The expressions of hexokinase IV (glucokinase, GK) and hexokinase (HK)-I genes were analysed during early ontogenesis of common carp (Cyprinus carpio). Unlike HK-I gene, which was expressed during all the stages of the development, GK was only induced by the first feeding with high levels of dextrin as a source of carbohydrate. This study confirms the high capacity of common carp to use glucose even at the very early stages of development.

The serum mineral levels, glucose disappearance rate (kg), total area under the glucose (ΔG) and insulin (ΔI) curves, and static insulin secretion were compared among rats fed a Mg-deficient diet for 6 (DF-6) or 11 (DF-11) weeks, and rats fed a control diet for the same periods (CO-6 and CO-11 groups). No change in glucose homeostasis was observed among DF-6, CO-6 and CO-11 rats. DF-11 rats showed an elevated kg and a reduced ΔG and ΔI. For evaluating the effect of supplementation, rats fed a control or Mg-deficient diet for 6 weeks were then fed a Mg- supplemented diet for 5 weeks (SCO and SDF groups respectively). The serum Mg levels in SDF rats were similar to those in CO-11 and SCO rats, but higher than in the DF-11 group. SDF rats showed similar kg, ΔG and ΔI compared with the CO-11 and SCO groups. However, a significantly lower kg and higher ΔG and ΔI were observed in SDF compared with DF-11 rats. Basal and 8.3 mmol glucose/l-stimulated insulin secretion by islets from DF-11 rats were higher than by islets from CO-11 rats. These results indicate that moderate Mg depletion for a long period may increase the secretion and sensitivity to insulin, while Mg supplementation in formerly Mg-deficient rats may prevent the increase in sensitivity and secretion of insulin.

Food energy values used for nutrition labelling and other purposes are traditionally based on the metabolisable energy (ME) standard, which has recent support from Warwick & Baines (2000). By reference to current practices and published data, the present review critically examines the ME standard and support for it. Theoretical and experimental evidence on the validity of ME and alternatives are considered. ME and alternatives are applied to 1189 foods to assess outcomes. The potential impact of implementing a better standard in food labelling, documentation of energy requirements and food tables, and its impact on users including consumers, trade and professionals, are also examined. Since 1987 twenty-two expert reviews, reports and regulatory documents have fully or partly dropped the ME standard. The principal reason given is that ME only approximates energy supply by nutrients, particularly fermentable carbohydrates. ME has been replaced by net metabolisable energy (NME), which accounts for the efficiency of fuel utilisation in metabolism. Data collated from modern indirect calorimetry studies in human subjects show NME to be valid and applicable to each source of food energy, not just carbohydrates. NME is robust; two independent approaches give almost identical results (human calorimetry and calculation of free energy or net ATP yield) and these approaches are well supported by studies in animals. By contrast, the theoretical basis of ME is totally flawed. ME incompletely represents the energy balance equation, with substantial energy losses in a missing term. In using NME factors an account is made of frequent over-approximations by the ME system, up to 25 % of the NME for individual foods among 1189 foods in British tables, particularly low-energy-density traditional foods. A new simple general factor system is possible based on NME, yet the minimal experimental methodology is no more than that required for ME. By accounting for unavailable carbohydrate the new factor system appears as specific to foods as the USA's food-specific Atwater system, while it is more representative of energy supply from food components. The NME content of foods is readily calculable as the sum from fat (37 kJ/g), protein (13 kJ/g), available carbohydrate (16 kJ/g), fully-fermentable carbohydrate (8 kJ/g), alcohol (26 kJ/g) and other components. Obstacles to the implementation of NME appear to be subjective and minor. In conclusion, the ME standard is at best an approximate surrogate for NME, and inadequately approximates food energy values for the purpose of informing the consumer about the impact on energy balance of the energy supply for equal intake of individual foods. NME is superior to ME for nutrition labelling and other purposes.

