Differential effects of exposure to parasites and bacteria on stress response in turbot Scophthalmus maximus simultaneously stressed by low water depth.

The stress response of turbot Scophthalmus maximus was evaluated in fish maintained 8 days under different water depths, normal (NWD, 30 cm depth, total water volume 40 l) or low (LWD, 5 cm depth, total water volume 10 l), in the additional presence of infection-infestation of two pathogens of this species. This was caused by intraperitoneal injection of sublethal doses of the bacterium Aeromonas salmonicida subsp. salmonicida or the parasite Philasterides dicentrarchi (Ciliophora:Scuticociliatida). The LWD conditions were stressful for fish, causing increased levels of cortisol in plasma, decreased levels of glycogen in liver and nicotinamide adenine dinucleotide phosphate (NADP) and increased activities of G6Pase and GSase. The presence of bacteria or parasites in fish under NWD resulted in increased cortisol levels in plasma whereas in liver, changes were of minor importance including decreased levels of lactate and GSase activity. The simultaneous presence of bacteria and parasites in fish under NWD resulted a sharp increase in the levels of cortisol in plasma and decreased levels of glucose. Decreased levels of glycogen and lactate and activities of GSase and glutathione reductase (GR), as well as increased activities of glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and levels of nicotinamide adenine dinucleotide phosphate (NADPH) occurred in the same fish in liver. Finally, the presence of pathogens in S. maximus under stressful conditions elicited by LWD resulted in synergistic actions of both type of stressors in cortisol levels. In liver, the presence of bacteria or parasites induced a synergistic action on several variables such as decreased activities of G6Pase and GSase as well as increased levels of NADP and NADPH and increased activities of GPase, G6PDH and 6PGDH.

Glucosensing capacity of rainbow trout telencephalon.

To assess the hypothesis of glucosensing systems present in fish telencephalon, we first demonstrated in rainbow trout, by in situ hybridisation, the presence of glucokinase (GK). Then, we assessed the response of glucosensing markers in rainbow trout telencephalon 6 hours after i.c.v. treatment with glucose or 2-deoxyglucose (inducing glucoprivation). We evaluated the response of parameters related to the mechanisms dependent on GK, liver X receptor (LXR), mitochondrial activity, sweet taste receptor and sodium-glucose linked transporter 1 (SGLT-1). We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (agouti-related protein, neuropeptide Y, pro-opiomelanocortin, and cocaine- and amphetamine-related transcript), as well as the abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression, such as protein kinase B (AkT), AMP-activated protein kinase (AMPK), mechanistic target of rapamycin and cAMP response element-binding protein (CREB). The responses obtained support the presence in the telencephalon of a glucosensing mechanism based on GK and maybe one based on LXR, although they do not support the presence of mechanisms dependent on mitochondrial activity and SGLT-1. The mechanism based on sweet taste receptor responded to glucose but in a converse way to that characterised previously in the hypothalamus. In general, systems responded only to glucose but not to glucoprivation. Neuropeptides did not respond to glucose or glucoprivation. By contrast, the presence of glucose activates Akt and inhibits AMPK, CREB and forkhead box01. This is the first study in any vertebrate species in which the response to glucose of putative glucosensing mechanisms is demonstrated in the telencephalon. Their role might relate to processes other than homeostatic control of food intake, such as the hedonic and reward system.

Gradation of the stress response in rainbow trout exposed to stressors of different severity: the role of brain serotonergic and dopaminergic systems.

After an intense acute stressor, fish develop a metabolic and behavioural response that usually lasts for several hours. Brain monoaminergic systems, particularly the serotonergic system, appear to play a key role in the central regulation of the stress response. However, the influence of stressor severity on brain monoaminergic systems and on the induced stress responses is yet poorly understood. We hypothesise that serotonergic system could have a direct role in the integration of sensory information during stressor exposure and in the organisation of the subsequent integrated stress response. According to our hypothesis, a low stressor intensity would induce a low response of brain serotonergic system and therefore stress responses of low magnitude and duration. To test this hypothesis, we exposed fish to handling disturbance for 5 s, 15 s or 3 min. We sampled fish at 0 (controls), 3, 15, 45 and 240 min after the start of the stress protocol. Brain levels of serotonin, dopamine and their respective main oxidative metabolites were quantified, along with plasma levels of stress markers (catecholamines, cortisol, glucose and lactate). Regarding stress markers, the 5-s and 15-s stress protocols induced similar and relatively low elevations in all parameters assessed. As expected, the 3-min protocol induced responses of a higher intensity and duration in all plasma parameters. Interestingly, the alterations of brain monoaminergic systems did not follow the same trend. The three stress protocols induced increases in the serotonergic activity in all brain regions analysed (hypothalamus, telencephalon and medulla oblongata), independently of the duration of the handling disturbance, whereas the effects on the dopaminergic system were minor and brain region-dependent. These data suggest that the brain serotonergic system, although likely involved in the recognition of the stressor stimuli, is not the only actor determining the magnitude and duration of the acute stress response in trout.

