Two experiments were carried out with piglets, 3–5 kg live weight, to evaluate the effects of feeding a tryptophan (TRP)-deficient diet for 2 weeks on protein synthesis rates measured in vivo 2 h after a meal. In the first experiment on twenty piglets fed on 250 g protein/kg diets, TRP deficiency (0.77 g/16 g nitrogen) as compared with adequacy (1.17 g/16 g N) significantly decreased feed intake, growth performance and fractional protein synthesis rates (FSR), without variation of RNA in longissimus dorsi (LD) and with parallel increases in RNA in semitendinosus (ST) muscle and liver. In the second experiment thirty-two piglets were tube-fed deficient and adequate diets at the two feeding levels (LF) previously achieved. Both TRP and LF significantly increased growth performance and FSR, but not RNA, in LD and ST muscle, with a trend to a synergy between the two factors (TRP x LF interaction). In another muscle, trapezius (TR), the same interaction was only apparent in RNA content. Among the three muscles it was in LD that FSR was the most responsive to dietary TRP (significant muscle x TRP interaction). In the liver the TRP x LF interaction on FSR and not RNA was the major significant effect, indicating that higher TRP and higher LF were both required to get the maximum protein synthesis rate. At 30 min after a meal the same significant interaction effect was shown on plasma glucose, whilst the higher LF increased plasma insulin with both diets. After a further 30 min the appearance of a similar significant effect of the TRP x LF interaction on plasma insulin resulted from its abatement when the deficient diet had been fed at high LF. These results suggest that dietary TRP deficiency decreased muscle and liver protein synthesis rates in relation to a decrease in the post-prandial release of insulin following a decreased rate of nutrient absorption.

Effects of 24 h mesenteric vein infusion of L-alanine (75 mmol/h) and diet forage: concentrate ratio on net nutrient metabolism by portal-drained viscera (PDV) and liver were measured in four Hereford-Angus heifers. Heifers were fed on diets containing approximately 750 g lucerne (Medicago sativa) or 750 g concentrate/kg every 2 h at similar metabolizable energy intakes in a balanced single reversal design with 6 weeks for diet adaptation. Measurements of blood flow and net metabolism of nutrients were obtained at 30 min intervals starting immediately before (four measurements) and after (five measurements) beginning, immediately before ending (four measurements) and 1.5 h after ending (three measurements) alanine infusion. Only values obtained immediately before beginning and ending alanine infusion were compared statistically. Net total splanchnic (PDV plus liver) release of glucose was greater when heifers were fed on the 750 g concentrate/kg ν. 750 g lucerne/kg diet due to greater net PDV absorption. Net PDV absorption of ammonia-nitrogen, β-hydroxybutyrate (BOHB) and lactate, and net liver and total splanchnic release of urea-N (UN) were greater when heifers were fed on the 750 g lucerne/kg ν. 750 g concentrate/kg diet. Infusion of alanine increased net liver removal of alanine and α-amino-N, net liver release of UN and net total splanchnic release of alanine, UN and lactate. Infusion of alanine decreased net liver release of BOHB and removal of lactate. Mesenteric vein infusion of alanine altered the net availability of precursors for liver glucose synthesis, but did not affect net glucose release by liver in these beef heifers

Intrinsically-labelled foods are required to validate extrinsic-labelling techniques used to study the bioavailability of trace elements. Wheat (Triticum aestivum), peas (Pisum sativum), goat's milk, human milk, eggs and chicken meat were selected for intrinsic-labelling studies with 67Zn. Peas were grown hydroponically in enriched nutrient solution and wheat was grown in sand and watered with enriched nutrient solution. Some of the wheat plants were also given stem injections of 67Zn solution. Eggs and chicken meat were prepared by administering 67Zn intravenously to chickens, and human milk was collected after an oral dose of 67Zn in a cola drink. All the foods investigated were sufficiently enriched with 67Zn for Zn absorption studies except wheat prepared by the sand and water-culture method.

