The nutritional and physiological modifications that occur during the weaning period induce adaptations of tissue metabolism in all mammal species. Among the adaptations due to weaning in ruminants, the regulation of lipoprotein lipase (LPL) activity, one of the rate-limiting steps of fatty acid utilization by tissues, was still unknown. The present study aimed at comparing LPL activity and gene expression in the heart, seven skeletal muscles and three adipose tissue sites between two groups of seven preruminant (PR) or ruminant (R) calves having a similar age (170 d), similar empty body weight (194 kg) at slaughter, and similar net energy intake from birth onwards. Triacylglycerol content of adipose tissues was 16 % lower in R than in PR calves, (P<0·01). This could be partly the result from a lower LPL activity (-57 %, P<0·01). LPL mRNA levels were also lower in R calves (-48 % to -68 %, P<0·01) suggesting a pretranslational regulation of LPL activity. Activity and mRNA levels of LPL did not differ significantly in the heart and skeletal muscles except in the masseter in which LPL activity and mRNA levels were higher (+50 % and +120 % respectively, P<0·01) in the R calves. Regulation of LPL in masseter could be explained by the high contractile activity of this muscle after weaning due to solid food chewing. In conclusion, weaning in the calf affects LPL activity and expression in adipose tissues, but not in skeletal muscles except the masseter.

A computational framework to represent nutrient utilization for body protein and lipid accretion by growing monogastric animals is presented. Nutrient and metabolite flows, and the biochemical and biological processes which transform these, are explicitly represented. A minimal set of calibration parameters is determined to provide five degrees of freedom in the adjustment of the marginal input–output response of this nutritional process model for a particular (monogastric) animal species. These parameters reflect the energy requirements to support the main biological processes: nutrient intake, faecal and urinary excretion, and production in terms of protein and lipid accretion. Complete computational details are developed and presented for these five nutritional processes, as well as a representation of the main biochemical transformations in the metabolic processing of nutrient intake. Absolute model response is determined as the residual nutrient requirements for basal processes. This model can be used to improve the accuracy of predicting the energetic efficiency of utilizing nutrient intake, as this is affected by independent diet and metabolic effects. Model outputs may be used to generate mechanistically predicted values for the net energy of a diet at particular defined metabolic states.

Prebiotics are non-digestible food ingredients that target selected groups of the human colonic microflora, thus having the ability to alter the composition towards a more ‘beneficial’ community, i.e. selectively increasing populations of bifidobacteria and/or lactobacilli. In the present study the prebiotic potential of partially hydrolysed guar gum (PHGG) and fructo-oligosaccharides (FOS) in a biscuit was assessed in human volunteers. Fluorescent in situ hybridization using oligonucleotide probes targeting Bacteroides spp., Bifidobacterium spp., Clostridium spp. and Lactobacillus–Enterococcus spp. were used for the bacteriology and total bacteria were enumerated using the fluorescent stain 4′,6-diamidino-2-phenylindole. Thirty-one volunteers consumed daily either three experimental biscuits (providing a total (g/d) of 6·6 FOS and 3·4 PHGG) or three placebo biscuits for two 21-d crossover periods. Bifidobacteria significantly increased in number on ingestion of the experimental biscuits compared with pre-treatment and placebo population levels. Bifidobacterial numbers returned to pretreatment levels within 7 d of the cessation of intake of experimental biscuits. A correlation was observed between the initial faecal bifidobacterial numbers and the magnitude of bifidogenesis, with volunteers who possessed low initial population levels of bifidobacteria experiencing the greatest increase in bifidogenesis. No changes were observed in the other bacterial groups monitored during the trial. Thus, the prebiotic nature of FOS and PHGG was maintained in a final food product as evidenced from the selective increase in bifidobacterial numbers.

