There is little age-specific information on changes in dietary intake over time in this country, yet this is valuable in assessing the effectiveness of health education programmes particularly in vulnerable groups such as adolescents. In 1990, 379 children aged 12 years completed two 3 d dietary records. They were interviewed by one dietitian on the day after completion of each diary to verify and enlarge on the information provided and, with the aid of food models, obtain a quantitative record of food intake. Nutrient intake was calculated using computerized food tables. These children attended the same seven Middle schools in Northumberland as 405 children of the same age who recorded their diet using the same method, 10 years previously. Heights and weights were also recorded in both studies in the same manner. Comparing the nutrient intakes in 1990 with 1980, energy intake fell in the boys (to 8.6 MJ) but not in the girls (8.3 MJ). The contribution of fat to energy intake was unchanged at about 40% (about 90 g/d). Likewise, intake of sugars was unchanged at about 22% of energy (about 118 g/d). Calcium intake remained the same in the girls (763 mg/d in 1990) but fell in the boys (786 mg/d in 1990). Iron, vitamin C and unavailable carbohydrate intakes increased in both sexes, and the nutrient density of the diet improved in all sex and social-class groups. However, a social trend evident in 1980 still existed in 1990 with low social groups having the poorest-quality diet. It is concluded that there is little evidence of substantial progress towards improving the diet of adolescents in this country.

A computational method for constructing individually acceptable diets by modifying a chosen diet to meet nutritional requirements is described. The effects on food quantities of imposing different nutrient requirements on a sample diet are demonstrated and techniques which can ensure the acceptability to the individual of the modified diet are described. The starting point in the calculation is the person's current dietary intake. This is modified using linear programming methods which make the smallest changes to the food quantities to meet specific targets. Sequential modification can be used to identify changes that are acceptable to the individual. The computer program has been developed in collaboration with practising dietitians and is in use in some leading UK hospitals.

Yellow discoloration often develops in rice kernels during post-harvest storage, due possibly to fungal activity. The present study examined the changes in nutrient composition taking place during yellowing of rice, and the effects of feeding rats and broiler chicks on a moderately yellow rice at 600 g/kg diet. Nitrogen content was found to be higher in rice grains that had become more yellow, only part of the increase being in non-protein-N; however, relative to crude protein (N x 6.25) the concentrations of lysine, methionine, cystine and arginine were lower. There were no significant differences between white and yellow rice in the food intake, weight gain and efficiency of food utilization (EFU) of rats and chicks when diets were formulated to contain similar nutrient concentrations, or the same basal ingredient composition. Diet pelleting increased food intake and weight gain in both animal species, but reduced dry matter and energy digestibility in rats; effects on nutrient retention in chicks were largely non-significant. Liver weights of rats and chicks and pancreas weights of chicks were unaffected by yellow rice; however, chicks fed on mash had a larger pancreas on average than those fed on pellets. Thus, whilst the nutrient composition of rice is altered during yellowing, a moderately yellow rice is unlikely to produce major adverse effects when fed to rats and broiler chicks.

Tissue-specific alterations in insulin sensitivity occur in response to fasting and refeeding, as part of the integrated adaptive mechanisms employed to adjust to major changes in nutritional status. In the present study the effects of fasting and refeeding on insulin-receptor, actin and myosin mRNA levels in skeletal muscle, and insulin-receptor and uncoupling-protein mRNA in brown adipose tissue of rats have been examined. Insulin-receptor mRNA levels increased markedly in both skeletal muscle and brown adipose tissue after a 40 h fast, the increase being greater in brown fat (8-fold) than in muscle (2-fold). On refeeding for 4 h, the insulin-receptor mRNA level in both tissues declined rapidly to control levels. An increase in insulin-receptor mRNA level was also observed in brown adipose tissue after a 16 h fast, although not in skeletal muscle. In contrast to the insulin-receptor mRNA, the level of the mRNA for the mitochondrial uncoupling protein declined markedly in brown adipose tissue during a 40 h fast. These results indicate that insulin-receptor mRNA levels are modulated in response to the alterations in nutritional status that occur during fasting and refeeding; this may reflect a nutritional influence on transcription of the receptor-protein gene

