Effects of Zinc Status on Expression of Zinc Transporters, Redox-Related Enzymes and Insulin-like Growth Factor in Asian Sea Bass Cells.

Since Asian sea bass is one of the economically most important fish, aquaculture conditions are constantly optimized. Evidence from feeding studies combined with the current understanding of the importance of zinc for growth and immune defense suggest that zinc supplementation may be a possible approach to optimize aquacultures of Asian sea bass. To investigate the effects of zinc deficiency and zinc supplementation, cells from Asian sea bass were incubated in culture medium with different zinc contents. The expression of genes, important for zinc homeostasis, redox metabolism, and growth hormones was analyzed using RT-PCR. Zinc deficiency induced the expression of certain zinc transporters (ZIP14, ZIP10, ZIP6, ZIP4, ZnT4, ZnT9) as well as of SOD1, IGF I and IGF II, while expression of ZnT1 and metallothionein (MT) was reduced. Zinc supplementation decreased the expression of ZIP10, while expression of ZnT1 and MT were elevated. No differences in the effects of zinc supplementation with zinc sulfate compared to supplementation with zinc amino acid complexes were observed. Thus, extracellular zinc conditions may govern the cellular zinc homeostasis, the redox metabolism and growth hormone expression in cells from Asian sea bass as reported for other fish species. Our data indicate that supplementing aquacultures with zinc may be recommended to avoid detriments of zinc deficiency.

Vitamin D3 deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy.

Vitamin D3 (VD3) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD3/VDR on intestinal inflammation, autophagy, and apoptosis of turbot in vivo and in vitro. Triple replicates of 30 fish were fed with each of three diets with graded levels of 32.0 (D0), 1012.6 (D1), and 3978.2 (D2) IU/kg VD3. Obvious intestinal enteritis was observed in the D0 group and followed with dysfunction of intestinal mucosal barriers. The intestinal inflammatory response induced by VD3 deficiency was regulated by the NF-κB/inflammasome signalling. The promotion of intestinal apoptosis and suppression of intestinal autophagy were also observed in the D0 group. Similarly, VD3 deficiency in vitro induced more intense inflammation regulated by NF-κB/inflammasome signalling. The mutually exclusive apoptosis and autophagy were also observed in the group without 1,25(OH)2D3 in vitro, accompanied by similar changes in apoptosis and autophagy increased apoptosis. The gene expression of VDRs was significantly increased with the increasing VD3 supplementation both in vivo and in vitro. Moreover, VDR knockdown in turbot resulted in intestinal inflammation, and this process relied on the activation of inflammasome mediated by NF-κB signalling. Simultaneously, intestinal apoptosis was promoted, whereas intestinal autophagy was inhibited. In conclusion, VD3 deficiency could induce intestinal inflammation via activation of the NF-κB/inflammasome pathway, intestinal apoptosis, and autophagy formed a mutually exclusive relation in teleost. And VDR is the critical molecule in those processes.

Effects of Chromium-L-Methionine in Combination with a Zinc Amino Acid Complex or Selenomethionine on Growth Performance, Intestinal Morphology, and Antioxidative Enzymes in Red Tilapia Oreochromis spp.

To consider diet optimization for the growth and health of fish under intensive aquaculture systems, with a focus on the farming of Nile tilapia and red tilapia in Thailand, we conducted an experiment based on a completely randomized design (CRD), with three treatments and four replicates. Three diets, supplemented with different trace minerals, were applied to selected groups of fish: (a) a control diet, without organic trace minerals supplementation; (b) a T1 diet of chromium-L-methionine at 500 ppb, in combination with a zinc amino acid complex at 60 parts per million (ppm); and (c) a T2 diet of chromium-L-methionine at 500 ppb in combination with selenomethionine at 300 ppb. Red tilapia with an initial mean weight of 190 ± 12 g/fish were randomly distributed into cages of 2 × 2 × 2.5 m in a freshwater pond (12 cages in total), with 34 fish per cage and a density of 17 fish/m3. During the 8 week feeding trial, the fish were fed 3−4% of their body weight twice a day. The fish were weighed, then blood samples were collected to study their immune responses. The intestines were collected, measured, and analyzed at the end of the feeding trial. The results showed that the red tilapia that were fed with diets of chromium-L-methionine in combination with a zinc amino acid complex in the T1 treatment had significantly (p < 0.05) higher final weights, weight gains, average daily gains (ADGs), and better feed conversion ratios (FCRs), compared with fish that were fed with the control diet without organic trace minerals and with fish that were fed with the T2 diet (p < 0.05). The midgut and hindgut villus heights of the group fed with chromium-L-methionine in combination with a zinc amino acid complex in the T1 treatment were significantly higher than those of the other groups (p < 0.05). The levels of the antioxidative enzyme superoxide dismutase (SOD) and lysozyme activity were not significantly different from those of fish that were fed with the control diet (p > 0.05), whereas the glutathione level tended to increase (p < 0.1) in fish that were fed with chromium-L-methionine in combination with selenomethionine in the T2 treatment. Therefore, we concluded that chromium-L-methionine in combination with a zinc amino acid complex or selenomethionine clearly enhanced red tilapia's growth performance and feed utilization through the promotion of antioxidative enzyme activity and immune response.

Replacing Fish Meal with Defatted Insect Meal (Yellow Mealworm Tenebrio molitor) Improves the Growth and Immunity of Pacific White Shrimp (Litopenaeus vannamei).

Recently, ecological and economic issues have affected fish meal (FM) supply, the main source of protein for shrimp. This triggered a search for alternative dietary protein sources for shrimp production. We studied the consequences of replacing FM with a defatted insect meal, ŸnMealTM (YM), comprised of yellow mealworm (Tenebrio molitor). Growth and immune parameters of juvenile Pacific white shrimp (Litopenaeus vannanmei) were compared after an eight-week feeding trial. Shrimp were kept in aquaria with densities of 60 and 40 shrimp/m2 and fed one of five diets in which a proportion of FM was replaced by YM. All diets were isoproteic, isoenergetic, and balanced in lysine and methionine. After the feeding trial, shrimp were challenged with pathogenic bacteria (Vibrio parahaemolyticus). Growth and feed conversion parameters improved when YM was included in shrimp diets; with the highest weight gain and best food conversion ratio (FCR) achieved when 50% of FM was replaced by YM versus the control diet that contained no YM (initial weight: 1.60 g/shrimp; growth: 5.27 vs. 3.94 g/shrimp; FCR 1.20 vs. 1.59). In challenged shrimp, mortality rates were significantly less among groups that received YM, with a 76.9% lower mortality rate in the 50% FM replacement group versus the control.

Stability of carotenoid diets during feed processing and under different storage conditions.

The stability of formulated carotenoid diets during feed processing and under different storage conditions were studied. All carotenoid diets were split into two groups with one group containing BHT (acting as an antioxidant) at 250 ppm and the other without BHT. The experiment was divided into two parts. First, all diets were evaluated in total carotenoid (TC) loss during feed processing, in dry mixed feeds after being processed and dried. In the final part, the completed dietary carotenoids were stored in an aluminum foil bag, the top of which was sealed with a bag sealer and kept under different storage conditions at 26-28 °C and 4 °C. The stability of the TC was observed during an 8-week trial period. The results showed that the diet pelleting process did not affect the carotenoid content of the diets, and the best storage temperature for the formulated carotenoid diet was at 4 °C. However, an antioxidant was added to assist in energy saving before feed processing. Thus, the addition of BHT at 250 ppm can be done at normal room temperature in order to reduce oxidation that might cause a loss of TC quantities in diets.