The effects of 12 weeks of antioxidant supplementation on exercise-induced oxidative stress were investigated in older adults (60 (SE 1) YEARS; BMI 26 (se 1) kg/m2). Subjects were randomly divided in two groups: supplementation (n 11) with 100 mg dl-α-tocopheryl acetate, 200 mg ascorbic acid, and 2 mg β-carotene, and placebo (n 9). Before and after the 12 week supplementation period, subjects cycled for 45 min at submaximal intensity (50 % maximal workload capacity). Antipyrine was used as marker for oxidative stress. Antipyrine reacts quickly with hydroxyl radicals to form para- and ortho-hydroxyantipyrine. The latter metabolite is not formed in man through the mono-oxygenase pathway of cytochrome P450. Daily supplementation significantly increased plasma concentrations of α-tocopherol and β-carotene in the supplemented group (Δ 14·4 (se 3·2) and 0·4 (se 0·1) μmol/l; P<0·001 and P<0·01). No significant differences, within and between groups, were observed in the exercise-induced increase in the ratios para- and ortho-hydroxyantipyrine to antipyrine. In addition, supplementation did not affect the exercise-induced increase in thiobarbituric acid reactive substances in plasma. In conclusion, in 60-year-old subjects antioxidant supplementation had no effect on the exercise-induced increase in oxidative stress as measured by free radical products of antipyrine.

Statistical analysis of data collected in experimental or observational studies is an important part of nutritional research. If it is not done appropriately, there is a risk that information in the data is lost, or that conclusions are misleading. The present article does not attempt a full review of the subject of statistics, but attempts to list aspects where care is needed.

In an attempt to prevent decreases in piglet 20 : 4n-6 status at birth while increasing 22 : 6n-3 status, multiparous sows (eight per treatment) were allocated to one of three different treatments: a basal diet fed from day 63 of pregnancy to term; basal diet supplemented with tuna oil (17·5 g/kg) from day 63 to day 91 and then basal diet alone from day 92 to term; basal diet alone from day 63 to day 91 and then basal diet supplemented with tuna oil from day 92 to term. Tuna oil supplementation increased mainly 22 : 6n-3 intake. Supplementation with tuna oil between day 92 and term increased 22 : 6n-3 to a greater extent in all piglet tissues (brain, liver, retina and the remaining carcass) at birth than supplementation with tuna oil between days 63 and 91. However, while piglet 20 : 4n-6 decreased to a greater extent in liver and carcass when diets were supplemented with tuna oil between days 92 and term than between days 63 and 91, in the brain and retina, the reverse was true; 20 : 4n-6 was decreased to a greater extent between days 63 and 91 than between 92 and term. The effect of pregnancy nutrition on the growth of piglets until 7 d postweaning (35 d of age) was assessed after removing any residual effects of pregnancy treatment by cross-fostering some piglets at birth. Piglets, the diets of whose dams had been supplemented with tuna oil during pregnancy, grew faster during the first 35 d of life than the progeny of sows fed only the basal diet. Feeding tuna oil to sows at different times during pregnancy therefore did not prevent decreases in piglet 20 : 4n-6 status at birth, but did suggest that changes in piglet brain 20 : 4n-6 status between days 63 and 91 of pregnancy were not reversible by later nutrition. Supplementing the diet of the pregnant sow with tuna oil had beneficial effects on postnatal piglet growth.