Nutrition is a critical determinant of the outcome of host microbe interactions through a modulation of the immune response. Besides macronutrient malnutrition, deficiencies of several macronutrients also influence immune homeostasis and thus affect infection-related morbidity and mortality. Deficiencies of micronutrients like vitamin A, iron and zinc are widely prevalent among populations living in developing countries. Besides their severe deficiencies, subclinical deficiencies are known to impair biological functions in the host, immune function being one of them. The effects of these micronutrients on various immune mechanisms are briefly reviewed in this article.

The trace element zinc is an essential micronutrient for the proper functioning of the immune system. Zinc deficiency leads to impaired function of the unspecific and specific immune response and consequently to an increased susceptibility to bacterial, viral and fungal infections. Immunological defects are not only seen in pronounced but even in marginal and moderate zinc deficiency. Lack of zinc is especially harmful for the development of the immune system, which stresses the importance of a balanced zinc level during pregnancy. However, gestational zinc deficiency due to an imbalance between intake and increased requirements is a common problem world-wide. In animals, gestational zinc deficiency results in reduced thymic and spleen size and depressed active and passive immunity in the infant. For example, depressed immunoglobulin levels, altered antibody repertoire, reduced proliferative response of lymphocytes and diminished neutrophil functions have been reported. Interestingly, immune defects caused by prenatal zinc deficiency, such as depressed antibody levels and lymphocyte proliferation, may even persist in subsequent generations and are not reversible by postnatal zinc administration. Since gestational zinc deficiency is a common problem throughout all cultures and socioeconomic levels, it might have immense consequences for the health status of the population. Based on a summary of the immunobiology of zinc, this article reviews the significance of zinc deficiency during pregnancy and the effect of gestational zinc deficiency on passive and active immunity in the infant. It provides a rational basis for both immunological laboratory investigations and field studies, such as large community-based zinc supplementation trials in pregnant women.

The racemic mixture, [6RS]-5-formyltetrahydrofolate, is widely used clinically. In human subjects, orally-administered pure unnatural C-6 isomers, [6R]-5-formyltetrahydrofolate and [6S]-5,10-methenyltetrahydrofolate, were recently shown to be metabolized to the natural isomer, [6S]-5-methyltetrahydrofolate. We re-analysed the data from human studies published during the past four decades in which oral doses (≤10 mg) of racemic mixtures of these folates were used. We re-evaluated the data to determine whether these racemic mixtures are only 50 % bioactive or, as we now predict, more than 50 % bioactive. Our analyses indicate that, in human subjects, oral doses of the racemic mixture of the two formyltetrahydrofolates are 20–84 % more bioactive than would be predicted. These data are consistent with the following pathway: chemical conversion of these folates to 10-formyltetrahydrofolate; oxidation of 10-formyltetrahydrofolate to 10-formyldihydrofolate; subsequent enzymic conversion of 10-formyldihydrofolate to dihydrofolate by 5-amino-4-imidazolecarboxamide ribotide transformylase; and finally the well-established metabolism of dihydrofolate to [6S]-5-methyltetrahydrofolate. An additional review of the literature supports the in vivo oxidation of 10-formyltetrahydrofolate occurring to a certain extent, as 10-formyl-folic acid is rapidly formed after the administration of folic acid (pteroylglutamic acid) or 5-formyltetrahydrofolate in human subjects. The dogma that an oral dose of the unnatural C-6 isomer of 5-formyltetrahydrofolate is not bioactive in human subjects does not withstand scrutiny, most probably due to the previously unrecognized in vivo oxidation of 10-formyltetrahydrofolate. This discovery unveils new folate metabolism in human subjects.