The essential role of taurine in the diet of the cat has been well documented and a deficiency of this nutrient is known to be responsible for a number of clinical conditions. At present, the National Research Council (1986) recommendation for the minimum dietary requirement of the kitten is 400 mg/kg dry matter and for a pregnant cat is 500 mg/kg dry matter. However, these minima were established by feeding the animals on semi-purified diets and, therefore, may be inappropriate for other dietary regimens. The aim of the present study was to investigate the effect of feeding a series of specially prepared diets containing different concentrations of taurine (canned diets 1475–5750 mg/kg dry matter, dry diets 811–1240 mg/kg dry matter) on the plasma taurine concentration of the cat. All diets were fed solus for 6 weeks and plasma taurine concentration was measured every 2 weeks. The results showed that to maintain plasma taurine values in the ‘normal’ range (> 60 μmol/l), a canned diet must supply at least 39 mg taurine/kg body-weight per d and a dry diet at least 19 mg/kg body-weight per d; a cat fed on a semi-purified diet need only achieve a daily intake of at least 10 mg taurine/kg body-weight to maintain an adequate circulating level of taurine. The cause of the reduced availability of taurine from these diets is not yet known. Furthermore, repletion of plasma concentration above 60 μmol/l can be achieved within 2 weeks of feeding an adequate diet.

Twelve lambs, paired on the basis of live weight, were cannulated in the abomasum, in the proximal jejunum approximately 4 m distal to the pylorus and in the terminal ileum. Six were infected with 3000 Trichostrongylus colubriformis and 3000 Ostertagia circumcincta larvae each day for 18 weeks and the remainder were pair-fed to individual infected lambs. All animals were offered ryegrass (Lolium perenne)–white clover (Trifolium repens) pasture, cut daily. Dry matter (DM) intake, live weight, faecal egg concentration, plasma pepsinogen and plasma protein concentrations were measured weekly. During weeks 7 and 17 after commencement of infection, the flow of digesta along the gastrointestinal tract was measured together with enteric plasma loss and true digestion and absorption of 125I-labelled albumin in the small intestine. DM intake was depressed by parasitism, being 1331, (se 70), 423 (se 32) and 529 (se 52) g/d during weeks 3, 7 and 17 respectively. The flow of nitrogen at the proximal jejunum and in faeces was increased by parasitism during week 7 and at the abomasum and ileum during week 17. Plasma protein-N loss (g/d) into the gastrointestinal tract was 0.68 (se 0.091) and 1.97 (se 0.139) during week 7, and 0.85 (se0.158) and 1.96 (se 0.396) during week 17, in control and infected sheep respectively. True digestion and absorption of albumin in the proximal small intestine, the site of infection, was very low (mean 0.08) and was not affected by parasitism. Between the abomasum and terminal ileum absorption of albumin was high (mean 0.87) and again was not affected by parasitism. It was calculated that of the total increase in endogenous protein passing from the ileum tract as a result of infection, plasma protein comprised only a small percentage (10–36%). The major proportion of digestion and absorption of protein occurred in the distal small intestine beyond the site of infection and was not affected by infection.

A variety of foods (peas (Pisum sativum), chicken meat, eggs, goat's milk, human milk) enriched with the stable isotope 67Zn were prepared by means of intrinsic- and extrinsic-labelling procedures. They were fed to rats and apparent absorption of 67Zn determined from faecal excretion measurements using thermal ionization mass spectrometry. There were significant differences in the absorption of the extrinsic and intrinsic label which differed in magnitude between the foods tested. The extrinsic 67Zn was less well absorbed in peas, chicken meat, eggs, and human milk than intrinsic 67Zn, but in goat's milk the extrinsic 67Zn was better absorbed than the intrinsic label. These results demonstrate that extrinsically-added stable Zn isotopes do not fully exchange with endogenous Zn in many foods, and illustrate the need for caution when using extrinsic labels for Zn bioavailability studies.

Intravenous infusion of L-[3H] phenylalanine (Phe) was carried out for 8 h in dry, non-pregnant and lactating dairy goats. Nitrogen balance was positive in the dry group and negative in the lactating group. Whole-body Phe flux was 50% greater in lactating goats (P < 0.01). Fractional synthesis rates (Ks) of tissue proteins were estimated from plasma- (Ksp) and tissue- (Ksh) specific radioactivities of Phe. In lactating goats, Ksp for mammary gland, duodenum and diaphragm was increased (P < 0.05). Ksp also tended to increase in liver, kidney and rumen (P < 0.08) of lactating goats, but was not different in uterus, spleen, caecum or heart. Values of Ksh were higher than Ksp; however, these measures agreed qualitatively. When absolute rates of protein synthesis were calculated, an increased contribution of mammary and visceral organs was seen in lactating goats. Ks and absolute rates of protein synthesis of hind-limb skin were less in lactating goats (P < 0.05). A decreased proportion of skeletal muscle (P < 0.01) and decreased Ks resulted in lower absolute synthesis of hind-limb muscle protein in lactating animals (P < 0.05). Decreased rates of muscle and skin protein synthesis would appear to participate in alterations of protein metabolism, permitting lactation to occur at the expense of body reserves.