Effects of insulin treatment on the response to oleate and octanoate of food intake and fatty acid-sensing systems in rainbow trout.

We hypothesized that food intake and the response of fatty acid (FA)-sensing systems in hypothalamus, liver, and Brockmann bodies of rainbow trout to raised levels of oleate (OL) or octanoate (OCT) is modified by insulin treatment. To assess this hypothesis, 15 fish per group received intraperitoneally 10-mL/kg injection of saline solution alone (control), or containing insulin (2-mg bovine insulin/kg body mass), OL (300 µg/kg), OCT (300 µg/kg), insulin + OL, or insulin + OCT to be sampled 6 h later to assess parameters related to FA sensing. Our results suggest that the modulatory role of insulin on the responses of hypothalamic FA-sensing systems to changes in circulating levels of OL or OCT was of minor importance in contrast to the mammalian model. However, this is in contrast with the effects observed in another experiment assessing changes in food intake after similar treatments because insulin treatment enhanced the anorectic effects of FA alone, and the effect was especially relevant (P < 0.001) for OCT, in contrast with the mammalian model where this FA is not inducing an anorectic response. In liver and Brockmann bodies, insulin treatment enhanced the responses to OL or OCT treatment in parameters related to FA sensing. Therefore, we provide for the first time in fish, and in a non-mammalian vertebrate, evidence for the modulation of FA-sensing systems by insulin.

Arginine vasotocin treatment induces a stress response and exerts a potent anorexigenic effect in rainbow trout, Oncorhynchus mykiss.

The peptide arginine vasotocin (AVT), homologous to mammalian arginine vasopressin, is involved in many aspects of fish physiology, such as osmoregulation, regulation of biological rhythms, reproduction, metabolism or responses to stress, and the modulation of social behaviours. Because a decrease in appetite is a general response to stress in fish and other vertebrates, we investigated the role of AVT as a possible food intake regulator in fish. We used i.c.v. injections for central administration of AVT to rainbow trout (Oncorhynchus mykiss). In a first experiment, we evaluated the temporal response of food intake after AVT treatment. In a second experiment, we investigated the effects of central AVT administration on the response of typical stress markers (plasma cortisol, glucose and lactate), as well as brain serotonergic, noradrenergic and dopaminergic activity. In addition, the mRNA levels of genes involved in food intake regulation [neuropetide Y, pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART) and corticotrophin-releasing factor (CRF)] and in CRF- (CRF-binding protein) and AVT-signalling (pro-VT and AVT receptor), were also assessed after AVT treatment. Our results showed that AVT is a potent anorexigenic factor in fish. Increases of plasma cortisol and glucose after AVT treatment strongly suggest that AVT administration induced a stress response and that AVT action was mediated by hypothalamic-pituitary-interrenal axis activation, which was also supported by the increase of the serotonergic activity in trout telencephalon and hypothalamus. The increased hypothalamic levels of POMC and CART suggest that these peptides might have a role in the anorexigenic action of AVT, whereas the involvement of CRF signalling is unclear.

Oral administration of melatonin counteracts several of the effects of chronic stress in rainbow trout.