An increasing number of foods fortified with varying levels of folic acid are appearing in the market place, targeted either at the general population or at specific consumer groups. Although it is assumed that the folate in these products should be highly bioavailable, there is a need to carry out studies to ascertain that this is, in fact, the case. The present study investigated the ability of selected folic acid-fortified foods (targeted at different types of consumer) to increase the folate status of folate-deficient rats. Forty-two weanling male rats (Wistar strain) were fed a folate-deficient diet containing 1 % succinyl sulfathiazole (w/w) for 28 d. Following depletion, seven rats were randomly assigned to each of five repletion diets containing folic acid, Complan®, Slim Fast®, Opti-Fuel2® or Cola Coa® calculated to provide 200 μg folate/kg of each diet. Calculations were based on folate information from the product labels. After a further 28 d, plasma, liver and kidney folate concentrations were determined by microbiological assay. Plasma homocysteine was measured by HPLC as a functional indicator of folate status. The folate content of the foods was measured by tri-enzyme extraction followed by microbiological assay. Our analyses suggest that there may be considerable inaccuracies on the part of the manufacturers in relation to the folate declarations on the product labels. Despite this, the four foods evaluated were highly effective in elevating plasma, liver and kidney folate and lowering plasma homocysteine concentrations in rats. These results lend support to the policy of food fortification with folic acid as a means of raising the folate status of the population, and in particular to the fortification of specific foods which may target areas of the population where increased folate status is most needed.

Low-digestible carbohydrates (LDCs) are incompletely or not absorbed in the small bowel and fermented in the colon. They are usually well tolerated but may also have some dose-related undesirable effects due to their natural osmotic potential and/or excessive fermentation: borborygmi, excessive flatus, bloating, abdominal cramps and eventually diarrhoea. There is an important intersubject variability in the tolerance to LDCs because of differences in absorption capacity, motility pattern, colonic response and intestinal sensitivity. There is also a great intrasubject variability, depending on the type of LDC, dosage and type of consumption. Absorption of LDC in the small intestine can be assessed using hydrogen breath test or intubation techniques or analysis of ileostomy effluents. Double-blind, placebo-controlled studies are required to assess the subjective symptoms of intolerance, and the experimental conditions may influence the results.

Large (>1600 μm), ingestively masticated particles of bermuda grass (Cynodon dactylon L. Pers.) leaf and stem labelled with 169Yb and 144Ce respectively were inserted into the rumen digesta raft of heifers grazing bermuda grass. The concentration of markers in digesta sampled from the raft and ventral rumen were monitored at regular intervals over approximately 144 h. The data from the two sampling sites were simultaneously fitted to two pool (raft and ventral rumen–reticulum) models with either reversible or sequential flow between the two pools. The sequential flow model fitted the data equally as well as the reversible flow model but the reversible flow model was used because of its greater application. The reversible flow model, hereafter called the raft model, had the following features: a relatively slow age-dependent transfer rate from the raft (means for a gamma 2 distributed rate parameter for leaf 0.0740 v. stem 0.0478 h-1), a very slow first order reversible flow from the ventral rumen to the raft (mean for leaf and stem 0.010 h-1) and a very rapid first order exit from the ventral rumen (mean of leaf and stem 0.44 h-1). The raft was calculated to occupy approximately 0.82 total rumen DM of the raft and ventral rumen pools. Fitting a sequential two pool model or a single exponential model individually to values from each of the two sampling sites yielded similar parameter values for both sites and faster rate parameters for leaf as compared with stem, in agreement with the raft model. These results were interpreted as indicating that the raft forms a large relatively inert pool within the rumen. Particles generated within the raft have difficulty escaping but once into the ventral rumen pool they escape quickly with a low probability of return to the raft. It was concluded that the raft model gave a good interpretation of the data and emphasized escape from and movement within the raft as important components of the residence time of leaf and stem particles within the rumen digesta of cattle.

The uridine (5′-)diphosphate-glucuronosyltransferases (UGT) are involved in the phase II of various xenobiotics and endogenous compounds. They are responsible for glucuronidation of many substrates, especially including bilirubin (UGT1A1) and phenolic compounds (UGT1A6). We previously showed that the expression of both isoforms is regulated at the transcriptional level by thyroid hormone in rat liver. In this present study, effects of vitamin A dietary intake (0, 1.72, 69 ug retinol acetate/g food) on the regulation of UGT1A1 and UGT1A6 activity and expression by 3,5,3′ triiodo-L-THYRONINE (l-T3) were examined in the same organ. Activities were determined toward bilirubin and 4-nitrophenol. UGT mRNA were analysed by reverse transcription and amplification methods (reverse transcription–polymerase chain reaction) and quantified by capillary electrophoresis. In rats fed a vitamin A-balanced diet, a single injection of l-T3 (500 μg/kg body weight) increased UGT1A6 mRNA expression whereas this hormone decreased UGT1A1 mRNA expression. In addition we observed that the specific effect of l-T3 on UGT1A1 and UGT1A6 was reduced in animals receiving a vitamin A-enriched diet and disappeared in those fed a vitamin A-free diet. The modulations observed in mRNA expression are concomitant with those found for UGT activities. Our results demonstrate for the first time the existence of a strong interaction between vitamin A and thyroid hormone on the regulation of genes encoding cellular detoxification enzymes, in this case the UGT.

