Raw or germinated faba bean (Vicia faba minor var. Alameda) and chickpea (Cicer arietinum kabuli var. Athenas) seed meals were incorporated in essential amino acid-supplemented and energy-equalized diets for growing (65 (SD 1) g) male Wistar rats as the only sources of dietary protein. A lactalbumin-based diet was used as the control. Faecal dry weight and N excretion of animals fed legume-containing diets were greater (P<0·01) and DM digestibility lower (P<0·01) than controls. Apparent faecal digestibilities of amino acids were found to be not different or lower (P<0·01) than controls in rats fed diets containing legume seeds, either germinated or not. Total diaminopimelic acid (DAPA) and purine bases excretion were significantly (P<0·01) higher than controls in rats fed both legume seed meals. Faecal bacterial N calculated according to DAPA or purine bases values was similar and significantly higher (P<0·01) than controls in rats fed legume seed meals. Bacterial N accounted for 50 to 80 % of total faecal N in rats fed legume diets. Apparent faecal N digestibility values (53–65 %) of rats fed legume-based diets were lower (P<0·01) than controls, but became substantially higher (85–92 %) when calculated taking into account bacterial N values. Faecal NSP digestibility values for legume diets were 40–57 g/100 g ingested. Germination decreased starch faecal excretion (P<0·05) and increased (P<0·05) faecal starch and NSP digestibilities of faba bean seeds.

The present study examined the effects of a 3-week fish-oil supplementation (6 g/d) on the rate of plasma glucose disappearance (Rd glucose), hepatic glucose production (HGP), carbohydrate oxidation and lipid oxidation during exercise. Six untrained males (23±1 years; 67·6±2·7kg) performed two 90min cycling exercise sessions at 60% of maximal O2 output separated by 20 d. During the 20 d before the first test, they ingested 6g olive oil/d, then 6g fish oil/d during the 20 d before the second test. Plasma glucose fluxes and lipolysis were traced using 6,6-[2H2]glucose and 1,1,2,3,3-[2H5]glycerol respectively. Substrates oxidation was obtained from indirect calorimetry. At rest HGP and the Rd glucose were similar after olive oil and fish oil (1.83 (se 0·05) v. 1·67 (se 0·11) mg/kg per min). During exercise, fish oil reduced the stimulation of both the Rd glucose (5·06 (se 0·23) v. 6·37 (se 0·12) mg/kg per min; P<0·05) and HGP (4·88 (se 0·24) v. 5·91 (se 0·21) mg/kg per min; P<0·05). Fish oil also reduced glucose metabolic clearance rate (6·93 (se 0·29) v. 8·30 (se 0·57) ml/min). Carbohydrate oxidation tended to be less stimulated by exercise after fish oil than after olive oil (12·09 (se 0·60) v. 13·86 (se 1·11) mg/kg per min; NS). Lipid oxidation tended to be more stimulated by exercise after fish oil (7·34 (se 0·45) v. 6·85 (se 0·17) mg/kg per min; NS). Glycaemia, lactataemia, insulinaemia and glucagonaemia were similarly affected by exercise after fish oil and olive oil. Lipolysis at rest was similar after fish oil and olive oil (2·92 (se 0·42) v. 2·94 (se 0·28) μmol/kg per min) and similarly stimulated by exercise (6·42 (se 0·75) v. 6·77 (se 0·72) μmol/kg per min). It is concluded that fish oil reduced the Rd glucose by 26% by reducing glucose metabolic clearance rate, possibly by facilitating fat oxidation, and reduced HGP by 21%, possibly by a feedback mechanism.