To assess a possible antistress role of melatonin in fish, we orally administered melatonin to rainbow trout for 10 d and then kept the fish under normal or high stocking density conditions during the last 4 d. Food intake; biochemical parameters in plasma (cortisol, glucose, and lactate concentrations); liver (glucose and glycogen concentrations, and glycogen synthase activity); enzyme activities of amylase, lipase, and protease in foregut and midgut; and content of the hypothalamic neurotransmitters dopamine and serotonin, as well as their oxidized metabolites, 3,4-dihydroxyphenylacetic acid and 5-hydroxy-3-indoleacetic acid, were evaluated under those conditions. High stocking density conditions alone induced changes indicative of stress conditions in plasma cortisol concentrations, liver glycogenolytic potential, the activities of some digestive enzymes, and the 3,4-dihydroxyphenylacetic acid-to-dopamine and 5-hydroxy-3-indoleacetic acid-to-serotonin ratios in the hypothalamus. Melatonin treatment in nonstressed fish induced an increase in liver glycogenolytic potential, increased the activity of some digestive enzymes, and enhanced serotoninergic and dopaminergic metabolism in hypothalamus. The presence of melatonin in stressed fish resulted in a significant interaction with cortisol concentrations in plasma, glycogen content, and glycogen synthase activity in liver and dopaminergic and serotoninergic metabolism in the hypothalamus. In general, the presence of melatonin mitigated several of the effects induced by stress, supporting an antistress role for melatonin in rainbow trout.

Evidence for a gut-brain axis used by glucagon-like peptide-1 to elicit hyperglycaemia in fish.

In mammals, glucagon-like peptide-1 (GLP-1) produces changes in glucose and energy homeostasis through a gut-pancreas-brain axis. In fish, the effects of GLP-1 are opposed to those described in other vertebrates, such as stimulation of hyperglycaemia and the lack of an effect of incretin. In the present study conducted in a teleost fish such as the rainbow trout, we present evidence of a gut-brain axis used by GLP-1 to exert its actions on glucose and energy homeostasis. We have assessed the effects of GLP-1 on glucose metabolism in the liver as well as the glucose-sensing potential in the hypothalamus and hindbrain. We confirm that peripheral GLP-1 administration elicits sustained hyperglycaemia, whereas, for the first time in a vertebrate species, we report that central GLP-1 treatment increases plasma glucose levels. We have observed (using capsaicin) that at least part of the action of GLP-1 on glucose homeostasis was mediated by vagal and splanchnic afferents. GLP-1 has a direct effect in parameters involved in glucose sensing in the hindbrain, whereas, in the hypothalamus, changes occurred indirectly through hyperglycaemia. Moreover, in the hindbrain, GLP-1 altered the expression of peptides involved in the control of food intake. We have elaborated a model for the actions of GLP-1 in fish in which this peptide uses a mammalian-like ancestral gut-brain axis to elicit the regulation of glucose homeostasis in different manner than the model described in mammals. Finally, it is worth noting that the hyperglycaemia induced by this peptide and the lack of incretin function could be related to the glucose intolerance observed in carnivorous teleost fish species such as the rainbow trout.

Ghrelin effects on central glucosensing and energy homeostasis-related peptides in rainbow trout.

Although the role of ghrelin (GHRL) on fish appetite regulation had been widely studied in past years, its involvement in the regulation of glucose metabolism had been little explored. In the present study we hypothesize that GHRL may have a role in the regulation of glucose homeostasis in fish. Therefore, we carried out different experimental approaches in rainbow trout to assess brain glucosensing potential and glucose metabolism in response to GHRL treatment. We found that after either systemic or central GHRL administration to trout deprived of food, glycemia remained unaffected, whereas (in clear contrast with the mammalian model) a consistent activation of the main glucosensing markers (glucose transporter 2, glucokinase, and ATP-sensitive inward rectified K+ channel) was noticed in both hypothalamus and hindbrain. Some of these results were further confirmed by in vitro incubations of hypothalamus and hindbrain in the presence of GHRL. Despite the lack of changes in glycemia, we suggest that the changes elicited by GHRL on the glucosensing system are direct and could be related to a helper action of this hormone when glucose arrived in the postprandial phase. Moreover, we also studied the effect of GHRL treatment on the expression of several food intake-related neuropeptides, such as neuropeptide Y, cocaine- and amphetamine-regulated transcript, pro-opiomelanocortin, and corticotropin-releasing factor. We observed an important variability in the effects of GHRL attributable either to the route of GHRL administration or to the brain regions assessed, which could help explain the contradictory results described in fish literature about GHRL role in food intake control.

Brain glucose and insulin: effects on food intake and brain biogenic amines of rainbow trout.