Linoleic acid (LA) transport in rats with experimental short-term and long-term renal failure (RF) was compared with that of sham-operated normal animals on liberal food intake and pair-fed animals. The perfusions in vivo and incubations in vitro were conducted using a micellar solution containing a wide range of LA concentrations. Both absorption in vivo and uptake in vitro of LA were significantly reduced in animals with short-term RF. Lipid extraction and separation by thin-layer chromatography revealed a marked LA trapping as trilinolein (TL) in the perfused intestinal tissue in the short-term RF group. The esterification process, as defined by the rate of LA incorporation into TL, was moderately reduced in short-term RF animals. The thickness of the unstirred water layer showed no significant difference among the groups studied. In contrast, animals with long-term RF exhibited normal absorption of LA in vivo at all concentrations tested. In conclusion, LA absorption is reduced in short-term RF and restored in long-term RF. Several steps including LA transport into and TL transport out of the enterocyte and the esterification process were impaired in short-term RF. These changes are not due to alteration in the unstirred water layer, anorexia, weight loss or a rapid effect of uraemic chemical environment or circulatory factors.

Male broiler chicks (1-d-old; Ross one) were given either a control diet containing recommended levels of phosphorus, calcium and cholecalciferol or experimental diets low in P and with variable levels of Ca (normal and low) and cholecalciferol (normal or high). The low-P diet with normal levels of Ca and cholecalciferol induced a hypophosphataemia and a hypercalcaemia which was reflected in reduced tibia length and weight and in reduced Ca, P and magnesium contents of tibia. The phytate digestibility remained normal while the retention of P and Ca fell significantly. The lowering of Ca alone elevated phytate digestibility and restored P and Ca retention. The hypercalcaemia and hypophosphataemia remained and tibia mineralization remained impaired. The raising of cholecalciferol alone dramatically increased phytate digestibility and the retention of Ca and P. While this remedied the hypercalcaemia, the hypophosphataemia persisted as did the diminution of tibia weight. The simultaneous lowering of dietary Ca and elevation of cholecalciferol on low-P diets restored all variables to the levels for the control diet. Circulating levels of 1,25-dihydroxycholecalciferol were significantly elevated by low-P diets, more so with high cholecalciferol intakes. However, Ca did not influence 1,25-dihydroxycholecalciferol levels in plasma

The effects of salt (sodium chloride) supplementation of rat diets (80 g/kg diet), with or without lactose (150 g/kg), were studied in weanling rats over 14 d. Dietary salt increased water intake and reduced weight gain and food conversion efficiency, but these variables were unaffected by lactose. Salt-supplemented rats exhibited a three- to fivefold increase in urinary calcium excretion and a small increase in urinary magnesium and phosphorus excretion, irrespective of dietary lactose content. In addition, salt supplementation reduced plasma alkaline phosphatase (EC 3.1.3.1) activity. Lactose increased urinary Ca and Mg excretion and plasma Ca and P concentrations. Salt reduced tibia mass but not tibia mass expressed relative to body-weight, but neither variable was affected by lactose. Both tibia Mg content and concentration were reduced by salt but unaffected by lactose, and neither tibia P content nor concentration was affected by salt or lactose. Tibia Ca content was reduced by salt but this was prevented by lactose. Tibia Ca concentration was unaffected by salt or lactose, although there was a reduction (not significant) in tibia Ca concentration in animals fed on the lactose-free diet. These results show that lactose had no independent effect on bone and that reduced accretion of bone mass and mineral content in rats fed on the high-salt diets was due, at least in part, to reduced growth. Failure to offset sodium-induced hypercalciuria by a compensatory increase in net Ca absorption may have contributed to reduced bone Ca accretion. The protective effect of lactose against reduced bone Ca accretion may be due to increased Ca absorption.