Anaemia is a common complication of pulmonary tuberculosis. The precise mechanism of anaemia in pulmonary tuberculosis is not clearly known, but anaemia of inflammation as well as of Fe deficiency has been implicated. Both are common in developing countries. It is extremely difficult to distinguish anaemia of Fe deficiency from anaemia of inflammation with the haematological indices used routinely. Therefore, Fe preparations are usually prescribed for all anaemic patients irrespective of the aetiology. This approach has been questioned. The present study aimed to assess the effect of Fe supplementation on anaemic patients with pulmonary tuberculosis. Adult male patients 15–60 years of age with pulmonary tuberculosis and a blood haemoglobin concentration 80–110 g/l were included in the study; healthy adult males matched for age and socio-economic status were taken as controls. Blood haemoglobin concentration, total erythrocyte count (TEC), packed cell volume (PCV), mean corpuscular volume (MCV), mean corpuscular haemoglobin and serum Fe, total Fe-binding capacity and ferritin were estimated before treatment and 1, 2 and 6 months after treatment. The patients were divided randomly into three groups and during the initial 2 months of treatment were provided with one of three supplementary regimens consisting of placebo, Fe alone or Fe with other haematinics. Significant improvements in haematological indices and Fe status were noticed in all three groups. Blood haemoglobin concentration, MCV and PCV were significantly higher at 1 month in both Fe-supplemented groups than the placebo group. This difference, however, disappeared at 2 and 6 months with similar values in all three groups. The increase of other haematological indices was similar in all groups. Serum Fe and Fe saturation of transferrin were significantly higher in both Fe-supplemented groups than the placebo group up to 2 months; this effect, however, disappeared at 6 months. There was a consistent increase in TEC and decrease in ferritin values up to 6 months in all groups. Radiological and clinical improvement was similar in all three groups. These observations suggest that Fe supplementation in mild to moderate anaemia associated with pulmonary tuberculosis accelerated the normal resumption of haematopoiesis in the initial phases by increasing Fe saturation of transferrin. However, consistent improvement of haematological status was dependent only on the improvement of the disease process.

The effect of increased dietary intakes of α-linolenic acid (ALNA) or eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for 2 months upon plasma lipid composition and capacity for conversion of ALNA to longer-chain metabolites was investigated in healthy men (52 (SD 12) years). After a 4-week baseline period when the subjects substituted a control spread, a test meal containing [U-13C]ALNA (700 mg) was consumed to measure conversion to EPA, docosapentaenoic acid (DPA) and DHA over 48 h. Subjects were then randomised to one of three groups for 8 weeks before repeating the tracer study: (1) continued on same intake (control, n 5); (2) increased ALNA intake (10 g/d, n 4); (3) increased EPA+DHA intake (1·5 g/d, n 5). At baseline, apparent fractional conversion of labelled ALNA was: EPA 2·80, DPA 1·20 and DHA 0·04 %. After 8 weeks on the control diet, plasma lipid composition and [13C]ALNA conversion remained unchanged compared with baseline. The high-ALNA diet resulted in raised plasma triacylglycerol-EPA and -DPA concentrations and phosphatidylcholine-EPA concentration, whilst [13C]ALNA conversion was similar to baseline. The high-(EPA+DHA) diet raised plasma phosphatidylcholine-EPA and -DHA concentrations, decreased [13C]ALNA conversion to EPA (2-fold) and DPA (4-fold), whilst [13C]ALNA conversion to DHA was unchanged. The dietary interventions did not alter partitioning of ALNA towards β-oxidation. The present results indicate ALNA conversion was down-regulated by increased product (EPA+DHA) availability, but was not up-regulated by increased substrate (ALNA) consumption. This suggests regulation of ALNA conversion may limit the influence of variations in dietary n-3 fatty acid intake on plasma lipid compositions.

Alkylresorcinols (AR) are amphiphilic 1,3-dihydroxy-5-alkyl phenolic lipids. AR in food are only found in the outer layers of wheat and rye grains, and in whole grains are present at concentrations of 500–1000 μg/g. In wheat and rye, there are five main homologues, differing in the length of the odd-numbered alkyl chain (from seventeen to twenty-five C atoms long). Because AR may be bioactive, and might serve as biomarkers for these cereals, their absorption was investigated in model experiments with pigs and rats. Pigs with a cannula in the terminal ileum were fed four diets containing rye fractions with different levels of AR and the ileal effluents were analysed. The ileal recovery of AR was found to vary between 21 and 40 %, with no major difference between different chain-length homologues. The absorption of AR by rats was investigated by feeding 14C-labelled heneicosylresorcinol (C21:0). Of the total activity, about 34% was recovered in the urine, showing that the labelled AR was absorbed and metabolised by rats. AR were mostly cleared from rats by 60h. It is concluded that AR are absorbed in the small intestine of single-stomached animals and excreted in metabolised form in the urine, and might contribute to the nutritional qualities of wholegrain wheat and rye diets.