The objective of the present study was to examine the influence of energy supplementation and its cessation thereafter on the basal metabolic rates (BMR) of chronically undernourished individuals. Seven apparently healthy males were supplemented daily with 3.35 MJ (15 g protein, 35 g fat, 105 g carbohydrate) for 12 weeks. The average gain in body-weight was 1.9 kg (body fat, 58%; fat-free mass (FFM), 42%). The rise in BMR exceeded that accounted for by the increases in FFM during the 12 weeks of supplementation and was attributed to increases in the amount and activity of the visceral tissue as well as to an added cost of lipogenesis. At 12 weeks after cessation of the supplement, body-weights and FFM had decreased to presupplementation levels. BMR at this stage were significantly lower than at the 12th week of supplementation, when expressed per kg FFM or when adjusted for FFM using an analysis of covariance. These results suggest an increase in the metabolic efficiency during this negative energy balance period. The study demonstrates that, in the chronically undernourished, the changes in BMR are reversible and, hence, physiologically important to the process of adaptation to low-energy intakes.

The objective of the present experiment was to define the form of the relationship between varying levels of energy intake at constant, high protein intake and the performance of young pigs. By doing so it was expected that we could distinguish between four models that predict the pig's responses to its diet as rates of protein and lipid retention. Forty young pigs were assigned at 12 kg live weight either to an initial slaughter group (n 8) or to one of four allowances of starch intake at a constant intake of a high-protein feed (with 345 g crude protein (nitrogen x 6.25)/kg food). Half the pigs were killed after 4 weeks and half after 8 weeks on the treatments; at each slaughter point on each treatment half the pigs were entire males and half were females. Increasing the intake of starch (energy) resulted in significant increases in the rates of live weight, empty-body, protein and lipid gains of pigs slaughtered at both stages. There was no minimum positive lipid: protein ratio in the gain of the pigs. Male pigs deposited more protein and less lipid than females but this effect of sex on protein and lipid retention was seen only on the two highest allowances of starch intake. The calculated efficiency of protein utilization increased with increasing starch intake up to a maximum of 0.81, when probably the energy: protein in the diet became non-limiting. The results led to the rejection of two of the models that predict the rates of protein and lipid retention as responses to protein and energy intake, but the two remaining models could not be rejected, at least qualitatively.

The objective of the experiment was to define the form of the relationship between varying levels of protein and energy intake and the performance of young pigs. Forty-four young pigs were assigned at 12 kg live weight for 6 weeks either to an initial slaughter group (n 8) or to one of the nine feeding treatments (n 4); three allowances of a high-protein food with 355 g crude protein (nitrogen × 6.25; CP)/kg (P1, P2, P3) at three levels of feeding (L, M and H). Each feeding level was met by supplementing the allowance of feed P with the appropriate amount of starch and each treatment had two males and two females. The rate of protein deposition was not affected by feeding level at the two lowest allowances of basal feed P (P1 and P2), but it increased with increasing the feeding level for the pigs on treatment P3. Males deposited more protein than females, but this effect was more pronounced with treatment P3. The rate of lipid deposition increased with each increase in the level of feeding and decreased with increasing the allowance of feed P. The calculated efficiency of protein utilization (ep) was expressed as a function of the energy: protein ratio in the feed (MJ metabolizable energy/kg digestible CP). The best model to describe the relationship was a linear-plateau model, with the maximum value for ep of 0.814 at 73 MJ/kg. This relationship provided the basis of a model that could predict the response of a growing pig to its diet as rates of protein and lipid retention

