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The effects of constant temperatures on growth, food efficiency, and physiological status were studied in four different batches of juvenile turbot. The growth responses were studied in three experiments lasting 70–85 days under 8–20° C thermal conditions. There was a positive correlation between growth and temperature from 8 to 17° C and a plateau was observed from 17 to 20° C. In fish fed to satiety, specific growth rate was positively correlated to the food intake, which was double at 20° C, compared with 8° C. Minor changes were observed in food efficiency. Body fat deposition decreased as temperature increased (25% lower at 20° C, compared with 8° C). Apparent food conversion, PER (protein efficiency ratio) and PUC (protein utilization coefficient) ranges were 0.8–0.9, 2.1–2.3 and 33–38% respectively. In 70–300 g fish, routine MO2 increased (2.5–6.5 μmol O2 h−1 g bw−1) with temperature up to 20° C, while larger turbot (500–600 g) appeared relatively thermo-independent, with a lower oxygen consumption (1.5 imol h−1 g−1). The average daily total ammonia nitrogen (TAN) and urea-N excretion per fish biomass was positively related to temperature. TAN was 30% lower at 8° C, compared with 20° C. Ingested nitrogen was mainly excreted under the final form of TAN, urea-N representing 26% of the total amount. A post-prandial peak in TAN and a delayed peak in urea-N nitrogen were observed. The hydromineral status [osmolarity, sodium, chloride and potassium blood plasma, gill (Na+-K+)-ATPase activity] of turbot was not affected by progressive changes in temperature during the acclimation period. Juvenile turbots show remarkable homeostatic capacities and so they have a relatively thermo-independent physiology within the range of temperature studied.

Intestinal transport of nutrients coincides with their partial catabolism in the gut. The aim of the present study was to measure intestinal oxygen consumption and nutrient metabolism after a meal or during a short fast. Nutrient and oxygen balances across the small intestine were measured in conscious 50 kg (live wt) pigs. Jejunal enterocytes were also isolated from 1-hr postprandial, postabsorptive, or 3-day fasted pigs, in order to evaluate their capacities to metabolize 5 mM glucose and 2 mM glutamine. Whatever the nutritional state, intestinal oxygen consumption was high, since 26 +/- 2% (n = 6) of the oxygen arterial supply was extracted by the small intestine. Furthermore, the consumption of a mixed meal induced a rapid and transient rise in oxygen consumption. In the postabsorptive state, the intestinal uptake of glucose (0.31 +/- 0.08 mmole/min, n = 6) was twice higher than that of glutamine. The role of glucose as a fuel was also evidenced after a 3-day fast. During nutrient absorption, glutamine was highly utilized, and lactate was produced. The capacity of enterocytes isolated from fed pigs to metabolize glucose was dramatically reduced, as was 6-phosphofructo 1-kinase activity. In contrast, intestinal muscle presented a high glycolytic capacity from glucose, suggesting that the main site of intestinal lactate production during nutrient absorption would be the muscular rather than the epithelial layer.

The intestinal absorption of glucose and alpha-amino nitrogen, the appearance of D-and L-lactic acids in the protal vein and the consumption of oxygen by the organs of the abdominal extrahepatic splanchnic area were studied simultaneously in pigs either during the postprandial period or during a fasting period of the same length. For this purpose, 5 growing pigs (59.4 +/- 3.5 kg live weight) were fitted with permanent catheters in the portal vein and carotid artery and with an electro-magnetic flowmeter probe around the portal vein. This device was used to measure the exchanges between the blood and the intestinal lumen. For a period of 1 wk, the animal received a semi-synthetic diet containing 6% purified cellulose (R6) and then during the next wk, a diet containing 16% purified cellulose (R16), the order of distribution being alternated from one animal to the next. During each of these 2 wk and after a fasting period of 16 h, they were subjected to 2 successive tests of 5 h, either after intake of an 800-g meal (R) (R6 or R16), or after no meal intake (J6 or J16). During these tests, blood samplings were made at 15 to 30-min intervals, the consumption of oxygen was recorded by an ABL3 radiometer and the afore mentioned nutrients and metabolites analysed in these samples. The consumption of oxygen was higher (P > 0.01) during the postprandial period (5.41 +/- 0.19 mmol/kg/h) than during the fasting period (4.64 +/- 0.19 mmol/kg/h) while the availability of oxygen only increased slightly (P < 0.05) (14.01 +/- 0.66 vs 13.08 +/- 0.76 mmol/kg/h). By contrast, the oxygen extraction coefficient did not significantly increase with meal intake. The appearance of L-lactic acid in the portal blood was higher (P < 0.001) during the postprandial period (3.83 +/- 0.32 g/h) than during the fasting period (1.23 +/- 0.23 g/h). The energy expenditure due to the aerobic metabolism of the organs drained by the portal vein ranged from 35.7 to 37.8 kcal/h after meal intake, ie 1-18% more than after fasting. The anaerobic metabolism only represented 0.3-0.4% (fasting) and 1.1-1.3% (postprandial period) of this aerobic metabolism. Oxygen consumption was not changed by the dietary cellulose content.

Weanling male rats, born to dams bred on a diet low in linolenic acid (0.32 g/kg), were fed either the maternal diet or a diet high in linolenic acid (32.2 g/kg) for five months. The n-6 and n-3 polyunsaturated fatty acid (PUFA) contents of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and cardiolipin (CL) of heart and liver mitochondria were strongly influenced by the diet, but neither the total PUFA nor the saturated fatty acid contents of PC, PE and heart CL. Mitochondrial respiratory parameters were hardly affected by linolenic acid intake, indicating that the n-6/n-3 PUFA balance in membrane lipids is not critical for mitochondrial respiration.