Stanyl esters dissolved in margarine inhibit cholesterol absorption, lower sterol absorption in general, and lower serum total cholesterol, LDL-cholesterol and plant sterol levels. To find out whether stanyl esters inhibit absorption of fat-soluble vitamins and β-carotene in acute experiments, we performed two fat-tolerance tests fortified with vitamins (retinol 0.9–3.7 mg, α-tocopherol 70–581 mg), β-carotene (25–150 mg) and squalene (0.5 g) with and without 1 g of stanyl ester added to the test meal in ten healthy men. The concentrations or areas under the curves (AUC) of cholesterol, triacylglycerols, squalene and α-tocopherol, β-carotene and retinyl palmitate showed typical postprandial changes in serum, chylomicrons, VLDL and VLDL infranatant (intermediate-density lipoproteins, LDL and HDL) over 24 h after the test meal without stanyl esters, and they were not affected by the addition of stanyl esters. The post-absorptive serum campesterol concentration and campesterol : cholesterol were significantly lowered at 6–9 h by stanyl ester supplementation, reflecting reduced sterol absorption efficiency. Changes in vitamin and β-carotene AUC did not correlate with the given doses. In conclusion, the present study shows that stanyl esters dissolved in margarine do not detectably interfere in a short-term study with the absorption of α-tocopherol, β-carotene or retinol measured by a 24 h oral fat-load test.

Both plasma and red blood cells contain amino acids (AA), but the relative amount of AA transferred from each vascular compartment to the tissues remains unclear. For splanchnic tissues, the relative transfers between the plasma, the red blood cells and the tissues may vary with nutritional state, but whether the same situation pertains for other tissues is not known. The current study focused on the transfer of lysine from plasma and red blood cells across the hindquarters of sheep offered four levels of intakes (0.5, 1.0, 1.5 and 2.5×maintenance energy). This design, coupled with use of [U-13C]lysine as tracer, also allowed the effect of intake on protein kinetics to be examined. At all intakes, the concentration of lysine in the sheep’ red blood cells exceeded that in plasma by 50 % (P<0.001), while the distribution of labelled lysine between the plasma and the red blood cells was 0.71:0.29. Net lysine uptake by the hindquarters increased in a linear manner (P<0.001) with intake, with more than 90 % extracted from the plasma. Free lysine enrichments in plasma from the posterior vena cava were less than that from the artery (P<0.001), but those in red blood cells were not different between the artery and vein. The red blood cells thus play a minor role in the transfers to and from the hindquarter tissues, regardless of intake. Based on plasma transfers and the enrichment of lysine in arterial plasma, hindquarter protein synthesis increased linearly with intake (P<0.001). In contrast, protein breakdown was unaffected by intake. The contribution of hindquarter protein synthesis to whole-body lysine flux remained unchanged with intake (18–20 %).