The effects of central (intracerebroventricular, 9 microg fish(-1)) and peripheral (intraperitoneal, 4 mg kg(-1)) administration of bovine insulin, as well as the effect of hyperglycemia (oral administration of 1 g glucose fish(-1)) and brain glucodeprivation (intracerebroventricular administration of 2-deoxy-D-glucose) on food intake and levels of brain (telencephalon, preoptic area, and hypothalamus) biogenic amines (serotonin, dopamine, noradrenaline and their metabolites 5-hydroxyindoleacetic acid, and dihydroxyphenylacetic acid) were assessed on rainbow trout ( Oncorhynchus mykiss). Treatment with insulin inhibited food intake after 26 or 52 h of administration, central or peripheral, respectively. This effect was still apparent after 74 h of central treatment. When assessing changes in the levels of biogenic amines after 26 h of central insulin administration, there was a significant increase in the levels of 5-hydroxyindoleacetic acid, and in the ratio of dihydroxyphenylacetic acid/dopamine of insulin-treated fish, in telencephalon and hypothalamus, respectively. These results suggest that peripherally administered insulin is involved in a feedback regulatory loop with food intake and body weight. Moreover, at least part of the effects of insulin could be mediated by hypothalamic dopaminergic activity. The strong hyperglycemia induced by oral administration of glucose did not induce significant changes either on food intake (control versus treated), or in brain levels of biogenic amines. The intracerebroventricular administration of 2-deoxy-D-glucose induced an increase in food intake without altering plasma glucose levels, suggesting that fish brain possesses a control system for detecting hypoglycemia in plasma and therefore keep brain glucose levels high enough for brain function.

Glucagon effects on brain carbohydrate and ketone body metabolism of rainbow trout.

The levels of glycogen in brain, lactate and acetoacetate in brain and plasma, glucose in plasma and the activities of brain key enzymes of glycogen metabolism (glycogen phosphorylase, GPase, glycogen synthetase, GSase), gluconeogenesis (fructose 1,6-bisphosphatase, FBPase), and glycolysis (6-phosphofructo 1-kinase, PFK) were evaluated in rainbow trout, Oncorhynchus mykiss, from 0.5 to 3 hr after intraperitoneal injection of 1 ml/kg(-1) body weight of saline alone (controls) or containing bovine glucagon at three different doses: 10, 50, and 100 ng/g(-1) body weight. The results obtained demonstrate, for the first time in a teleost fish, the existence of changes in brain carbohydrate and ketone body metabolism following peripheral glucagon treatment. A clear stimulation of brain glycogenolytic potential was observed after glucagon treatment, as judged by the time- and dose-dependent changes observed in brain glycogen levels (up to 88% decrease), and GPase (up to 30% increase) and GSase (up to 42% decrease) activities. In addition, clear time- and dose-dependent increased and decreased levels were observed in brain of glucagon-treated rainbow trout for lactate (up to 60% increase) and acetoacetate (up to 67% decrease), respectively. In contrast, no significant changes were observed after glucagon treatment in those parameters related to glycolytic/gluconeogenic capacity of rainbow trout brain. Altogether, these in vivo results suggest that glucagon may play a role (direct or indirect) in the regulation of carbohydrate and ketone body metabolism in brain of rainbow trout.

Uptake of 3-O-methyl-D-[U-14C]glucose into brain of rainbow trout: possible effects of melatonin.

The influx of glucose into the brain and plasma glucose disappearance were estimated in rainbow trout (Oncorhynchus mykiss) intravenously injected (1 ml x kg(-1) body weight) with a single dose (15 microCi x kg(-1) body weight) of 3-O-methyl-D-[U-14C]glucose ([U-14C]-3-OMG) at different times (2-160 min), and after intravenous injection at 15 min of increased doses (10-60 microCi x kg(-1) body weight) of [U-14C]-3-OMG. Brain and plasma radiotracer concentrations were measured, and several kinetic parameters were calculated. The apparent brain glucose influx showed a maximum after 15-20 min of injection then decreased to a plateau after 80 min. Brain distribution space of 3-OMG increased from 2 min to 20 min reaching equilibrium from that time onwards at a value of 0.14 ml x g(-1). The unidirectional clearance of glucose from blood to brain (k1) and the fractional clearance of glucose from brain to blood (k2) were estimated to be 0.093 m x min(-1) x g(-1), and 0.867 min(-1), respectively. A linear increase was observed in brain and plasma radiotracer concentrations when increased doses of [U-(14)C]3-OMG were used. All these findings support a facilitative transport of glucose through the blood-brain barrier of rainbow trout with characteristics similar to those observed in mammals. The injection of different doses of melatonin (0.25-1.0 mg x kg(-1)) significantly increased brain glucose influx suggesting a possible role for melatonin in the regulation of glucose transport into the brain.