We examined the effects of ingestion of five types of insoluble fibre on growth and Zn absorption in rats fed a marginally Zn-deficient diet (6·75 mg (0·103 mmol) Zn/kg diet) with or without added sodium phytate (12·6 mmol/kg diet). The types of insoluble fibre tested were corn husks, watermelon skin, yam-bean root (Pachyrhizus erosus) and pineapple core, and cellulose was used as a control (100 g/kg diet). Body-weight gain in the cellulose groups was suppressed by 57 % by feeding phytate. Body-weight gain in phytate-fed rats was 80 % greater in the watermelon skin fibre and yam-bean root fibre group than that in the cellulose group. Zn absorption ratio in the cellulose groups was lowered by 46 and 70 % in the first (days 7–10) and second (days 16–19) measurement periods with feeding phytate. In the rats fed the phytate-containing diets, Zn absorption ratio in the watermelon skin, yam-bean root and pineapple core fibre groups was 140, 80 and 54 % higher respectively than that in the cellulose group, in the second period. Fe absorption was not suppressed by phytate, however, feeding of these three types of fibre promoted Fe absorption in rats fed phytate-free diets. The concentration of soluble Zn in the caecal contents in the watermelon skin fibre or yam-bean root fibre groups was identical to that in the control group in spite of a higher short-chain fatty acid concentration and lower pH in the caecum. These findings indicate that ingestion of these types of insoluble fibre recovered the growth and Zn absorption suppressed by feeding a high level of phytate, and factors other than caecal fermentation may also be involved in this effect of insoluble fibre.

A computational framework to represent energy utilization for body protein and lipid accretion by growing pigs is presented. Nutrient and metabolite flows, and the biochemical and biological processes which transform these, are explicitly represented in this nutritional process model. A calibration procedure to adjust the marginal input–output response is described, and applied, using reported experimental results, to determine a complete set of parameters for representing energy utilization by growing pigs. A reasonable value for minimum basal energy requirements is also determined. Although model inputs and outputs need not at any time be converted to equivalent energy flows, to facilitate comparison of model response with that of conventional energy-based models, a simple means to estimate energy flows from model-predicted nutrient flows is described. The well-known hierarchy of marginal (biological) energetic efficiencies with which pigs use different classes of nutrients is predicted by the model, based only on simple biological and biochemical principles. The significance of independent diet and metabolic effects on both energetic efficiency and maintenance requirements is examined using model predictions from simulated experiments.

The metabolic effects of feeding soyabean oil instead of an isoenergetic amount of maize starch plus glucose were studied in ponies. Twelve adult Shetland ponies were given a control diet (15 g fat/kg DM) or a high-fat diet (118 g fat/kg DM) according to a parallel design. The diets were fed for 45 d. Plasma triacylglycerol (TAG) concentrations decreased by 55 % following fat supplementation. Fat feeding also reduced glycogen concentrations significantly by up to 65 % in masseter, gluteus and semitendinosus muscles (P<0·05, P<0·01 and P<0·01 respectively). The high-fat diet significantly increased the TAG content of semitendinosus muscle by 80 % (P<0·05). Hepatic acetyl-CoA carboxylase and fatty acid synthase activities were 53 % (P<0·01) and 56 % (P<0·01) lower respectively in the high-fat group, but diacylglycerol acyltransferase activity was unaffected. Although carnitine palmitoyltransferase-I (CPT-I) activity in liver mitochondria was not influenced, fat supplementation did render CPT-I less sensitive to inhibition by malonyl-CoA. There was no significant effect of diet on the activity of phosphofructokinase in the different muscles. The activity of citrate synthase was raised significantly (by 25 %; P<0·05) in the masseter muscle of fat-fed ponies, as was CPT-I activity (by 46 %; P<0·01). We conclude that fat feeding enhances both the transport of fatty acids through the mitochondrial inner membrane and the oxidative capacity of highly-aerobic muscles. The higher oxidative ability together with the depressed rate of de novo fatty acid synthesis in liver may contribute to the dietary fat-induced decrease in plasma TAG concentrations in equines.