The effects of protein restriction on Δ9 desaturase (EC 1.14.99.5) activity were studied in growing rats. A control group was fed on a balanced diet (200 g casein/kg; BD) for 28 d. The experimental group was fed on the low-protein diet (20 g casein/kg; LP) for 26 d, then refed the balanced diet (BD-R) for 2 d. Rats were born to and suckled from normally fed dams. The enzyme activity was measured after 2 and 14 d of LP, and 26 d of LP plus 2 d of BD-R, by incubations in vitro of hepatic microsomal pellets with [1-14C]stearic acid. The results indicated a decreased Δ9 desaturase activity after 2 and 14 d of LP of -33 and -43% respectively. Refeeding for 2 d was sufficient to super-repair this activity (+ 66%). The fatty acid composition of total liver lipids and microsomal phosphatidylethanolamines (PE) and phosphatidylcholines (PC) were also investigated; 18:0 decreased in total liver lipids at 14 d of LP, when 18:1n-9 increased. Stearic acid (18:0) increased in PC at 2 d of LP and in PE at 14 d of LP; oleic acid (18:1n-9) did not change. Therefore, it is concluded that a defect occurred in the bioconversion of 18:0 into 18:1n-9 by Δ9 desaturation during protein depletion. As oleic acid is accumulated in total liver lipids during LP, we speculate that this is due to a decreased oxidation or transport of this fatty acid

The effects of zero-erucic acid rapeseed oil and rapeseed oil-containing margarine on plasma fatty acid composition and serum cholesterol were studied in butter users (n 43). Compliance to the substitution was followed by fatty acid analysis of total plasma and plasma phospholipids. The amount of substitute fats represented, on average, 21% of total fat and 8% of total energy intake. Changes in the relative fatty acid composition of plasma phospholipids indicated further fatty acid metabolism, and were closely related to the serum cholesterol level. The reduction in saturated fatty acids led to a significant increase in the proportion of n-3 and n-6 polyunsaturated fatty acids (PUFA) with the rapeseed oil diet, whereas the margarine caused a significant rise in n-6 PUFA only. The increase in the proportions of the two PUFA families occurred in accordance with their competitive order, most completely with the rapeseed oil diet. When butter was replaced by rapeseed oil, low-density-lipoprotein-cholesterol decreased by an average of 9.1% without a reduction in high-density-lipoprotein-cholesterol. During margarine substitution the reduction was 5.2%, on average. Of the plasma phospholipids, α-linolenic acid and the linoleic:stearic acid ratio, but not oleic acid, were the components most significantly correlated with serum cholesterol levels or the decrease in these levels. The results show that rapeseed oil can act primarily as a source of essential fatty acids, rather than that of monoenes, in the diet of butter users.

The present study reports results from two investigations to determine effects of a 6-week period of moderate n-3 fatty acid supplementation (2.7 g/d) on fasting and on postprandial triacylglycerol and metabolic hormone concentrations in response to standard test meals. In the first study postprandial responses were followed for 210 min after an early morning test meal challenge; in the second study responses to an evening test meal were followed during the evening and overnight for a total period of 12 h. In both studies postprandial triacylglycerol responses to the test meals were significantly reduced after compared with before fish-oil supplementation. In the second study the triacylglycerol peak response seen between 200 and 400 min in subjects studied before supplementation with fish oils was almost completely absent in the same subjects after 6 weeks of n-3 fatty acid supplementation. Analysis of fasting concentrations of metabolites and hormones was carried out on the combined data from the two studies. There were no significant differences in total, low-density-lipoprotein- or high-density-lipoprotein-cholesterol concentrations during fish-oil supplementation, although there was considerable individual variation in cholesterol responses to the supplement. Concentrations of Apo-B and Apo-A1 were unchanged during supplementation with fish oils. Fasting and early morning postprandial GIP concentrations were lower in subjects taking fish oils, possibly due to acute effects of fish-oil capsules taken on the evening before the studies. In both studies fasting insulin and glucose and postprandial insulin concentrations remained unchanged following fish-oil supplementation. The results do not support the view that triacylglycerol-lowering effects of n-3 fatty acids are due to modulation of insulin secretion mediated via the enteroinsular axis. Further studies are required to determine the precise mechanism by which fish oils reduce both fasting and postprandial triacylglycerol concentrations.