By using the isotopic equilibrium method in the young male Syrian hamster, the rates of cholesterol turnover processes, i.e. dietary cholesterol absorption, cholesterol synthesis, cholesterol excretion in the faeces and urine and cholesterol transformation into bile acids, were determined in the hamster receiving a control (C) or a lithogenic diet (L) for 7 weeks. At the end of this period the gall bladder of all animals in group L contained cholesterol gallstones. The coefficient of dietary cholesterol absorption was reduced by 26 %, cholesterol synthesis and cholesterol faecal excretion were twofold higher in group L than in group C. Bile acid content in the small intestine was diminished in group L, but bile acid composition was similar in the two groups. The increase in cholesterogenesis in lithiasic animals essentially took place in the liver. Bile acid biosynthesis did not significantly differ in the two groups, but represented only 35 % of total cholesterol input (dietary absorption + internal secretion) in group L ν. 52% in group C. Thus, in the lithiasic hamster, hepatic synthesis of cholesterol and bile acids are not coupled. The molar percentage of cholesterol in bile was twofold higher in group L than in group C but those of bile acids and of phospholipids were not modified. In the lithiasic hamster the specific activity of biliary cholesterol was similar to that in plasma and liver. Consequently, biliary cholesterol does not derive directly from cholesterol newly synthesized in the liver but from hepatic cholesterol rapidly exchangeable with plasma cholesterol.

Sodium selenite and selenomethionine were investigated as possible causative factors for the induction of Degnala disease syndrome in twelve buffalo (Bubalus bubalis) calves divided into three groups of four. Group 1 was the control group and received no additional selenium. Sodium selenite and selenomethionine were given daily as intramuscular injections on a selenium-equivalent basis, with a weekly increment in the dose of 0.05 mg Se/kg live weight from 0.05 to 0.20 mg Se/kg live weight per day, in groups 2 and 3 respectively. Only one animal from group 3 manifested the lesions of Degnala disease. The blood Se concentration and erythrocyte glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity were both greater in groups 2 and 3 than in control group 1. The overall blood Se concentration was 0.22 (se 0.01), 0.38 (se 0.12) and 0.77 (se 0.20) μg Se/ml in groups 1 to 3 respectively with corresponding GSH-Px activities of 63.84 (se 7.38), 88.37 (se 12.38) and 165.32 (se 40.62) enzyme units/mg protein. Erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2) activity was not affected by treatment but reduced glutathione content was lower in groups 2 and 3. Liver adenosylmethionine, estimated at autopsy, was lowest (22.87 (se 6.17) μmol/g) in group 3, and greatest (102.63 (se 9.39) μmol/g) in group 1 (P < 0.01). Organic Se sources seemed to accumulate in tissues more than inorganic sources, and might be the causative toxic factors of Degnala disease.

Hemicellulose consists primarily of pentose sugars, joined together in a polysaccharide chain with d-xylose as the most abundant component. Ileal digestibility and urinary excretion of d-xylose and associated effects of this pentose sugar on ileal and faecal digestibility of dry matter (DM), organic matter (OM), gross energy (GE) and nitrogen were studied in pigs. Castrated pigs were prepared with a post-valvular T-caecum cannula to measure ileal digestibility. Faecal digestibility was measured in non-cannulated pigs. d-xylose was given at dietary inclusion levels of 100 and 200 g/kg, and the control sugar, d-glucose, at a rate of 200 g/kg diet. Ileal digestibility of d-xylose as well as that of d-glucose was found to be close to 100%. The presence of d-xylose in the diet decreased ileal digesta pH and increased ileal flow of volatile fatty acids, suggesting the occurrence of microbial degradation of d-xylose in the pig small intestine. In pigs fed on the 100 g d-xylose/kg diet, 44.5% of the d-xylose intake appeared in the urine. This percentage increased significantly to 52.6 when pigs were fed on the 200 g d-xylose/kg diet. Ileal and faecal digestibility of DM, OM, GE and N, as well as N retention, decreased significantly in pigs fed on the 200 g d-xylose/kg diet.

