The purposes of the present study were to determine whether caffeine has an effect on zinc absorption and tissue levels of Zn. Under anaesthesia, one side of the intestine of female rats was connected to infusion pumps and an infused solution (first caffeine and later Zn solution) was collected from the other side of the intestine using either 300 mm or the whole small intestine to determine Zn absorption. In a further study, different doses of caffeine solution were injected directly into the femoral vein and a saline or Zn solution was infused into the intestine to measure Zn absorption and tissue Zn concentrations. The results consistently showed that the caffeine solution infused into the intestine did not affect intestinal Zn absorption nor was absorption affected by the direct injection of caffeine into the vein. In contrast, injection of different doses of the caffeine solution significantly decreased Zn tissue levels for the heart only. Calcium concentrations in the heart tissue were also decreased, but not magnesium concentrations. Tissue Zn levels recovered immediately on infusion of a Zn solution into the intestine.

1. Details are given of modifications to standard pH measuring equipment enabling it to be used to record continuously the pH in the bovine rumen for up to 4 weeks. The operation of the apparatus and examples of its use are presented.

Ten adult female mink (Mustela vison) were studied in a 7 d balance experiment consisting of a 2 d pre-surgery feeding period, followed by surgery, 1 d of recovery, 4 d of ad libitum feeding, and a 2d fasting period. In this experiment (Expt A) the animals had osmoticpumps implanted for continuous release of radioactively-labelled p–aminohippuric acid (p–aminobenzoyl-2-[3H]glycine; [3H]PAH;n10) and 14C-labelled inulin ([14C]IN; n 5). Repeated 24 h collections of urine, corrected to 100%[3H]PAH or [14C]IN recovery, were used for accurate determination of N balances, 24 h urinary excretion of urea, creatinine, and total N, and calculation of mean 24 h renal clearance rates for endogenous creatinine and inulin. N balances were slightly below zero, but not significantly different between feeding and fasting periods, indicating that correction to 100% [3H]PAH recovery resulted in slight overestimation of thefinal balances. During fasting, withdrawal of the dietary water and protein loads resulted in a dramatic decline in 24 h urinary volume, and urea and creatinine excretion. Large individualvariations in 24h urinary creatinine excretion (with relative variation coefficients up to 30%) confirmed that this is an unreliable index of the completeness of urine collection. In this respect, recovery rates of [3H]PAH proved far more consistent. Renal clearance values obtained in fed mink were in fair agreement with published data from cats, dogs and ferrets (Mustela putorius furo). Inulin clearance was about 30% higher than endogenous creatinine clearance, although its decline in response to fasting was not significant. In a separate study (Expt B)another ten female mink were equipped with osmotic pumps containing [3H]PAH for determination of 24 h excretion rates of purine derivatives. During feeding, allantoin accounted for more than 97 % of the excretion of purine derivatives in urine, uric acid making up less than 2·5%, xanthine and hypoxanthine less than 1 %. In fasted animals, urinary excretion of each of these purine derivatives declined to less than 50% of the feeding value. In conclusion, an experimental technique is presented for efficient and accurate measurements of daily urinary excretion of nitrogenous constituents, which allows for correct determination of N balances in adult mink and, presumably, in other mammalian species.

1. Glucosyl urea, lactosyl urea and galactosyl urea were prepared from pure sugars and urea and their purity confirmed by determination of their melting points, specific rotations and by mass spectrometry.

2. Using whey as a lactose source, a range of conditions were examined for the preparation of lactosyl urea on a laboratory scale. Yields of 60% were achieved when lactose and urea (molar ratio, urea: lactose 0:6) were reacted for 15 h in sulphuric acid at pH 2·0 and a temperature of 70°.

3. Methods of detection and estimation of all three ureides in whey preparations and ruminant digesta samples were developed. Two quantitative methods, one involving acid-hydrolysis, the other ion-exchange chromatography, were used. The latter method enabled determination of individual quantities of ureides in mixtures.

1. Three groups of rats of different mean weights were given a diet of milk treated with hydrogen sulphide and supplemented with copper-free minerals and vitamins. Also divided into three groups of similar weights were rats given the same diet supplemented with 500 μg Cu/week and stock rats which were given a commercial diet.