Low-digestible carbohydrates represent a class of enzyme-resistant saccharides that have specific effects on the human gastrointestinal tract. In the small bowel, they affect nutrient digestion and absorption, glucose and lipid metabolism and protect against known risk factors of cardiovascular disease. In the colon they are mainly degraded by anaerobic bacteria in a process called fermentation. As a consequence, faecal nitrogen excretion is enhanced, which is used clinically to prevent or treat hepatic encephalopathy. Low-digestible carbohydrates are trophic to the epithelia of the ileum and colon, which helps to avoid bacterial translocation. Short-chain fatty acids are important fermentation products and are evaluated as new therapeutics in acute colitis. They are considered in the primary prevention of colorectal cancer. The bifidogenic effect of fructo-oligosaccharides merits further attention. Unfermented carbohydrates increase faecal bulk and play a role in the treatment of chronic functional constipation, symptomatic diverticulosis and, possibly, the irritable bowel syndrome. In conclusion, low-digestible carbohydrates may play a role in the maintenance of human digestive health. However, the strength of evidence differs between disease entities.

Diets with protein of inferior quality may increase protein breakdown in skeletal muscle but the experimental results are inconsistent. To elucidate the relationship, pigs were fed isoenergetic and isonitrogenous diets based on soyabean-protein isolate or casein for 15 weeks, with four to six animals per group. A higher plasma level of urea (2.5-fold the casein group value, P=0.01), higher urinary N excretion (2.1-fold the casein group value, P=0.01), a postabsorptive rise in the plasma levels of urea, 3-methylhistidine and isoleucine in soyabean protein-fed pigs suggested recruitment of circulatory amino acids by protein breakdown in peripheral tissues. Significant differences between dietary groups were detected in lysosomal and ATP-dependent proteolytic activities in the semimembranosus muscle of food-deprived pigs. A higher concentration of cathepsin B protein was found, corresponding to a rise in the cathepsin B activity, in response to dietary soyabean protein. Muscle ATP-stimulated proteolytical activity was 1.6-fold the casein group value (P=0.03). A transient rise in the level of cortisol (2.9-times the casein group value, P=0.02) occurred in the postprandial phase only in the soyabean group. These data suggest that the inferior quality of dietary soyabean protein induces hormonally-mediated upregulation of muscle protein breakdown for recruitment of circulatory amino acids in a postabsorptive state.

The aim of the present study was to investigate the effects of photoperiod and feeding level on lipid metabolism in ovine perirenal and subcutaneous adipose tissues (AT) and in skeletal and cardiac muscles. Twenty dry non-pregnant ovariectomised ewes were divided into two groups and subjected to either 8 h or 16 h light/d, and underfed at 22 % energy requirements for 7 d. Half of the ewes in each group were slaughtered and the remaining ewes were refed at 190 % energy requirements for 14 d, until slaughtering. Refeeding increased (2.6–4.3-fold) malic enzyme (ME), fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH) and glycerol-3-phosphate dehydrogenase (G3PDH) activities in subcutaneous AT as well as lipoprotein lipase (LPL) activity in perirenal (3.5-fold) and subcutaneous (10-fold) AT and to a lesser extent (1.4-fold) in the skeletal longissimus thoracis and cardiac muscles. Moreover, variations of LPL mRNA level followed variations of LPL activity: refeeding increased perirenal AT- and cardiac muscle-mRNA levels (7.4- and 2-fold respectively). The main finding of this study is that, for a given level of food intake, long days (compared with short days) increased the LPL activity in the longissimus thoracis muscle and, in refed ewes, the activities of LPL and ME in subcutaneous AT. Furthermore, long days increased LPL mRNA level in cardiac muscle and perirenal AT. Thus, our results show that there are direct effects of photoperiod on sheep AT lipogenic potential, as well as on muscle LPL activity, which are not caused by changes in nutrient availability.

The present study was carried out to determine whether cephalic stimulation, associated with eating a meal, was sufficient stimulus to provoke the release of stored triacylglycerol (TAG) from a previous high-fat meal. Ten subjects were studied on three separate occasions. Following a 12 h overnight fast, subjects were given a standard mixed test meal which contained 56 g fat. Blood samples were taken before the meal and for 5 h after the meal when the subjects were randomly allocated to receive either water (control) or were modified sham fed a low-fat (6 g fat) or moderate-fat (38 g fat) meal. Blood samples were collected for a further 3 h. Compared with the control, modified sham feeding a low- or moderate-fat meal did not provoke an early entry of TAG, analysed in either plasma or TAG-rich lipoprotein (TRL) fraction (density <1.006 kg/l). The TRL-retinyl ester data showed similar findings. A cephalic phase secretion of pancreatic polypeptide, without a significant increase in cholecystokinin levels, was observed on modified sham feeding. Although these data indicate that modified sham feeding was carried out successfully, analysis of the fat content of the expectorant showed that our subjects may have accidentally ingested a small amount of fat (0.7 g for the low-fat meal and 2.4 g for the moderate-fat meal). Nevertheless, an early TAG peak following modified sham feeding was not demonstrated in the present study, suggesting that significant ingestion of food, and not just oro-sensory stimulation, is necessary to provoke the release of any TAG stored from a previous meal.

