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Submitted to: Aquaculture America Conference
Publication Type: Abstract Only Publication Acceptance Date: 9/3/2015 Publication Date: 2/22/2016 Citation: Cleveland, B.M., Weber, G.M. 2016. Effects of sexual maturation and 17ß-Estradiol on nutrient partitioning and mechanisms regulating growth and nutrient metabolism in Rainbow Trout Oncorhynchus mykiss [abstract]. Aquaculture America Conference. p. 44. Interpretive Summary: Technical Abstract: In female rainbow trout sexual maturation occurs parallel with declines in growth performance and mobilization of nutrient stores that partition energy away from growth and toward gonad development. For this reason sterile triploids are often reared for their ability to produce larger fillets and avoid the negative effects of sexual maturation. However, it is unknown to what extent increased 17ß-estradiol (E2) signaling versus a negative energy balance orchestrates the nutrient repartitioning effort. In the current study nineteen-month old triploid female rainbow trout were fed an E2-supplemented diet (30 mg/kg diet) for one month. Growth performance, nutrient partitioning, and expression of genes central to growth and nutrient metabolism were compared to triploids and age-matched diploids consuming a control feed. Specific growth rate was greater in maturing diploids compared to sterile triploids and was not affected by E2 supplementation in triploids. However, E2-treated triploids exhibited lower fillet protein content and fillet yield, losing fillet protein over the course of the study. In contrast, maturing diploids lost viscera fat while triploids, regardless of diet, continued to accrue visceral adipose tissue. Gene expression data indicate numerous genes in liver and muscle tissue that responded similarly in maturing diploids and E2-treated triploids, suggesting that E2 is a maturation-related signal that regulates mechanisms related to growth and nutrient metabolism. In liver these mechanisms included the growth hormone/insulin-like growth factor (IGF) axis, IGF binding proteins, as well as genes associated with lipid binding and transport, fatty acid oxidation, and PPAR transcription factors. In muscle these mechanisms included reductions in myogenic gene expression and increased proteolytic capacity, suggesting an E2-induced reduction in the capacity for muscle growth. This study suggests that during sexual maturation elevated E2 plays a significant role in the regulation of hepatic mechanisms related to growth and lipid metabolism and reduces the capacity for muscle growth. The collective result is the partitioning of nutrients and energy away from muscle in support of gonad development. In contrast, the mobilization of viscera lipid stores appear to be mediated less by E2 and more by energy demands associated with gonad development. These findings improve understanding of how steroids regulate nutrient metabolism to meet the high energy demands associated with gonad development during sexual maturation. |