Epidemiological and clinical trials suggest an inverse relationship between dietary K intake and blood pressure (BP). Most trials however have been of short duration, the dose of K was high, and the results have been conflicting. The aim of the present study was to evaluate the effect on BP of a low-dose supplementation (24 mmol/d) for an extended period. A double-blind placebo-controlled trial was conducted on fifty-nine volunteers, randomly assigned to receive 24 mmol slow-release KC1/d (n 30) or a placebo (n 29). Measures of BP, anthropometric characteristics and urine analysis for electrolytes were recorded during a 1-week baseline period. Supplementation was for 6 weeks during which BP and changes in weight were assessed and a second 24h urine collection made. The primary outcome was the change in mean arterial pressure (MAP); systolic BP(SBP) and diastolic BP(DBP) were secondary outcomes. After 6 weeks of supplementation MAP was reduced by 7·01 (95% CI −9·12, −4·89; P<0·001) mmHg, SBP was reduced by 7·60 (95% CI −10·46, −4·73; P<0·001) mmHg and DBP was reduced by 6·46 (95% CI −8·74, −4·19; P<0·001) mmHg. The reduction in MAP was positively associated with baseline urinary Na:K (P<0·034). A low daily dietary supplement of K, equivalent to the content of five portions of fresh fruits and vegetables, induced a substantial reduction in MAP, similar in effect to single-drug therapy for hypertension.

Conjugated linoleic acids (CLA) have been shown to decrease body fat content in pigs. It is possible that feeding pigs diets rich in CLA may increase carcass lipid CLA to levels that could provide health benefits when included as a part of a healthy diet. Therefore, the aim of the present study was to determine whether dietary CLA supplementation has any effect on the fatty acid composition of subcutaneous and intramuscular adipose tissue in pigs. Thirty-five female cross bred (Large White×Landrace) pigs (initial weight 57·2kg and initial P2 back fat 11·5mm) were used in the present study. Pigs were housed individually and randomly allocated to one of six dietary treatments (0·00, 1·25, 2·50, 5·00, 7·50 and 10·00g CLA55 (55g CLA isomers/100g total fatty acids; Natural Lipids Ltd, Hovdebygda, Norway)/kg) and fed their respective diets for 8 weeks. Twelve CLA isomers in the diet and in pig tissue lipids were separated by Ag+-HPLC. CLA was incorporated at fivefold higher levels in subcutaneous fat as compared with intramuscular fat and in a dose-dependant manner. Overall, the transfer efficiency of CLA was maximized at 5·00g CLA55/kg. However, there was clear selectivity in the uptake or incorporation of cis,trans-9,11 isomer over the trans,cis-10,12 isomer. In general, CLA supplementation produced significant changes in skeletal muscle and adipose tissue fatty acid composition, indicating that dietary CLA had a potent affect on lipid transport and metabolism in vivo. Significant increases in myristic, palmitic and palmitoleic acids and a reduction in arachidonic acid were observed, suggesting an alteration in activity of Δ5-, Δ6- and Δ9-desaturases in pig adipose tissue. In conclusion, feeding pigs diets supplemented with CLA increases carcass lipid CLA, but also results in changes in the fatty acid profile in pig fat that could potentially outweigh the benefits of CLA.

