C. Vachot

TL;DR: The studies strongly suggest that low dietary carbohydrate utilization in rainbow trout is not due to the absence of inducible hepatic GK as previously suggested, and suggest that other biochemical mechanisms are implicated in the inability of rainbow trout and gilthead seabream to control blood glucose closely.

TL;DR: It is found that even a single meal containing 24% of glucose is sufficient to induce the GK expression (mRNA and activity) as in mammals, and suggests that in carnivorous rainbow trout, the liver is capable to strongly regulate the utilisation of glucose but not the synthesis of glucose.

TL;DR: The model combines genetic selection and dietary treatment to produce a model to study metabolic pathways involved in genetic and nutritional control of fat deposition in fish muscle, suggesting that the two factors used in this study to modify muscle lipid content exerted some additive but mostly independent effects on these metabolic actors.

TL;DR: The data confirm that ornithine urea cycle is incomplete in the liver and that argininolysis plays a major role in ureogenesis in both species.

TL;DR: A small but sufficient endogenous Arg synthesis is suggested to maintain whole body N balance and differences between freshwater and marine species as regards Arg requirement are suggested.