The effects of two monounsaturated fatty acid (MUFA)-rich diets, containing virgin olive oil (OO) and high-oleic-acid sunflower oil (HOSO), on development of vascular response from isolated thoracic rat aorta and lipid composition and fatty acid composition were studied and compared with samples from rats fed on a control diet. Dietary MUFA oils were fed for 6 weeks to spontaneously hypertensive (SHR) and Wistar–Kyoto (WKY) rats from 4 weeks of age. The maximum contraction of aortic ring preparations in response to phenylephrine (10-6 M) WAS SIGNIFICANTLY DECREASED IN SHR RATS FED WITH OO (0·81 (sem 0·05) v. 1·18 (sem 0·09) g, P<0·01) and treatment with HOSO did not alter the phenylephrine-induced contractions. The relaxant responses to acetylcholine (10-5 m) were significantly enhanced (30·03 (sem 0·70) v. 18·47 (sem 0·28) %, P<0·001) in the rings from SHR rats treated with OO, and were more pronounced than in WKY rats (P<0·05). In the same way, OO attenuated the dose–response curves induced by phenylephrine (10-8–10-5 m) from SHR rats, accompained with a slower contraction. These results suggest that only the chronic feeding of OO diet was able to attenuate the vascular response of rat aorta. In addition, an increase in phospholipid content (186·7 (sd 3·2) v. 159·1 (sd 11·3) g/kg, P<0·01) and changes in the fatty acid composition of aorta (mainly a decrease in arachidonic acid) could contribute to improving endothelial function. Therefore, the effects can not be attributed exclusively to the content of MUFA (mainly oleic acid). Other components of OO, such as polyphenols, not present in HOSO, may help to explain the vascular protective effect of OO consumption.

It has been suggested that protein synthesis in peripheral tissues: (1) responds in a curvilinear manner to increasing feed intake over a wide range of feeding levels; and (2) has a greater sensitivity to intake than protein breakdown. The aim of the present experiment was to test these hypotheses across the ovine hindlimb. Six growing sheep (6–8 months, 30–35 kg), with catheters in the aorta (two), posterior vena cava and jugular vein, received each of four intakes of dried grass pellets (0·5, 1·0, 1·5 and 2·5×maintenance energy; M) for a minimum of 7 d. A U-13C-labelled algal hydrolysate was infused intravenously for 10 h and from 3–9 h para-aminohippuric acid was infused to measure plasma flow. Arterial and venous plasma were obtained over the last 4 h and the concentrations and enrichments of thirteen 13C-labelled amino acids (AA) were determined by GC–MS. As intake increased, a positive linear response was found for plasma flow, arterial concentrations of the aromatic and branched-chain AA, total flow of all AA into the hindquarters and net mass balance across the hindquarters (except glycine and alanine). Based on two separate statistical analyses, the data for protein synthesis showed a significant linear effect with intake (except for phenylalanine, glycine and alanine). No significant curvilinear effect was found, which tends not to support hypothesis 1. Nonetheless, protein synthesis was not significantly different between 0·5, 1·0 and 1·5×M and thus the 2·5×M intake level was largely responsible for the linear relationship found. There was no significant response in protein breakdown to intake, which supports hypothesis 2.

The regulation of intracellular ascorbic acid (AsA) levels may be under the control of an AsA-specific membrane transporter. The present study investigates AsA uptake and expression of Na-dependent vitamin C transporter (SVCT) mRNA in the mouse osteoblastic cell line, MC3T3-E1. Among eight compounds tested, dexamethasone (Dex) all-trans retinoic acid, transforming growth factor β, prostaglandin E2 and transferrin significantly (P<0·01, P<0·01, P<0·05 and P<0·01 respectively) stimulated the update of AsA into MC3T3-E1 cells. Among these five, Dex was the most active, inducing mSVCT2 mRNA and the uptake of AsA in a time- and concentration-dependant manner. Dex did not induce mSVCT1 mRNA. These results suggest that the Dex-induced stimulation of AsA incorporation into osteoblastic cells is mediated by the induction of mSVCT2. Since Dex reduced alkaline phosphatase activity in MC3T3-E1 cells in our culture conditions, Dex-induced stimulation of AsA incorporation might not be the result of differentiation. Hormone-regulated changes of SVCT expression may have an important role in cell functions.