The present study was designed to examine the effects of mixed high-carbohydrate meals with different glycaemic indices (GI) on substrate utilization during subsequent exercise. Nine healthy male recreational runners (age 26·8 (sem 1·1) years, body mass 74·7 (sem 2·4) kg, V˙O2max 58·1 (sem 1·7) ml/kg per min) completed three trials: high-glycaemic-index meal (HGI), low-glycaemic-index meal (LGI) and fasting (FAST), separated by 7 d. The test meals contained 2 g carbohydrate/kg body mass, they were isoenergetic and the GI values were 77·4, 36·9 and 0·0 respectively. In each trial, subjects consumed the test meal 3 h before performing a 60 min run at 65 % V˙O2max on a motorized treadmill. Ingestion of the HGI and LGI resulted in hyperglycaemia and hyperinsulinaemia during the postprandial period compared with the FAST (P<0·05). The incremental area under the curve for plasma glucose was 2-fold higher for HGI compared with LGI (108·7 v. 48·9 mmol/l per min). In contrast, plasma non-esterified fatty acid concentrations were significantly lower following HGI and LGI compared with FAST (P<0·05). During the subsequent submaximal exercise, plasma glucose declined to below the fasting value in HGI compared with LGI and FAST (P<0·05). The estimated total fat oxidation was significantly higher for the LGI than the HGI during exercise (P<0·05). In summary, both pre-exercise carbohydrate meals resulted in lower rates of fat oxidation during subsequent exercise than when subjects performed exercise in the fasting state. However, the LGI resulted in a higher rate of fat oxidation during exercise than following the consumption of the HGI.

The malnutrition caused by liver cirrhosis (LC) often worsens the course of the disease. Patients affected by LC often have a low bioavailability of the anabolic liver peptide insulin-like growth factor (IGF)-I. The present study was undertaken to investigate the effect of low doses of IGF-I on the nutritional status and in vivo jejunal transport of d-galactose in anatomically, pathologically and biochemically confirmed moderate, non-ascitic, cirrhotic rats. LC was experimentally induced in growing rats by inhalation of CCl4 and addition of phenobarbital to drinking water. Both the nutritional status, as evaluated by N balance, and in vivo intestinal transport of d-galactose, were significantly impaired in cirrhotic rats. As compared with healthy rats, administration of 20μg human recombinant IGF-I/kg body weight for 14d to cirrhotic rats significantly improved N balance variables and restored in vivo intestinal transport of the sugar. However, IGF-I had no effect on the steatorrhoea associated with LC. These results suggest that low doses of IGF-I may have beneficial effects on the malnutrition associated with moderate LC.

Dietary fibre sources are fermented by the gut flora to yield short-chain fatty acids (SCFA) together with degraded phytochemicals and plant nutrients. Butyrate, a major SCFA, is potentially chemoprotective by suppressing the growth of tumour cells and enhancing their differentiation. Conversely, it could lead to a positive selection pressure for transformed cells by inducing glutathione S-transferases (GST) and enhancing chemoresistance. Virtually nothing is known about how butyrate's activities are affected by other fermentation products. To investigate such interactions, a variety of dietary fibre sources was fermented with human faecal slurries in vitro, analysed for SCFA, and corresponding SCFA mixtures were prepared. HT29 colon tumour cells were treated for 72 h with individual SCFA or complex samples. The growth of cells, GST activity, and chemoresistance towards 4-hydroxynonenal were determined. Fermentation products inhibited cell growth more than the corresponding SCFA mixtures, and the SCFA mixtures were more active than butyrate, probably due to phytoprotectants and to propionate, respectively, which also inhibit cell growth. Only butyrate induced GST, whereas chemoresistance was caused by selected SCFA mixtures, but not by all corresponding fermentation samples. In summary, fermentation supernatant fractions contain compounds that: (1) enhance the anti-proliferative properties of butyrate (propionate, phytochemical fraction); (2) do not alter its capacity to induce GST; (3) prevent chemoresistance in tumour cells. It can be concluded that fermented dietary fibre sources are more potent inhibitors of tumour cell growth than butyrate alone, and also contain ingredients which counteract the undesired positive selection pressures that higher concentrations of butyrate induce in tumour cells.

We analysed the effects of goats' milk (GM) on the nutritive utilization of Ca and P in rats with resection of 50% distal small intestine in comparison with cows' milk (CM) and a standard non-milk diet. The three test diets contained 200 g protein and 100 g fat/kg. The apparent digestibility coefficient (ADC) of Ca and P were considerably higher in the two groups of rats given the GM diet than those given the other two diets. Ca and P retention did not decrease by effect of intestinal resection with GM diet. In both groups of animals, serum Ca and P levels and ionic Ca were higher in the case of the GM diet than the other two diets, whereas the parathyroid hormone levels were lower. Ca content in femur, sternum and longissimus dorsi muscle was higher in rats given the GM diet. P content in femur and sternum was higher among the two groups of rats given a milk-based diet (GM or CM), especially with GM diet. The GM diet has beneficial effects on nutritive utilization of Ca and P in control rats and those with resection of the distal small intestine.