Indian River male broiler chickens growing from 7 to 28 d of age were fed on diets containing energy: protein values varying from 43 to 106 MJ/kg protein and containing 0 or 1 mg triiodothyronine (T3)/kg diet to study effects on growth, metabolic hormone concentrations and in vitro lipogenesis. In vitro lipid synthesis was determined in liver explants in the presence and absence of ouabain (Na+, K+-transporting ATPase (EC 3.6.1.37) inhibitor) to estimate the role of enzyme activity in explants synthesizing lipid. Growth and feed consumption increased (P < 0.01) when the energy: protein value decreased from 106 to 71 MJ/kg protein; however, both variables decreased as the value was further decreased from 53 to 43 MJ/kg protein. Triiodothyronine depressed (P < 0.01) growth, but not food intake. Large energy:protein diets (> 53 MJ/kg protein) and dietary T3 lowered (P < 0.01) plasma growth hormone. Large energy:protein diets (> 53 MJ/kg protein) increased (P < 0.01) lipogenesis, plasma growth hormone (GH) and decreased plasma insulin-like growth factor 1 (IGF-1). Also, T3 decreased plasma GH, IGF-1 in vitro lipogenesis. Ouabain inhibited a greater proportion of in vitro lipogenesis in those explants synthesizing fat at a high rate. Both dietary T3 and in vitro ouabain decrease lipogenesis, but, when combined, the effects are not cumulative

Thirty-eight male volunteers participated in a double-blind cross-over trial evaluating the effect of replacing the usual sources of saturated fat in the Dutch diet (animal fats and hydrogenated oils) by palm oil, which is virtually free of cholesterol and trans-fatty acids, on serum lipids, lipoproteins and apolipoproteins. Maximum (about 70%) replacement had no significant effect on serum total cholesterol or most lipoprotein fractions, but resulted in an 11% increase in serum high-density-lipoprotein (HDL)2-cholesterol relative to the control (P2 = 0.01). The palm-oil diet also caused an 8% decrease in low-density-lipoprotein (LDL):HDL2+HDL3-cholesterol ratio (P2 = 0.02) as well as a 9% decrease in triacylglycerols in the low-density-lipoprotein fractions (P2 = 0.01). Palm oil consumption resulted in a 4% increase in serum apolipoprotein AI (P2 = 0.008) and a 4% decrease in apolipoprotein B (P2 = 0.01) relative to the control diet; the B:AI apolipoprotein ratio was decreased by 8% (P2 < 0.0001). These results were not significantly affected by the different lipoprotein E phenotypes of the volunteers. Although the observed differences were relatively modest, the present study, nonetheless, indicates that dietary palm oil, when replacing a major part of the normal fat content in a Dutch diet, may slightly reduce the lipoprotein- and apolipoprotein-associated cardiovascular risk profiles

Six Large White pigs (mean body-weight 59 (se 1.7) kg) were surgically fitted with permanent catheters in the portal vein, the brachiocephalic artery and the right hepatic vein, as well as with electromagnetic flow probes around the portal vein and the hepatic artery, and allowed to recover. The non-anaesthetized animals were given a basal non-fibre diet (diet A) alone or together with 60 g guar gum/kg (diet B) or 150 g purified cellulose/kg (diet C) by substitution for mica. The diets were given for weekly periods and according to a replicated 3x3 Latin square design. On the last day of each such adaptation period, test meals of 800 g were given before blood sampling. Sampling was continued for 8 h. Guar gum strongly reduced glucose apparent absorption without changing the absorption and the hepatic uptake profiles. Production rates of insulin, gastric inhibitory polypeptide and insulin-like growth factor-1 (IGF-1) were lowest after guar gum ingestion. However, the reductions in peripheral blood insulin levels caused by guar gum were not associated with a change in hepatic insulin extraction. IGF-1 appeared to be strongly secreted by the gut, whereas the liver had a net uptake of the peptide. Ingestion of guar gum increased the hepatic extraction coefficient of gut-produced IGF-1. Guar gum ingestion appeared also to decrease glucagon secretion.