2. In a second experiment eight adult female rats were given the Cu-deficient diet for 2 weeks before mating and during pregnancy, and in a third experiment were mated and immediately after mating were given the Cu-deficient diet or the Cu-supplemented diet.

3. Cu deficiency reduced the growth rate of younger rats but had a much less marked effect on the weight of more mature rats. Achromotrichia appeared at 5 weeks; diarrhoea, with the faeces frequently containing undigested blood, and subcutaneous oedema were terminal changes. Deaths occurred in the youngest group of rats after 9 weeks and later in heavier, older rats.

4. Histological changes were seen in livers, spleens, testes and epididymes but not in blood vessels or bones.

5. Pups were not born to mothers given the deficient diet before mating, and the pups from mothers given the deficient diet only during pregnancy were born dead or showed congenital abnormalities.

6. Foetal and liver Cu concentrations for the various groups of animals are given.

7. Maintenance of the foetus appears to be the biological process most susceptible to Cu deficiency in the rat.

To obtain quantitative information on the digestibility of the non-starch polysaccharides (NSP) fraction of white and wholemeal breads, rats were fed on diets in which freeze-dried bread (white, wholemeal or mixtures of the two) provided all the complex carbohydrates. In a second experiment the possibility that dietary fat concentration might influence NSP digestibility was tested by feeding diets containing 30 or 170 g maize oil/kg and either white or wholemeal bread. Multiple linear regression analysis provided little evidence of associative effects of dietary components on NSP digestibility and in the two experiments digestibilities of NSP for white and wholemeal breads were 0·77–0·82 and 0·47–0·52 respectively. Xylose- and arabinose-containing polymers were better digested than was cellulose for both breads. Replacing white by wholemeal bread markedly increased the molar proportion of butyrate in caecal volatile fatty acids at the expense of acetate. This was associated with greater flows of organic matter to the large bowel (LB) and a reduction in caecal transit time (Expt 2). There was little detectable ettect of dietary maize oil concentration on NSP digestibility or on LB fermentation. All breads contained some starch resistant to pancreatic α-amylase (EC 3.2.1.1) without previous treatment with dimethyl sulphoxide. The digestibility of this starch fraction was not significantly different from 1·0 for all diets except that containing wholemeal bread and the higher maize oil concentration where the apparent digestibility was 0·89.

Urea kinetics were measured in normal women aged 22-34 years at weeks 16, 24 and 32 on either their habitual protein intake (HABIT.) or a controlled intake of 60 g protein/d (CONTROL), using primed-intermittent oral doses of [15N15N]urea and measurement of plateau enrichment in urinary urea over 18 h (ID) or a single oral dose of [15N15N]urea and measurement of enrichment of urea in urine over the following 48 h (SD). The intake of protein during HABIT-ID (80 g/d) was greater than that on HABIT-SD (71 g/d); urea production as a percentage of intake was significantly greater at week 16 for HABIT-ID than HABIT-SD, whereas urea hydrolysis at week 16 was greater for HABIT-SD than HABIT-ID and urea excretion at week 32 was greater for HABIT-ID than HABIT SD. The combined results for HABIT-ID and HABIT-SD showed a significant reduction in urea production at week 32 compared with week 24. Urea excretion decreased significantly from week 16 to week 24 with no further decrease to week 32 and urea hydrolysis was significantly greater at week 24 than either week 16 or week 32. Compared with HABIT, on CONTROL there was a decrease in urea production at week 16, and urea excretion was significantly reduced at week 16. For all time periods urea production was closely related to the sum of intake plus hydrolysis. Hydrolysis was greatest at week 24 and closely related to urea production. There was a significant inverse linear relationship overall for hydrolysis as a proportion of production and excretion as a proportion of intake. The results show that on HABIT N is more effectively conserved in mid-pregnancy through an increase in urea hydrolysis and salvage, and during late pregnancy through a reduction in urea formation. Lowering protein intake at any stage of pregnancy increased the hydrolysis and salvage of urea. The staging of these changes was later than that in pregnancy in Jamaica.