The present study examined the ontogeny of mitochondrial protein abundance in adipose tissue and lungs over the first month of life in the sheep and the extent to which this may be altered by maternal undernutrition during the final month of gestation. The ontogeny of uncoupling protein (UCP), voltage-dependent anion channel (VDAC) and cytochrome c abundance were determined in adipose tissue and lungs sampled from near-term fetuses and young sheep aged 4 h, 1, 7 and 30 d. In adipose tissue, the abundance of UCP1, VDAC and cytochrome c all peaked at 1 d of age and then decreased by 30 d of age, at which stage the brown adipose tissue-specific UCP1 was no longer detectable but UCP2 was clearly abundant. For the lungs, however, UCP2 and VDAC abundance both peaked 7 d after birth and then decreased by 30 d of age. During postnatal development, therefore, a marked change in mitochondrial protein abundance occurs within both adipose tissue and lungs. Maternal nutrient restriction had no effect on lamb growth or tissue weights at 30 d of age but was associated with increased abundance of UCP2 and VDAC but not cytochrome c in both adipose tissue and lungs. These mitochondrial adaptations within both adipose tissue and the lungs of offspring born to previously nutrient-restricted mothers may compromise adipose tissue and lung function during periods of environmental stress.

Many orange-coloured fruits contain β-cryptoxanthin in its non-esterified as well as its esterified form. Information concerning the absorption of β-cryptoxanthin, especially with regard to the metabolism of its fatty acid esters, is rather scarce. The present study assessed the plasma concentration reached after consumption of a single dose of native β-cryptoxanthin esters from papaya (Carica papaya L.) or non-esterified β-cryptoxanthin in equal total amounts. In a randomized, single-blind crossover study, twelve subjects were served a portion of yoghurt containing esterified or non-esterified β-cryptoxanthin (1.3 mg absolute) together with a balanced breakfast. Between the two intervention days, there was a 2-week depletion period. After a fasting blood sample had been taken, futher samples were taken from the subjects at 3, 6, 9, 12 and 24 h. The concentration of non-esterified β-cryptoxanthin in the whole plasma was determined by HPLC; β-cryptoxanthin identification was confirmed by liquid chromatography–atmospheric pressure chemical ionization–MS analyses. Irrespective of the consumed diet, the plasma β-cryptoxanthin concentrations increased significantly (P=0·05) and peaked after 6–12 h. The concentration curves, as well as the areas under the curves, were not distinguishable according to two-sided F and t tests (P=0·05). Standardization of β-cryptoxanthin concentrations to plasma triacylglycerol and cholesterol had no impact on the results. Thus, the present study indicates comparable bioavailability of both non-esterified β-cryptoxanthin and mixtures of β-cryptoxanthin esters. The results support the existence of an effective enzymatic cleavage system accepting various β-cryptoxanthin esters.

The glycaemic index (GI) of commonly consumed bakery products supplemented with increasing levels of coconut (Cocos nucifera) flour was determined in ten normal and ten diabetic subjects. Using a randomized crossover design, the control and test foods were fed in random order on separate occasions after an overnight fast. Blood samples were collected through finger prick before and after feeding and were analysed for glucose levels using a clinical chemistry analyser. The significantly low-GI (< 60) foods investigated were: macaroons (GI 45·7 (sem 3·0)) and carrot cake (GI 51·8 (sem 3·3)), with 200–250 g coconut flour/kg (P<0·05). The test foods with 150 g coconut flour/kg had GI ranging from 61·3 to 71·4. Among the test foods, pan de sal (GI 87·2 (sem 5·5)) and multigrain loaf (GI 85·2 (sem 6·8)) gave significantly higher GI with 50 and 100 g coconut flour/kg respectively (P<0·05). On the other hand, granola bar and cinnamon bread with 50 and 100 g coconut flour/kg respectively gave a GI ranging from 62·7 to 71·6 and did not differ significantly from the test foods with 150 g coconut flour/kg (P < 0·05). A very strong negative correlation (r– 0·85, n 11, P < 0·005) was observed between the GI and dietary fibre content of the test foods supplemented with coconut flour. In conclusion, the GI of coconut flour-supplemented foods decreased with increasing levels of coconut flour and this may be due to its high dietary fibre content. The results of the present study may form a scientific basis for the development of coconut flour as a functional food. However, the fat content of coconut flour-supplemented food should always be considered to optimize the functionality of coconut fibre in the proper control and management of diabetes mellitus.