The effects of magnesium or zinc deficiency on growth, tissue contents of Mg or Zn and protein synthesis have been compared in 4–13-week-old rats. When maintained on Mg-deficient fodder (1.6 mmol/kg) or Zn-deficient fodder (27 μmol/kg) rats showed a reduced weight gain, whereas repletion caused increased growth rates. Pair-feeding experiments showed that this could not be attributed to reduced energy intake only. In rats maintained on Mg-deficient fodder for 14 d [3H]leucine incorporation into skeletal muscle and the heart was reduced by 24–38% compared with pair-fed controls (P <0.001–0.002). The incorporation of [3H]phenylalanine was reduced by 19–31%. Tissue Mg contents, however, were only reduced by 6–7% (not significant). The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib. fed animals. In rats maintained on Zn-deficient fodder for 15 d [3H]leucine incorporation into skeletal and heart muscle was reduced by 57–64% compared with pair-fed controls. The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib. fed animals. In the Zn-deficient animals the content of Zn was not reduced in the skeletal muscles, whereas there was a small (15%) but significant loss of Zn in the heart. In another experiment, Zn depletion for 17 d caused a reduction in [3H]leucine incorporation of 35–41 %. After 5 d of Zn repletion this defect was restored, and the [3H]leucine incorporation was above control level in the skeletal muscles. It is concluded that the intact organism is very sensitive to dietary Mg or Zn deficiency, and that the reduced growth and protein synthesis cannot easily be attributed to the reduction of tissue Mg or Zn content per se. This points to the existence of other control mechanisms mediating down-regulation of growth and protein synthesis in response to reduced dietary supplies and the ensuing drop in the plasma concentrations of Mg and Zn.

Glycogen synthase (GS) activity was characterized in rat brown adipose tissue (BAT) and the activity was found to be much higher than that in white adipose tissue. Prolonged starvation had no effect on the active form of GS, as found in the liver and muscle. The GS activity was similar in BAT of rats housed in an animal room (21+± 1°) whether they were fed on high-carbohydrate, high-fat, or stock diets. Acclimatizatioin of rats to cold (4+± 1°) for 2 weeks significantly increased GS activity. This increase in the cold was fivefold greater when rats were fed on high-carbohydrate diets than in control rats at room temperature fed on an identical diet. The increase was accompanied by a large accumulation of glycogen in BAT. It was concluded that GS may play an important role in BAT and may contribute to the control of blood glucose in a cold environment. Its relevance to thermogenesis requires further elucidation.

The aim of the present work was to show that cottonseed flour introduced into rehabilitation diets is not nutritionally harmful. The cottonseed flour obtained from glandless seeds contains traces of gossypol. As gossypol is known to have pathological hepatic and testicular actions, the effects on hepatic variables and on the histological appearance of liver and testis of diets containing cottonseed flour were compared with those without cottonseed flour. Seventy growing male Wistar rats were divided into two groups. The control group (C) received a balanced diet (200 g casein+3 g methionine/kg) for 78 d and the experimental group was fed on a low-protein diet (20 g casein+3 g methionine/kg) for 29 d. After the period of protein deprivation, the depleted rats were divided into four groups and each group was refed with a different diet, for 49 d: a balanced diet (200 g casein+3 g methionine/kg; rC), maize–soya-bean flour–milk (60:30:5, by wt; MSM), maize–cottonseed flour–milk (60:30:5, by wt; MCM) or rice–cottonseed flour–milk (60:30:5, by wt; RCM). Each diet was supplemented with a vitamin mixture (10 g/kg) and a salt mixture (40 g/kg). In the liver, protein, total lipid, fatty acid composition and nucleic acid contents were determined after 29 d of protein deprivation and after 2, 14, 29, 49 d of refeeding. The refeeding of rats with either diet MSM or RCM promoted a higher growth than that with diet MCM or diet rC. In all groups, a progressive decrease in relative liver weights with age was observed. The highest values were obtained with diets rC and MSM. After 49 d of refeeding, the lowest values for lipid, DNA and protein: RNA and the highest values for RNA and RNA:DNA were obtained with the cottonseed diets (MCM and RCM). Rats fed on the cottonseed-flour diets for a 49 d period after severe protein malnutrition showed no change in size or shape of their hepatocytes compared with those obtained with the control casein diet, and all stages of spermatogenesis occurred normally and spermatozoa were accurately formed. Therefore, our findings show that a low level of gossypol administrated during 49 d, even to an organism weakened by protein malnutrition, does not affect hepatic variables and the histological appearance of liver and testis.

The effect of protein deprivation on plasma concentration of insulin-like growth factor-binding proteins (IGFBP) was studied in rats. A significant decrease in the concentration of IGFBP of molecular weight (mass) approximately 40 kDa was observed in protein-deprived rats. There was no prominent effect of protein deprivation on the concentration of IGFBP with molecular weights of about 30 kDa or 22–24 kDa. The binding capacity to plasma IGFBP of exogenously-added 125I-labelled insulin-like growth factor-1 (125I-IGF-1) was also studied. IGFBP of molecular weight about 30 and 22–24 kDa (the native form of this protein is presumed to be 29 kDa) in protein-deprived rat plasma bound more 125I-IGF-1 than those in protein-fed rat plasma. This suggested that these IGFBP in protein-deprived rat plasma are relatively unsaturated by endogenous IGF-1. The response of IGFBP to protein deprivation which was elucidated in the present investigations add further evidence to our previous assumption that IGFBP play an important role in protein nutrition.