The present paper offers a dual 14CO2 breath test approach to study the metabolic utilization of free amino acids in the body. Using the carboxyl-[14C]isotopomer of an amino acid as the test substrate the percentage recovery of the isotope as 14CO2 reflects which part of the labelled amino acid flux has been decarboxylated. The residual C fragments may flow to total oxidation at least to the level recovered for the universal [14C]isotopomer. In the case that recovery for total oxidation is less than for decarboxylation, part of the [14C]fragments are retained in the body by either exchange or non-oxidative pathways. Utilization of tyrosine and leucine was measured in the post-absorptive phase in adult rats conditioned on isoenergetic diets containing 210, 75 or 0 g protein/kg. It was shown that the level of dietary protein exerts an influence on both decarboxylation and total oxidation. Although the responses of leucine and tyrosine were not different for total oxidation, there was a difference between the amino acids in their relative rate of decarboxylation. That this dual 14CO2 breath test approach can be used as a tool to evaluate whether the protein and amino acid supply has been adequate to support actual requirements is discussed.

Amino acid utilization: Amino acid requirements: Leucine: Tyrosine

The present study compared leucine kinetics and acute-phase-protein concentrations in three groups of marasmic, acutely infected Malawian children fed one of three isoenergetic diets. These were: an enhanced-protein-quality diet (egg-white+tryptophan, providing 1.2 g protein/kg per d; n 14); an increased-protein-content diet (egg-white+tryptophan, providing 1·8 g protein/kg per d; n 14); a standard-protein diet (1·2 g milk protein/kg per d; n 25). The hypotheses tested were that children receiving a diet with more protein would have greater rates of non-oxidative leucine disposal and that children receiving an isonitrogenous diet with a higher protein quality would have lower rates of leucine oxidation. The children were studied after 24 h of therapy using standard [13C]leucine stable-isotope tracer techniques. The children receiving the higher-protein-content diet had greater leucine kinetic rates than those receiving the standard-protein-content diet; non-oxidative leucine disposal was 170 (SD 52) v. 122 (SD 30) μmol leucine/kg per h (P<0·01). Leucine oxidation was less in the children receiving the enhanced-protein-quality diet than in those receiving the standard-protein-quality diet; 34 (SD 12) v. 45 (SD 13) μmol leucine/kg per h (P<0·05). The children receiving the high-protein-content diet increased their serum concentration for five of six acute-phase proteins 24 h after starting therapy, while those receiving the standard-protein-content diet did not. These data suggest that there was greater whole-body protein synthesis, and a more vigorous acute-phase response associated with the higher-protein-content diet. The clinical benefits associated with a higher protein intake in marasmic, acutely infected children need further study.

Consumption of carbohydrate-containing foods leads to transient postprandial rises in blood glucose concentrations that vary between food types. Higher postprandial glycaemic exposures have particularly been implicated in the development of chronic cardiometabolic diseases. Reducing such diet-related exposures may be beneficial not only for diabetic patients but also for the general population. A variety of markers have been used to track different aspects of glycaemic exposures, with most of the relevant knowledge derived from diabetic patients. The assessment of glycaemic exposures among the non-diabetic population may require other, more sensitive markers. The present report summarises key messages of presentations and related discussions from a workshop organised by Unilever intended to consider currently applied markers of glycaemic exposure. The particular focus of the meeting was to identify the potential applicability of glycaemic exposure markers for studying dietary effects in the non-diabetic population. Workshop participants concluded that markers of glycaemic exposures are sparsely used in intervention studies among non-diabetic populations. Continuous glucose monitoring remains the optimal approach to directly assess glycaemic exposure. Markers of glycaemic exposure such as glycated Hb, fructosamine, glycated albumin, 1,5-anhydroglucitol and advanced glycation end products can be preferred dependent on the aspect of interest (period of exposure and glucose variability). For all the markers of glycaemia, the responsiveness to interventions will probably be smaller among the non-diabetic than among the diabetic population. Further validation and acceptance of existing glycaemic exposure markers applied among the non-diabetic population would aid food innovation and better design of dietary interventions targeting glycaemic exposure.

