SUMMARYTo assess the potential involvement of TORC1 (target of rapamycin complex 1) signalling in the regulation of post-prandial hepatic lipid and glucose metabolism-related gene expression in trout, we employed intraperitoneal administration of rapamycin to achieve an acute inhibition of the TOR pathway. Our results reveal that rapamycin inhibits the phosphorylation of TORC1 and its downstream effectors (S6K1, S6 and 4E-BP1), without affecting Akt and the Akt substrates Forkhead-box Class O1 (FoxO1) and glycogen synthase kinase 3α/β (GSK 3α/β). These results indicate that acute administration of rapamycin in trout leads to the inhibition of TORC1 activation. No effect is observed on the expression of genes involved in gluconeogenesis, glycolysis and fatty acid oxidation, but hepatic TORC1 inhibition results in decreased sterol regulatory element binding protein 1c (SREBP1c) gene expression and suppressed fatty acid synthase (FAS) and glucokinase (GK) at gene expression and activity levels, indicating that FAS and GK activity is controlled at a transcriptional level in a TORC1-dependent manner. This study demonstrates for the first time in fish that post-prandial regulation of hepatic lipogenesis and glucokinase in rainbow trout requires the activation of TORC1 signalling.

We examined the long-term effect of feeding coconut oil (CO; rich in lauric acid, C12) on voluntary food intake and nutrient utilisation in rainbow trout (Oncorhynchus mykiss), with particular attention to the metabolic use (storage or oxidation) of ingested medium-chain TAG. Trout were fed for 15 weeks one of the four isoproteic diets containing fish oil (FO) or CO as fat source (FS), incorporated at 5 % (low fat, LF) or 15 % (high fat, HF). Fat level or FS did not modify food intake (g/kg 0·8 per d), despite higher intestinal cholecystokinin-T mRNA in trout fed the HF-FO diet. The HF diets relative to the LF ones induced higher growth and adiposity, whereas the replacements of FO by CO resulted in similar growth and adiposity. This, together with the substantial retention of C12 (57 % of intake), suggests the relatively low oxidation of ingested C12. The down-regulation of carnitine palmitoyl-transferase-1 (CPT-1) confirms the minor dependency of mediumchain fatty acids (MCFA) on CPT-1 to enter the mitochondria. However, MCFA did not up-regulate mitochondrial oxidation evaluated using hepatic hydroxyacyl-CoA dehydrogenase as a marker, in line with their high retention in body lipids. At a low lipid level, MCFA increased mRNA levels of fatty acid synthase, elongase and stearoyl-CoA desaturase in liver, showing the hepatic activation of fatty acid synthesis pathways by MCFA, reflected by increased 16 : 0, 18 : 0, 16 : 1, 18 : 1 body levels. The high capacity of trout to incorporate and transform C12, rather than to readily oxidise C12, contrasts with data in mammals and may explain the absence of a satiating effect of CO in rainbow trout.Key words: Medium-chain fatty acids: Coconut oil: Fatty acid oxidation: Satiety Medium-chain fatty acids (MCFA), which are the principal constituents of medium-chain TAG (MCT), are saturated with a chain length of six to twelve carbons (1,2) . In mammalian vertebrates, the consumption of MCT has been reported to decrease food intake (3 -5) and to reduce fat deposition (6,7) . The satiety effect of MCT compared with long-chain TAG has been attributed to the metabolic discrimination in fatty acid utilisation. Long-chain fatty acids (LCFA), after being packed into chylomicrons, enter the lymphatic system that favours their uptake by peripheral tissues such as adipose tissues and muscle (1,2) . In contrast, MCFA can enter directly into the portal vein that accelerates their uptake and oxidation by the liver. As a result, minor amounts of MCFA are recovered in the different tissues (8,9) . Moreover, the transport of MCFA across the mitochondrial membrane does not require carnitine palmitoyltransferase-1 (CPT-1) (10) , considered as a rate-limiting step in the mitochondrial oxidation of LCFA.In this context, the satiating effect of MCFA has been explained by their rapid oxidation and the limited 'storage' of MCFA by the organism. The possible link between oxidative metabolism, satiety and food intake has been documented in rats and human subjects (11 -13) , but has been litt...

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