Cellulose at the level consumed had very few effects on the variables considered.

It is suggested that the modulation of intestinal mechanisms by guar gum was sufficient to mediate the metabolic effects described

An attempt was made to unravel further the mechanism by which high dietary concentrations of ascorbic acid influence copper metabolism. The addition of ascorbic acid to the diet of rats caused about a twofold increase in plasma ascorbate concentrations and reduced group mean plasma and tissue concentrations of Cu. The effect of 10 g ascorbic acid/kg diet was greater than that of 1 g/kg. Ascorbic acid feeding reduced blood haemoglobin concentrations and packed cell volume values. Dietary ascorbic acid caused a significant decrease in apparent Cu absorption from the intestine. Ascorbate, intravenously administered together with 64Cu, caused an increase in 64Cu in the liver. Ascorbate, at concentrations occurring in plasma after ascorbic acid feeding, promoted the uptake of 64Cu by isolated hepatocytes. Thus, ascorbate stimulated the efficiency of hepatic uptake of Cu. Ascorbate, intravenously administered together with 64Cu, stimulated accumulation of 64Cu in bile of rats with a bile duct cannula. In rats fed on ascorbic acid, intravenously administered 64Cu was recovered in bile at increased rates. Dietary ascorbic acid enhanced the recovery of intraperitoneally administered 64Cu in faeces. The ascorbate-induced stimulation of biliary 64Cu excretion may reflect an increased hepatic uptake of 64Cu and be caused by an increased specific activity of Cu in liver pools. It is suggested that dietary ascorbic acid reduces tissue Cu concentrations primarily by interfering with intestinal Cu absorption. Ascorbate increases the efficiency of hepatic uptake of Cu, but this effect may not be causatively related with the reduced tissue Cu concentrations after ascorbic acid feeding

The purpose of the present study was first to assess the extent to which unlabelled ascorbate in the diet of guinea-pigs can exchange with labelled ascorbate within their organs when the dietary intake is varied over a wide range, and second to determine whether the retention of label might be used to assess either the amount of ascorbate intake or its biological availability where these are not known. The retention of [14C]ascorbate in the body and in various organs of guinea-pigs were, therefore, measured following a 13 d period of graded dietary intakes of ascorbate. It was found first, that the amount of label retained in each of the organs, 13 d after the initial dose of labelled ascorbate, was much more closely related to the amount of ascorbate intake after labelling than to the intake (and tissue ascorbate levels) before and at the time of labelling. Second, most of the individual internal organs exhibited a constant relationship between the specific activity at 13 d and the dietary intake, except for brain which was flushed to a smaller extent. Third, in agreement with several previous studies a high proportion of the radioactive label in the tissues was found to be still present in ascorbate. The specific activity of column-purified ascorbate was very similar to the estimated specific activity in the crude extract, which implies that it may be possible to estimate specific activities (or stable isotope enrichments) at certain sites without rigorous isolation procedures. Fourth, the amount of radioactivity appearing in the urine 2 d before killing the animals was correlated with the amount of ascorbate intake and with tissue specific activities, suggesting that intakes (or bioavailability) might be predicted from the patterns of label-appearance in the urine