Healthy male volunteers consumed hot lunches consisting of cooked white rice, fried chicken fillet, raisins, bigarreaus (sweet cherries) and curry sauce with carbohydrate: fat ratios of either 0·77 or 2·04, and polysaccharide: (mono+di)saccharide ratios (P: MD) varying between 5·3 and 0·95. Before and at various time intervals after the start of the meal, blood samples were analysed for glucose, insulin, triacylglycerol (TG), free glycerol (FG), free fatty acids (FFA) and cholesterol. Elevated postprandial glucose and insulin peaks were induced by the meals containing a larger amount of carbohydrate. The type of carbohydrate in the meal appeared to have little or no effect on the peak maximum. A small second glucose peak was seen at 2 h after the meals with P: MD > 3·1. The TG concentration in the blood showed a similar and rapid rise. After the meal containing the largest amount of simple sugars, the TG curve levelled off 1 h after the start of the meal and then remained at a nearly constant level (1·5 mM). In contrast, a larger amount of complex carbohydrates induced a TG concentration which rapidly rose to a maximum of 1·75 mM, and subsequently decreased slowly to somewhat below that of the simple sugar-rich meal at 4 h. The postprandial curves after the fat-rich meals showed a continuous rise of TG up to a maximum of about 2 mM at 2 h, and a subsequent slow decrease. FG and FFA all showed a rapid drop immediately after the start of the consumption of the meals, followed by a rebound at 1 h. The postprandial curves of total cholesterol, as well as the areas below the curve of both total cholesterol and free, unesterified cholesterol were lower after the carbohydrate-rich meals than after the fat-rich meals. This is attributed to the larger amount of cholesterol in the fat-rich meals.

The consumption of food with MUFA has been associated with improvement of inflammation and oxidative stress in overweight individuals. In the present study, we evaluate the effect of high-oleic peanut intake within a hypoenergetic diet on inflammatory and oxidative status markers in overweight men. Sixty-four overweight men (BMI 26–35 kg/m2, 18–50 years old) participated in this randomised controlled study for 4 weeks, allocated into three groups: control (CT, n 22), conventional peanut (CVP, n 21) and high-oleic peanut (HOP, n 21). They followed a hypoenergetic diet (−250 kcal/d; −1045 kJ/d) with or without 56 g of high-oleic or conventional peanuts. After the intervention, the inflammatory markers did not show significant changes in fasting concentrations or postprandial response among the experimental groups (P > 0·05). The activity of oxidative status markers remained unchanged after the intervention. However, in the CT, malondialdehyde showed lower concentration in comparison with the baseline (P = 0·020) and among the groups (P = 0·002). In the present study, the daily intake of high-oleic peanuts within a hypoenergetic diet did not modify the inflammatory markers and oxidative status in overweight men. More studies are needed to better understand the effect of high-oleic peanut intake on health outcomes.

Resistant starch can alter the intestinal nutrient availability and bulk of digesta, thereby modulating the substrate available for microbial metabolic activity along the gastrointestinal tract. This study elucidated the effect of transglycosylated starch (TGS) on the retention of digesta in the upper digestive tract, ileal flow and hindgut disappearance of nutrients, and subsequent bacterial profiles in pigs. Fourteen ileal-cannulated growing pigs were fed either the TGS or control (CON) diet in a complete crossover design. Each period consisted of a 10-d adaptation to the diets, followed by 3-d collection of faeces and ileal digesta. Consumption of TGS decreased the retention of digesta in the stomach and small intestine, and increased ileal DM, starch, Ca and P flow, leading to enhanced starch fermentation in the hindgut compared with CON-fed pigs. TGS increased ileal and faecal total SCFA, especially ileal and faecal acetate and faecal butyrate. Gastric retention time positively correlated to Klebsiella, which benefitted together with Selenomonas, Lactobacillus, Mitsuokella and Coriobacteriaceae from TGS feeding and ileal starch flow. Similar relationships existed in faeces with Coriobacteriaceae, Veillonellaceae and Megasphaera benefitting most, either directly or indirectly via cross-feeding, from TGS residuals in faeces. TGS, in turn, depressed genera within Ruminococcaceae, Clostridiales and Christensenellaceae compared with the CON diet. The present results demonstrated distinct ileal and faecal bacterial community and metabolite profiles in CON- and TGS-fed pigs, which were modulated by the type of starch, intestinal substrate flow and retention of digesta in the upper digestive tract.