performances, higher death, and there were incidences of green liver and hemolytic anemia. In this group, hepatic and plasma taurine concentrations, serum osmolality and osmotic tolerance of erythrocytes (EC50 value) were significantly lower, and plasma hydroperoxide concentration was markedly higher than in the taurine supplemented groups. These conditions markedly improved corresponding with the increase of dietary taurine concentration. These results indicate that taurine plays a role in hemolytic suppression through osmoregulation and biomembrane stabilization in fish. In addition, it is suggested that yellowtail requires dietary taurine as an essential nutrition for maintaining physiological condition normally.
This study was performed to evaluate the efficacy of taurine supplementation for preventing green liver syndrome and improving growth performance in red sea bream Pagrus major fed a low-fishmeal (FM) diet. Yearling red sea bream were fed for 34 weeks on low-FM diets either supplemented with taurine, or without taurine, and the tissue taurine and bile pigment concentrations were measured. Compared to the fish fed the FM diet, fish fed the low-FM diet without taurine supplementation resulted in inferior feed performances and higher incidence of green liver related to the morphological transformation of the erythrocytes. In these fish, the hepatopancreatic taurine concentration was significantly lower and hepatopancreatic biliverdin concentration was high compared to the fish fed the FM diet. These parameters were markedly improved by taurine supplementation of the low-FM diet and were similar in levels to the fish fed the FM diet. These results indicate that green liver appearance and inferior feed performances of red sea bream fed the low-FM diet without taurine supplementation were caused by dietary taurine deficiency, and indicate the requirement of taurine supplementation to low-FM diets for red sea bream.KEY WORDS: alternative protein, bile pigment, green liver syndrome, low-fishmeal diet, red sea bream, taurine.
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