Micronutrient deficiency, whether clinical or subclinical, may affect growth, cognition and reproductive performance. In pregnant women moderate to severe deficiencies of iron, zinc and folic acid have been shown to increase risk of low birth weight, pregnancy complications and birth defects. Any attempt to introduce a micronutrient supplementation programme during pregnancy must be based on adequate data on the prevalence of micronutrient deficiencies, their adverse effects and the potential for reversing these through supplementation. This paper reviews parameters for assessment of iron, zinc and folic acid deficiencies in pregnancy and the available data on prevalence of these in pregnant women in South Asia. Iron deficiency and anemia affect 50 % or more of pregnant women, the prevalence of folic acid deficiency may be up to 30–50 % and there is evidence to suggest that zinc deficiency is likely to be widespread but supportive data are scarce.

The objective of the present study was to evaluate the oxidative susceptibility of LDL in human volunteers following supplementation with various low doses (<1 g/d) of n–3 polyunsaturated fatty acids (PUFA). Sixty-two healthy volunteers (thirty-seven males and twenty-five females, aged 19–63 years) were recruited to take part in a randomised placebo-controlled trial. Volunteers were required to take 0.9, 0.6 or 0.3 g n–3 PUFA as fish oil or placebo capsules daily for 16 weeks. Susceptibility of LDL to oxidative modification was assessed by measuring the production of conjugated dienes and thiobarbituric acid-reactive substances in LDL oxidised by Cu2+ (15 μM) OR 2,2″-AZOBIS(2-AMIDINOPROPANE) DIHYDROCHLORIDE (1 Mm) for 5 h. Plasma fatty acid and LDL-fatty acid composition, cholesterol levels and antioxidant concentrations were also measured. While post-treatment n–3 PUFA compositions of plasma and LDL reflected the capsule contents, no meaningful differences in antioxidant concentrations or cholesterol levels were observed between the groups. Supplementation with low doses of n–3 PUFA as fish oil did not influence the oxidative susceptibility of LDL. The results of the present study suggest that moderate dietary intakes of n–3 PUFA do not significantly influence the susceptibility of LDL to oxidative modification in vitro.

I in the chain sow diet → blood serum of sow → sow milk → piglet serum was investigated in two experiments with a total of eighty-one sows and their piglets. In experiments conducted during the last trimester of gravidity and the 28 d of lactation, diets with glucosinolates (1.9 mmol/kg diet via 100 g ground rapeseed/kg diet (Expt 1) and 2.1 and 4.2 mmol/kg diet via 75 and 150 g rapeseed press cake/kg diet (Expt 2)) were compared with control groups without rapeseed products. From 0 to 600 μg I/kg was added to sow diets during lactation. Diets without supplementary I decreased the I concentration particularly in milk and piglet serum. The presence of rapeseed and rapeseed press cake were indicated by a thiocyanate concentration increase, mainly in sow serum. The diets with glucosinolates decreased the milk and piglet serum I concentration. Spot urine and faeces samples from sows eating the rapeseed-press cake diets had increased I concentration. The sows’ serum I and thyroxine did not respond to glucosinolates (Expt 1) or these diets caused an increase in concentration (Expt 2). Both these criteria seem unsuitable for the diagnosis of I status of adult animals. Glucosinolates and their degradation compounds may affect the thyroid and the mammary glands resulting in lower I milk transfer and higher renal and intestinal I excretion.