Acute effects of L-tryptophan on tryptophan hydroxylation rate in brain regions (hypothalamus and medulla) of rainbow trout (Oncorhynchus mykiss).

Levels of 5-hydroxytryptophan (5-HTP) in brain regions (hypopthalamus and medulla) of rainbow trout were analysed by HPLC-EC 0, 10, 30, and 40 min after intraperitoneal administration of different doses of L-tryptophan (Trp) (0, 12.5, and 25 mg. kg(-1) body weight) in fish treated with 3-hydroxybenzylhydrazine (NSD1015; 75 mg. kg(-1)). The results show that, in control fish, 5-HTP levels in hypothalamus (58.03 +/- 6.36 pg. mg(-1) brain tissue) were significantly higher than those observed in medulla (28.04 +/- 4.32 pg. mg(-1) brain tissue). Basal tryptophan hydroxylation rates (after 0 mg. kg(-1) Trp administration) were 0.42 +/- 0.07 pg 5-HTP. mg(-1). min(-1), and 0.63 +/- 0.24 pg 5HTP. mg(-1). min(-1), for hypothalamus and medulla respectively. On the other hand, the results demonstrate that L-tryptophan administration induced significant increases in the rate of tryptophan hydroxylation, both in hypothalamus and medulla. These findings indicate that, in a way similar to that observed in mammals, brain tryptophan hydroxylase is unsaturated by its substrate (tryptophan) under normal physiological conditions. J. Exp. Zool. 286:131-135, 2000.

Brain serotonin and the control of food intake in rainbow trout (Oncorhynchus mykiss): effects of changes in plasma glucose levels.

The levels of 5-hydroxytryptamine and its main metabolite 5-hydroxyindoleacetic acid were assessed in two brain regions, hypothalamus and telencephalon, of rainbow trout (Oncorhynchus mykiss) submitted to increases or decreases in plasma glucose levels through different experimental approaches. Thus, intraperitoneal glucose treatment (500 mg kg(-1)) increased 5-hydroxytryptamine telencephalic levels. Long-term food deprivation up to 3 weeks significantly increased hypothalamic (2 weeks and 3 weeks) and telencephalic (1 week, 2 weeks, and 3 weeks) levels of 5-hydroxyindoleacetic acid, whereas the ratio 5-hydroxyindoleacetic acid/5-hydroxytryptamine significantly increased throughout the food-deprivation period assessed. Intraperitoneal treatment with bovine insulin (4 mg kg(-1)) decreased the 5-hydroxyindoleacetic acid/5-hydroxytryptamine ratio in hypothalamus after 1 h. Intraperitoneal administration of fenfluramine (3 mg kg(-1)) caused a depression in food intake coincident with a significant decrease of the hypothalamic 5-hydroxyindoleacetic acid/5-hydroxytryptamine ratio. These data are discussed in the context of the involvement of serotonergic system in the control of food intake in rainbow trout.

HCO3(-)-ATPase and Ca2+ dependent ATPase activities in the gills of the rainbow trout after the transfer to brackishwater and seawater.

The effect of seawater and brackishwater exposure on gill HCO3(-)-ATPase and Ca2+ dependent ATPase activity in rainbow trout (Oncorhynchus mykiss) was investigated at different periods of time. HCO3(-)-ATPase activity decreased after the transfer to either brackishwater or seawater. Ca2+ dependent ATPase activity decreased during the initial period (1 to 4 days) in both salinities and recovered freshwater values from the 7th day onwards. No effect from fish size was detected in both parameters after saltwater transfer. The results are discussed in terms of salinity and long-term saltwater adaptation.

Glucose, lactate, and beta-hydroxybutyrate utilization by rainbow trout brain: changes during food deprivation.

In order to evaluate the normal (fed conditions) substrate utilization rates of rainbow trout (Oncorhynchus mykiss) brain, CO2 production from glucose, lactate, and beta-hydroxybutyrate was tested in pooled brains. Oxidation rates, as well as the capacity for metabolism of carbohydrate and ketone bodies, were also evaluated in brain of rainbow trout that were food-deprived for 14 d. Under normal (fed) conditions, rainbow trout brain oxidized glucose and lactate at rates higher than those described for mammals; oxidation rates of beta-hydroxybutyrate were lower in rainbow trout brain than those observed for lactate and glucose, and also lower than those described for mammals. Under food-deprivation conditions, glucose and lactate oxidation rates decreased in brains, suggesting the existence of brain metabolic depression, and beta-hydroxybutyrate oxidation rates sharply increased, suggesting increased utilization of ketone bodies.