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisons P≤0·01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0·001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisons P≤0·05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0·03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0·001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.

The beneficial effect of bovine whey protein (WP) on bone metabolism has been shown in adult human subjects and ovariectomised rats. However, its effect on bone formation in earlier life, particularly during periods of bone mineral accrual, has not been investigated. Twenty-one male rats (4 weeks old, Wistar strain) were randomised by weight into three groups of seven rats each and fed ad libitum on a semi-purified low-Ca diet (3·0 g Ca/kg diet) containing 0 (control), 10 (diet WP1) or 20 (diet WP2) g bovine WP/kg for 47 d. On day 34 of the dietary intervention, all rats had two gelatine capsules containing demineralised bone powder implanted subcutaneously in the thorax region (a well-established in vivo model of ectopic bone formation). At 14 d after implantation, alkaline phosphatase activity (reflective of bone formation) in the bone implants from animals fed WP1 and -2 diets was almost 2-fold (P<0·01) that of control animals. Insulin-like growth factor (IGF)-I mRNA levels were about 3-fold (P<0·05) higher in implants from animals fed the WP diets compared with those from control animals. Serum- and urine-based biomarkers of bone metabolism and bone mineral composition in intact femora were unaffected by WP supplementation. In conclusion, the present findings suggest that bovine WP can enhance the rate of ectopic bone formation in young growing rats fed a Ca-restricted diet. This effect may be mediated by an increased synthesis of IGF-I in growing bone. The effect of WP on bone formation warrants further investigation.

The influence of propionate supplementation on the splanchnic metabolism of amino acids (AA) and other N compounds (urea-N and NH3-N) and the supply of AA and NH3-N to the hindlimb was investigated in growing lambs. Six rumen-cannulated and multicatheterised lambs (32·2kg) were fed frozen rye grass at 690kJ metabolisable energy intake/d per kg average metabolic body weight. They were infused intraruminally with a salt solution (control) or with propionate solutions at 0·23mol/l (P1) or 0·41mol/l (P2) infused at a maximal rate of 1·68 (sd 0·057) ml/min according to a repeated Latin square design. The propionate infusion did not increase the net portal appearance of total AA (TAA)-N but increased that of some branched-chain AA (valine and to a lesser extent isoleucine). Simultaneously, the propionate treatment (especially P2) induced an increased TAA utilisation by the liver. This was due mainly to an increased (+79%; P<0·07) utilisation of the essential AA and particularly the branched-chain AA. A stimulation of protein synthesis in the liver is hypothesised since (1) propionate stimulated insulin secretion and (2) utilisation of non-essential AA were less influenced by the propionate treatment in the liver (except for alanine), suggesting that the AA utilised by the liver were directed towards protein synthesis rather than towards oxidation or urea synthesis. At the splanchnic level, the propionate treatment did not have any effect on the TAA, non-essential AA and essential AA, except for a net splanchnic release that was decreased for leucine (P<0·02) and methionine (P<0·01) and increased for threonine (P<0·05). The propionate treatment did not have any effect on the hindlimb uptake of AA (essential and non-essential). As a consequence, even though the propionate treatment induced some major alterations in the splanchnic metabolism of AA, there were no changes in the net AA balance in the hindlimb (and hence probably on muscle growth). The role of the splanchnic tissues in the regulation of the AA supply to the peripheral tissues (such as muscle) therefore appears to be prominent in the regulation of muscle growth. Whether the peripheral tissues regulate their own supply by interacting with the splanchnic tissues (and especially the liver) or the liver is the only regulator of the AA supply to the muscle remains in doubt.