Nutritional deficiencies of magnesium or zinc lead to a progressive and often marked growth retardation. We have evaluated the effect of Mg and Zn deficiency on growth, serum insulin-like growth factor-1 (s-IGF-1), growth hormone (s-GH) and insulin (s-insulin) in young rats. In 3-week-old rats maintained on Mg-deficient fodder for 12 d the weight gain was reduced by about 34%, compared with pair-fed controls. This was accompanied by a 44% reduction in s-IGF-1, while s-insulin showed no decrease. After 3 weeks on Mg-deficient fodder, growth had ceased while serum Mg (s-Mg) and s-IGF-1 were reduced by 76 and 60% respectively. Following repletion with Mg, s-Mg was completely normalized in 1 week, and s-IGF-1 reached control level after 2 weeks. Growth rate increased, but the rats had failed to catch up fully in weight after 3.5 weeks. Absolute and relative pair-feeding were compared during a Mg repletion experiment. Absolute pair-fed animals were given the same absolute amount of fodder as the Mg-deficient rats had consumed the day before. Relative pair-fed animals were given the same amount of fodder, on a body-weight basis, consumed in the Mg-deficient group the day before. In a repletion experiment the two methods did not differ significantly from each other with respect to body-weight, muscle weight, tibia length and s-IGF-1, although there was a tendency towards higher levels in the relative pair-fed group. The peak in s-GH after growth hormone-releasing factor 40 (GRF 40) was 336 (se 63) μg/l in 5-week-old rats that had been Mg depleted for 14 d, whereas age-matched control animals showed a peak of 363 (se 54) μg/l (not significant).

In 3-week-old rats maintained on Zn-deficient fodder for 14 d weight gain was reduced by 83% compared with pair-fed controls. Serum Zn (s-Zn) and s-IGF-1 were reduced by 80 and 69% respectively, while s-insulin was reduced by 66%. The Zn-deficient animals showed a more pronounced growth inhibition than that seen during Mg deficiency and after 17 d on Zn-deficient fodder s-IGF-1 was reduced by 83%. Following repletion with Zn, s-Zn was normalized and s-IGF-1 had increased by 194% (P <0.05) after 3 d. s-IGF-1, however, was not normalized until after 2.5 weeks of repletion. Growth rate increased but the catch-up in weight was not complete during 6 weeks. The maximum increase in s-GH after GRF 40 was 774 (se 61) μg/l in control animals ν. 657 (se 90) μg/l in 6-week-old rats that had been Zn-depleted for 12 d (not significant). In conclusion, both Mg and Zn deficiency lead to growth inhibition that is accompanied by reduced circulating s-IGF-1, but unchanged s-GH response. Zn deficiency, but not Mg deficiency, caused a reduction in s-insulin. The reduction in s-IGF-1 could not be attributed to reduced energy intake, but seems to be a specific effect of nutritional deficiency of Mg or Zn. It is suggested that the growth retardation seen during these deficiency states may be mediated through reduced s-IGF-1 production.

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial β-oxidation was unaffected and peroxisomal β-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC 1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and glutathione peroxidase (EC 1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC 3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.

Plasma corticosterone clearance in anaesthetized rats was measured from the disappearance of radioactivity after a bolus injection of [3H]corticosterone. Mean fractional clearance rates were significantly (P < 0.05) reduced after a 48 h fast, by 32 and 22% for males and females respectively. Plasma corticosterone concentrations were increased by fasting in both sexes. Corticosterone secretion rates, calculated as the product of fractional clearance and plasma corticosterone concentration, did not differ between fed and fasted groups in either sex. The mean activity (U/liver) of the rate-limiting enzyme for corticosterone degradation, hepatic 4,5-dihydrocorticosterone:NADP+ Δ4-oxidoreductase, was significantly reduced by 51 and 78% after fasting in males and females respectively. This was due to changes in both the soluble and microsomal forms of the enzyme. The binding capacity of corticosterone-binding globulin in plasma was significantly reduced by fasting in females (P < 0.001), but was not altered in males. The results suggest that reduced hormone clearance is the dominant cause of fasting hypercorticosteronaemia in the rat.