Direct transfer of rainbow trout to seawater induces several changes in kidney carbohydrate metabolism.

The levels of glycogen and glucose, and the activities of several key enzymes of glycogenolysis, glycolysis, gluconeogenesis and the pentose phosphate shunt were assessed in kidneys of rainbow trout (Oncorhynchus mykiss) of two sizes (80 and 140 g) after transfer to seawater (28 p.p.t.) during 7 days. The results indicated changes, mainly size-independent, in kidney carbohydrate metabolism during transfer of rainbow trout to seawater. An enhanced glycogenolysis and a concomitant increase in gluconeogenic enzyme activity were clearly observed in kidneys of both sizes of animals during transfer to seawater. Changes are suggested to be related to the known role of kidney as a glucose producer tissue thus satisfying, at least in part, the high energetic requirements of the osmoregulatory work performed by other tissues using glucose as fuel, such as the gills, during adaptation to seawater.

Food deprivation and refeeding in Atlantic salmon,Salmo salar: effects on brain and liver carbohydrate and ketone bodies metabolism.

The capacity of carbohydrate and ketone bodies metabolism in brain and liver was evaluated in fed and food-deprived Atlantic salmon (Salmo salar) in a time period covering from 1 to 7 days (Experiment I), and in Atlantic salmon food deprived for 6 weeks, and food deprived for 4 weeks and refed for 2 weeks (Experiment II). The results obtained demonstrate for the first time in a teleost the existence of changes in brain metabolism due to food deprivation. Thus, decreased glucose levels in plasma are reflected in the brain by an increased mobilization of glycogen reserves, and by a decreased glycolytic capacity. Also, ketone bodies appear to increase their importance as a metabolic fuel from day 7 of food deprivation onwards. A possible increase in the gluconeogenic potential in brain simultaneously is not discarded. All these metabolic changes are reversed under refeeding conditions.

Kidney ATPase response in seawater-transferred rainbow trout (Oncorhynchus mykiss). Effect of salinity and fish size.

Two sizes of domesticated rainbow trout (Oncorhynchus mykiss, 40 +/- 0.67 and 180 +/- 3.9 g) were directly transferred to brackish water (9 ppt) and seawater (28 ppt). Kidney Na(+)-K(+)-ATPase and Mg(2+)-ATPase activities were measured in fresh water, and after long-term seawater adaptation (up to 21 days). Renal Na(+)-K(+)-ATPase activity increased after saltwater loading in small trout, while large trout displayed an unmodified ATPase activity. The smallest trout showed a low but progressive increase in renal Mg(2+)-ATPase activity after the transfer to both salinities. However, ATPase activity remained unchanged or significantly decreased in large trout after the transfer to seawater or brackish water, respectively.

Effects of an acute exposure to lindane (gamma-hexachlorocyclohexane) on brain and liver carbohydrate metabolism of rainbow trout.

The capacity of carbohydrate and ketone bodies metabolism in brain and liver was evaluated in rainbow trout control and exposed to lindane (0.05 mg.L-1) for 12 hr. The results obtained demonstrate the existence of changes in several parameters of brain carbohydrate metabolism due to lindane treatment. Thus, increased plasma glucose levels are reflected in brain by the mobilization of glycogen stores and increased lactate levels probably reflecting an increased anaerobic use. Also, ketone bodies appear to be used under this stressful condition. In liver, the main results obtained suggest that glycogen stores are being mobilized to be probably used as glucose in pathways other than glycolysis.

Post-feeding carbohydrate and ketone bodies metabolism in brain and liver of Atlantic salmon.

A study of several pathways of carbohydrate and ketone bodies metabolism was carried out in Atlantic salmon (Salmo salar) to assess the basal metabolism of the brain, and the possible existence of post-feeding changes in brain and liver metabolism. The main results obtained in brain of Atlantic salmon indicate a use of exogenous glucose as a main fuel source since important hexokinase activities were noticed, and brain glycogen levels were usually very low. Several post-feeding changes were observed in brain including an apparent decrease in glycolytic potential, as well as a decreased use of ketone bodies. In contrast, no major post-feeding changes were detected in liver metabolism. A role for ketone bodies as a metabolic fuel in brain of Atlantic salmon is supported by both the high levels of acetoacetate found in brain, and the presence of an active beta-hydroxybutyrate dehydrogenase.