A series of experiments was designed to evaluate inert markers employed in studies of ileal and faecal apparent digestibilities of nitrogen and amino acids in pigs fitted with simple ‘T’ piece cannulas. Trial 1 assessed the palatability of diets containing (a) 5 g chromic oxide/kg, (b) 1 and (c) 5 g titanium dioxide/kg at two levels of feeding. The results indicated that there were slight problems in terms of period of feed consumption associated with diets (a) and (c), but that these effects were transitory and disappeared following acclimatization, although higher levels of feeding may compound the problem. Trial 2 estimated N balance, faecal apparent digestibility of amino acids as determined by both total collection and ratio of markers, ileal apparent digestibility of amino acids and recovery of markers using diets containing (a) 1 and (b) 5 g Cr2O3/kg, (c) 1 and (d) 5 g TiO2/kg. An additional assessment of acid-insoluble lignin present within the diet was also undertaken. Cr2O3 was associated with the lowest recovery, whilst calculations based on TiO2 gave lower standard errors. Trial 3 examined diurnal variation in digesta sampling and its effect on faecal apparent digestibility of N and amino acids. There were no evident effects. In general, it was concluded that the most appropriate marker to use in studies of this nature was TiO2 at a rate of 1 g/kg.

The effect of the weaning diet on the subsequent colonic metabolism of bran and pectin in the adult rat has been investigated. Feeding a fibre-reduced diet on its own or supplemented with bran (WB) and pectin (P) from weaning (fibre-reduced (weaning)) was compared with introducing the same diet to age-matched rats reared on a standard laboratory diet from weaning (fibre-reduced (6 weeks)). The effects of the diets on colonic metabolism were measured by wet and dry caecal contents and stool weights, caecal sac weight, and caecal and faecal short-chain fatty acids (SCFA). Final body-weights were greater for fibre-reduced (6 weeks) and fibre-reduced (6 weeks)+P groups, but not fibre-reduced (6 weeks)+WB, than those of the fibre-reduced (weaning) rats. Rats fed on fibre-reduced (6 weeks) diet had a higher total caecal SCFA content than fibre-reduced (weaning) control rats. Fibre-reduced (weaning)+P-fed rats had a threefold higher caecal concentration of both propionate and butyrate than the matched fibre-reduced (6 weeks)+P group. Fibre-reduced (weaning)+WB animals had a significantly higher butyrate caecal concentration compared with their matched fibre-reduced (6 weeks)+WB group. Fibre-reduced (weaning)+P-fed rats had a lower faecal output than the fibre-reduced (6 weeks)+P rats. There was no difference in faecal output in rats fed on either fibre-reduced (6 weeks)+ WB or fibre-reduced (weaning)+WB. The faecal concentration of SCFA was in general higher in the rats fed on fibre-reduced (weaning) alone, +P, or +WB than in those fed on fibre-reduced (6 weeks) alone, +P or +WB. Faecal output of total and individual SCFA was increased on the fibre-reduced (weaned)+WB diet compared with fibre-reduced (6 weeks)+WB-fed animals. The diet at weaning may be important in determining the pathways of caecal bacterial metabolism in the adult rat. In studying the effect of a dietary fibre on caecal metabolism and faecal output, when the diet is changed appears to be important

The effect of vitamin A deficiency or the lentogenic La Sota strain of Newcastle disease virus (NDV) infection, or both, on immunoglobulin (IgA and IgM) levels in bile and plasma were investigated. In addition, tissue distribution of IgA-, IgG- and IgM-containing cells was studied to establish the source of these Ig. Chickens (1-d-old) with limited vitamin A reserves were fed ad lib. on diets containing either marginal or adequate levels of vitamin A. At 4 weeks of age, half the chickens in each group were infected with NDV. The number of IgA- and IgM-containing cells was not significantly affected by vitamin A deficiency, demonstrating that neither class-switching nor homing of Ig-containing cells is influenced by vitamin A deficiency. Although bile IgM levels were not significantly different in vitamin A-deficient chickens compared with normal chickens, IgA levels were significantly lower. This decrease was even more pronounced in deficient NDV-infected chickens, despite the higher number of IgA-containing cells found in these birds. These results, together with the slightly increased levels of IgA in plasma of vitamin A-deficient chickens, suggest that the hepatobiliary transport of IgA is impaired by vitamin A deficiency and possibly also by NDV infection, although disturbed secretion by IgA-containing cells cannot be excluded