A low Ca intake by both rats and man increases bone resorption, decreases bone mass and increases the risk of osteoporosis. The skeletal effect of high Ca intakes is less clear, particularly during periods of bone mineral accrual. Twenty-four female 5-week-old rats, Wistar strain, were randomized by weight into three groups of eight rats each and fed ad libitum a semi-purified diet containing 2 (Ca-restricted), 5 (normal) or 20 (Ca-supplemented) g Ca/kg for 3 weeks. When compared with the normal Ca diet, urinary Ca excretion was unaffected by the dietary restriction of Ca for 3 weeks, but was greater (P<0·001) in Ca-supplemented rats. Urinary pyridinoline (Pyr) and deoxypyridinoline (Dpyr) levels were significantly greater during weeks 2 (Pyr P<0·05, Dpyr P<0·001) and 3 (Pyr P<0·01, Dpyr, P<0·001) of dietary Ca restriction, but were unaffected by Ca supplementation. Femoral dry weight and the concentration of Mg and P in femora were unaffected by dietary Ca concentration. Femoral Ca concentration was reduced (P<0·05) in the Ca-restricted group compared with the other two groups. In conclusion, these results suggest that increasing dietary Ca intake, well above the recommended level, had no effect on bone mineral composition or bone resorption (as assessed with urinary pyridinium crosslinks) in young growing female rats. In addition, these results confirm the findings of previous studies which have shown that bone Ca content in young growing rats was reduced by dietary Ca restriction and that this reduction results, at least in part, from an increased rate of bone resorption.

The effects of dietary supplementation with either sucrose or starch (50 g/kg regular food for 2 weeks) on central 5-hydroxytryptamine (5HT; serotonin) release were investigated in freely-moving rats. It has been suggested that the amount of transmitter that serotoninergic neurons release might be altered by food intake. We monitored the effects of sucrose and starch on concentrations of extracellular 5HT, its metabolite 5-hydroxyindoleacetic acid (5HIAA), γ-aminobutyric acid (GABA) and dopamine in the hippocampus, using in vivo microdialysis. The major finding was that baseline levels of extracellular hippocampal 5HT in rats with ad libitum access to food supplemented with sucrose were significantly higher compared with the starch control group. We then verified that sucrose supplementation affected the potency of S(+)fenfluramine to increase hippocampal 5HT levels. In both groups of rats, acute intraperitoneal injection (1 mg/kg) of this anorectic drug induced a response curve of the extracellular hippocampal 5HT levels, with a shape that corresponded with earlier data for different brain areas often using up to 10-fold higher doses of S(+)fenfluramine. Nevertheless, we showed that throughout the experiment the absolute values of the sucrose response curve remained higher than in the starch group. On the other hand, S(+)fenfluramine exerted longer lasting effects in the starch group, as compared with the sucrose group. Significant decreases in levels of extracellular hippocampal 5HIAA levels following S(+)fenfluramine administration were simultaneously observed. A practical implication of the present findings is that dietary sucrose may bias the results of studies investigating brain serotoninergic mechanisms and the effects of (anorectic) drugs interacting with 5HT systems in the hippocampus.

