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Abstract: This study investigates the effect of diet during early development on growth and metabolic capacity in the juvenile stage of Atlantic cod. Growth in three groups of Atlantic cod juveniles (10–70g) was measured at two salinities (15‰ or 32‰) in combination with two temperatures (10°C or 14°C). Groups of cod from a single egg batch differed by having been fed with rotifers (R) or natural zooplankton (Z) during the first 36days post hatch. A third group was fed zooplankton from 1 to 22dph, after which diet changed to rotifers from 22 to 36dph (ZRZ). All fish were weaned at 36dph. Juveniles from the Z and ZRZ groups performed equally well under all experimental conditions, but fish that had received rotifers as a larval diet showed overall significantly lower growth rates. Growth was significantly enhanced by reduced salinity. Metabolic enzyme activity and relative myosin mRNA expression levels were not affected by larval diet. Muscle AAT and MDH were affected by salinity while these enzymes in liver tissue were affected by the interaction between salinity and temperature. Metabolic enzymes were stronger correlated with fish size than growth rates. Our results indicate that larval diet has a pronounced effect on juvenile growth rates under varying environmental conditions as optimal larval diet (zooplankton) increased juvenile growth rates significantly. Metabolic enzyme activity and relative myosin mRNA expression were not affected by larval history, which suggests that the persisting juvenile growth difference is not a result of differing metabolic capacity. [Copyright &y& Elsevier]

Abstract: The catabolic and energy metabolism capacities during spotted wolffish (Anarhichas minor) embryogenesis were investigated. We assessed the embryo''s ability to catabolize proteins (trypsin-like proteases) and lipids (triglyceride lipase) and examined the development of metabolic capacities using enzymatic assays: ability to use carbohydrates (pyruvate kinase), amino acids (aspartate aminotransferase) and fatty acids (hydroxyacyl-CoA dehydrogenase) for energy production, and aerobic (citrate synthase) and anaerobic (lactate dehydrogenase) energy production. Functional enzymatic systems were detected from the eyed stage (350 degree-days), except for fatty acids, which was detected from 540 degree-days. To compare the development of 1) aerobic and anaerobic pathways and 2) the capacity to mobilize the different energy substrates, enzymatic ratios were calculated. Anaerobic capacity appeared to increase at a significantly higher rate than the aerobic capacity. Ratios revealing the relative capacity to use specific energy substrates showed a significantly slower increase during development in the capacity to use carbohydrates than amino acids and fatty acids. The end of embryogenesis was characterized by a significant decrease in the use of carbohydrates for aerobic energy production but an increasing capacity to use amino acids. Egg survival as affected by the variability in metabolic parameters is discussed. [Copyright &y& Elsevier]

Abstract Refeeding, following a period of food deprivation will often lead to compensatory growth. Although many studies have focused on molecular mechanisms behind this accelerated growth response in fish, little is known on the roles of protein and metabolism. We also assessed, for the first time, the potential roles of miRNAs in regulating compensatory growth. Artcic charr, Salvelinus alpinus , a northern freshwater species, was deprived of food for 101 days and then fed to satiety for 126 days. The refeeding period resulted in compensatory growth, with a partial compensation of body mass. The feed deprivation period lead to a decrease in hepatosomatic index (HSI) and intestinal somatic index (ISI). HSI and ISI were then gradually replenished during early refeeding, following a lag phase prior to the compensatory growth response. mRNA transcripts regulating protein degradation via the autophagy pathway (Cathepsin D and Cathepsin L) in muscle were upregulated during feed restriction and downregulated after refeeding, which could allow for greater protein accretion in muscle, facilitating compensatory growth. Transcript levels from the ubiquitin proteasome pathway (Mafbx and Murf1) and the calpain system (Calpain 7 and Calpastatin) suggested that these pathways were not involved in regulating compensatory growth. Furthermore, we've shown that miRNAs (miR-29a and miR-223) could be involved in fish glycogen homeostasis during the early stages of refeeding. These findings provide a deeper understanding of the molecular mechanisms regulating growth in fish. [ABSTRACT FROM AUTHOR]

Cardiac mitochondrial metabolism provides 90% of the ATP necessary for the contractile exertion of the heart muscle. Mitochondria are therefore assumed to play a pivotal role in heart failure (HF), cardiovascular disease and ageing. Heat stress increases energy metabolism and oxygen demand in tissues throughout the body and imposes a major challenge on the heart, which is suspected of being the first organ to fail during heat stress. The underlying mechanisms inducing heart failure are still unclear. To pinpoint the processes implicated in HF during heat stress, we measured mitochondrial respiration rates and hydrogen peroxide production of isolated Arctic char ( Salvelinus alpinus ) heart mitochondria at 4 temperatures: 10 °C (acclimation), 15 °C, 20 °C and 25 °C (just over critical maximum). We found that at temperature ranges causing the loss of an organism's general homeostasis (between 20 °C and 25 °C) and with a substrate combination close to physiological conditions, the heat-induced increase in mitochondrial oxygen consumption levels off. More importantly, at the same state, hydrogen peroxide efflux increased by almost 50%. In addition, we found that individuals with low mitochondrial respiration rates produced more hydrogen peroxide at 10 °C, 15 °C and 20 °C. This could indicate that individuals with cardiac mitochondria having a low respiratory capacity, have a more fragile heart and will be more prone to oxidative stress and HF, and less tolerant to temperature changes and other stressors. Our results show that, at temperatures close to the thermal limit, mitochondrial capacity is compromised and ROS production rates increase. This could potentially alter the performance of the cardiac muscle and lead to heat-induced HF underlining the important role that mitochondria play in setting thermal tolerance limits. [ABSTRACT FROM AUTHOR]