Recent advances in understanding the molecular basis of taste physiology in fish could open new opportunities to optimize feeding performance in aquaculture. This is particularly relevant at a time when alternative ingredients are being increasingly used, often reducing the digestibility and acceptability of fish diets, even if they are nutritionally balanced. The molecular characterization of fish taste receptors T1Rs and T2Rs revealed common taste discrimination mechanisms among vertebrates. In addition, data so far appear to indicate that taste signaling elements are conserved from fish to mammals. Nevertheless, fundamental differences between ligand specificities of taste receptors, and the presence of multiple T1R2s in fish species, underlines evolutionary adaptations of the T1R2 receptor to sense metabolically important nutrients, with a shift from sugars in mammals to amino acids in teleosts. This fits well with electrophysiological and behavioral studies on ligand specificities and taste preferences in several fish species. On the other hand, synergistic responses between different attractants could result from additive effects of independent receptor sites and response mechanisms, and this knowledge can be of practical interest to specifically design stimulant mixtures to modulate feed intake in aquaculture. Mammalian taste receptors and signaling elements have also been identified in the gastrointestinal tract, where they trigger multiple endocrine and neuronal pathways regulating digestion, nutrient absorption, feeding, and metabolism. Evidence for the existence of these receptors and signaling pathways in fish guts have recently been uncovered, suggesting that sensory properties of the diet might also have functional effects beyond oral taste sensations and palatability.

An 8-week feeding trial was conducted to investigate the effects of high-starch diets and the supplementation of an olive extract (OE) on the growth performance, liver health and lipid metabolism of largemouth bass (Micropterus salmoides). Four isonitrogenous and isolipidic diets were prepared: two basal diets containing low (9.0%) and high (14.4%) levels of starch (named as LS and HS), and 0.125% OE was supplemented to each basal diet (named LSOE and HSOE). The results show that high-starch diets had significant negative effects on growth performance, with lower FR, SGR and higher FCR, whereas OE significantly lowered FCR, determined by two-way ANOVA analysis. High-starch diets induced oxidative stress, inflammatory response and liver function injury, with significant increases in the content of plasmatic AKP, AST, ALT, hepatic SOD and MDA, and up-regulation of hepatic TNFα, IL1β, and TGFβ1 gene expression. In addition, a high-starch diet decreased the phosphorylation of AMPK and upregulated the expression of SREBP, together with higher hepatic liver lipid and HSI. The oxidative stress and lipid metabolism disorders indicate metabolic liver disease (MLD) of largemouth bass fed high-starch diets. Feeding on OE-supplemented diets increased the hepatic antioxidant capacity by decreasing the content of MDA and SOD. Fish fed the HSOE diet had an activated phosphorylation of JNK and decreased expression of pro-inflammatory IL1β compared with those fed the HS diet, which strongly indicated that the degree of inflammatory responses was reduced after OE supplementation. Interestingly, this study demonstrated that OE regulates hepatic lipid metabolism in fish by inhibiting the expression of hepatic lipogenesis genes (ACC1 and FASN) and promoting lipolysis (ATGL) and β-oxidation (CPT1α) to prevent TG accumulation. In conclusion, high-starch feed induced oxidative stress and lipid metabolic disorder of largemouth bass, while supplementation with OE improved its antioxidant capacity, anti-inflammatory responses and lipid metabolism. However, hepatic histopathological results suggested that OE supplementation could not completely repair the MLD caused by the high level of starch in largemouth bass.

A 10-week growth trial was conducted to investigate the effects of a phytogenic feed additive (PFA) containing olive by-products and green tea extracts supplemented to a reduced fishmeal/high soybean meal diet on the growth performance, hepatic antioxidant capacity, lipid metabolism, and liver health of largemouth bass (Micropterus salmoides). Three experimental diets were tested: (1) a control high fishmeal (40%) and low soybean meal (15.57%) diet (named HFM), (2) a reduced fishmeal (30%) and high soybean meal (30.97%) diet (named HSB), and (3) a HSB diet supplemented with the PFA at 500 mg/kg (named HSB+P). Each diet was assigned to four replicate tanks, each containing 30 largemouth bass (initial body weight, IBW = 48.33 ± 0.01 g). The results showed that increasing the soybean meal content in the diet did not negatively affect growth performance, whereas supplementation with PFA significantly increased weight gain and specific growth rate of largemouth bass compared to both HFM and HSB groups. Reducing fishmeal and increasing soybean meal in the diet caused oxidative stress with a higher content of ROS in the liver. However, the hepatic antioxidant capacity was enhanced, with reduced ROS and increased GSH-Px levels in the HSB+P group. Moreover, the decrease of plasma TG, LDL-C, and LDL-C/TC, and downregulation of lipogenesis and cholesterol synthesis gene expression in liver, indicated that supplementation with the PFA improved fish lipid metabolism. Protein retention efficiency was also significantly increased in largemouth bass fed the diet with PFA supplementation, which regulated (enhanced) AKT-mTOR phosphorylation. These results clearly indicated that a PFA containing olive by-product and green tea extracts can positively improve growth performance, protein retention efficiency, antioxidant capacity, and lipid metabolism of largemouth bass fed a reduced fishmeal/high soybean meal diet.

A plethora of molecular and functional studies in tetrapods has led to the discovery of multiple taste 1 receptor (T1R) genes encoding G-protein coupled receptors (GPCRs) responsible for sweet (T1R2 + T1R3) and umami (T1R1 + T1R3) taste. In fish, the T1R gene family repertoires greatly expanded because of several T1R2 gene duplications, and recent studies have shown T1R2 functional divergence from canonical mammalian sweet taste perceptions, putatively as an adaptive mechanism to develop distinct feeding strategies in highly diverse aquatic habitats. We addressed this question in the carnivore fish gilthead seabream (Sparus aurata), a model species of aquaculture interest, and found that the saT1R gene repertoire consists of eight members including saT1R1, saT1R3 and six saT1R2a-f gene duplicates, adding further evidence to the evolutionary complexity of fishT1Rs families. To analyze saT1R taste functions, we first developed a stable gene reporter system based on Ca²⁺-dependent calcineurin/NFAT signaling to examine specifically in vitro the responses of a subset of saT1R heterodimers to L-amino acids (L-AAs) and sweet ligands. We show that although differentially tuned in sensitivity and magnitude of responses, saT1R1/R3, saT1R2a/R3 and saT1R2b/R3 may equally serve to transduce amino acid taste sensations. Furthermore, we present preliminary information on the potential involvement of the Gi protein alpha subunits saGαi1 and saGαi2 in taste signal transduction.