Addition of marine oils containing long-chain n-3 polyunsaturated fatty acids to the diet of pregnant sows may reduce piglet mortality. In previous experiments, when marine oils have been fed to pregnant sows, improvements in piglet tissue 22 : 6n-3 status have been accompanied by potentially undesirable decreases in 20 : 4n-6. The objective of the present experiment was to establish an amount of dietary salmon oil which would enhance piglet 22 : 6n-3 status while minimising reductions in 20 : 4n-6. Twenty-four pregnant multiparous sows were used in the experiment which began on day 60 of pregnancy (gestation length 115 d). To give four diets, salmon oil was added in increasing amounts (0, 5, 10 and 20 g/kg diet) to a basal diet; the diets were made isoenergetic by adding palm oil to each diet to give a total of 20 g oil/kg diet. Diets were offered to the sows in fixed amounts (2·5 kg/d) until parturition. Piglet tissue samples (brain, liver and retina) were obtained at birth before consumption of colostrum. The greatest increase in piglet tissue 22 : 6n-3 proportions occurred between 0 and 5 g salmon oil/kg diet, with only small increases between 10 and 20 g salmon oil/kg diet. In contrast, tissue 20 : 4n-6 proportions declined progressively as the amount of salmon oil fed to the sow increased. In brain, the change in the value 22 : 6n-3/22 : 5n-6 was greatest between 0 and 5 g salmon oil/kg diet, whereas in liver the value increased linearly with added salmon oil. In addition, piglet brain weight (g/kg live weight) increased to a maximum at 10 g salmon oil/kg diet. The optimum amount of supplementary salmon oil in the current experiment, defined as that which gave the greatest response in brain 22 : 6n-3 proportions with minimum reduction in 20 : 4n-6,was 10 g salmon oil/kg diet. This corresponds to an intake of approximately 2·4 g 20 : 5n-3 plus 3·6 g 22 : 6n-3/d or 0·6 % digestible energy.

A method for the measurement of the rate of lipogenesis in ruminants using a continuous intravenous infusion of [1-14C]acetate and measuring the rate of [1-14C]acetate incorporation into adipose tissue lipid was evaluated. Subcutaneous adipose tissue samples obtained by biopsy over the course of a 6 h continuous intravenous infusion of [1-14C]acetate into a wether and a steer maintained in a ‘metabolic steady state’ demonstrated that the incorporation of [1-14C]acetate into subcutaneous adipose tissue lipid was linear for the duration of the infusion period. Subsequent measures of rates of [1-14C]acetate incorporation into adipose tissue lipid were made on adipose tissue samples taken at a single time point during the infusion period. The technique was used to measure rates of lipogenesis in the subcutaneous adipose tissue of fourteen Hereford × Friesian steers that had been fed a pelleted diet of dried grass at a range of metabolizable energy (ME) intakes from 1·1 × ME requirement for maintenance to ad libitum for 11 weeks. Rates of lipogenesis increased linearly (P<0·001) with increasing ME intake. It was concluded that the method is an effective technique for measuring rates of lipogenesis in specific adipose tissue depots in vivo in ruminants.

The effects of increasing levels of Fe on serum fatty acids, cholesterol, triacylglycerol, liver and heart were examined in male Sprague–Dawley rats fed either Fe-deficient or carbonyl Fe-supplemented diets with 35 (control), 350, 3500 and 20 000 μg Fe/g for 12 weeks. As intake of Fe increased, serum total cholesterol increased from 2·0 mmol/l in controls to 5·2 mmol/l at the highest level of Fe. Also, the total serum phospholipid fatty acids increased from 609 mg/dl in controls to 1292 mg/l at the highest level of Fe. Except for the highest dose of Fe, the ratio of saturated to unsaturated phospholipid fatty acids increased from 1·2 to 1·7. The serum total free fatty acid levels remained constant among all groups with a range from 162 to 228 mg/l, while a ratio of 0·6 to 0·8 for saturated to unsaturated fatty acids was maintained. A dose-related increase in liver non-haem Fe from 18 to 3500 μg/g correlated with increases in lipid peroxidation (r 0·87), measured by the lipid-conjugated diene assay. Oxidative changes in the liver may have resulted in alterations in sterol synthesis, leading to increased serum cholesterol levels with increases in serum phospholipids and changes in the ratios of their saturated to unsaturated fatty acids. Animals with heart damage showed myocardial degeneration and cardiomyopathy with haemosiderin in interstitial macrophages or myocardial fibres and, when these were coupled with the findings of increased non-haem Fe in the heart and lipid peroxidation in the liver, suggested that oxidative stress is involved in the pathogenesis of the lesions.