The effects of altering the type of n-3 polyunsaturated fatty acid (PUFA) in the mouse diet on the ability of monocytes and neutrophils to perform phagocytosis were investigated. Male weanling mice were fed for 7 d on one of nine diets which contained 178 g lipid/kg and which differed in the type of n-3 PUFA and in the position of these in dietary triacylglycerol (TAG). The control diet contained 4·4 g α-linolenic acid/100 g total fatty acids. In the other diets, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) replaced a proportion (50 or 100 %) of the α-linolenic acid, and were in the sn-2 or the sn-1(3) position of dietary TAG. There were significant increases in the content of n-3 PUFA in spleen-cell phospholipids when EPA or DHA was fed. These increases were largely independent of the position of EPA or DHA in dietary TAG except when EPA was fed at the highest level, when the incorporation was greater when it was fed in the sn-2 than in the sn-1(3) position. There was no significant effect of dietary DHA on monocyte or neutrophil phagocytic activity. Dietary EPA dose-dependently decreased the number of monocytes and neutrophils performing phagocytosis. However, when EPA was fed in the sn-2 position, the ability of active monocytes or neutrophils to engulf bacteria was increased in a dose-dependent fashion. This did not occur when EPA was fed in the sn-1(3) position. Thus, there appears to be an influence of the position of EPA, but not of DHA, in dietary TAG on its incorporation into cell phospholipids and on the activity of phagocytic cells.

Sun-dried raisins are a source of dietary fibre and tartaric acid. The effects of tartaric acid on colon function have not been the focus of extensive research. The purpose of the present study was to evaluate the effects of dietary fibre and tartaric acid from sun-dried raisins on colon function and on faecal bile acid and short-chain fatty acid (SCFA) excretion in healthy adults. Thirteen healthy subjects were fed 120 g sun-dried raisins/d or 5 g cream of tartar (equivalent to the tartaric acid in 120 g sun-dried raisins)/d for 9 weeks, divided into 3-week cycles. The experimental diets were fed in a crossover design after an initial control period. Faeces were collected for the last 4 d of each cycle for analysis of SCFA and bile acids. Intestinal transit time decreased from 42h on the baseline diet to 31h on cream of tartar (P<0·1) and to 28h on sun-dried raisins (P<0·05). Faeces were softer on both sun-dried raisins and cream of tartar, but sun-dried raisins increased faecal wet weight (P<0·05), while cream of tartar did not. Sun-dried raisins caused significant reductions from baseline values in total bile acid concentration (from 1·42 (sd 1·03) to 1·09 (sd 0·76) mg/g, P<0·05), whereas cream of tartar did not (1·40 (sd 1·06) mg/g). Sun-dried raisins also significantly reduced the lithocholic (LC):deoxylithocholic acid (DC) ratio (from 1·63 (sd 0·85) to 1·09 (sd 0·50), P<0·02), whereas cream of tartar reduced the ratio, but to a lesser extent (1·29 (sd 0·79), NS). Both faecal bile acids and the LC:DC ratio are indicators of reduced risk for colon cancer. Sun-dried raisins increased total SCFA excretion (from 5·6 (sd 3·4) to 7·6 (sd 3·0) g/4d, P<0·05), which remained unchanged with cream of tartar (5·6 (sd 3·0) g/4d). Both sun-dried raisins and cream of tartar appear to be good stool softeners and to shorten intestinal transit time, although the fibre in sun-dried raisins has the added benefit of increasing faecal weight. Both sun-dried raisins and cream of tartar modulate the composition of faecal bile acids and SCFA in a way that has potential health benefits.

Retinoids have been reported to produce regressions in metaplastic changes of the mucosal epithelium. In order to define the role of these micronutrients in the prevention of squamous metaplasia of the oral cavity, it is necessary to measure their uptake in target tissues such as the buccal mucosal epithelium. We demonstrated in a trial that retinyl palmitate applied topically via a toothpaste is taken up by buccal mucosal cells in young healthy volunteers. In the randomised, parallel-designed, placebo-controlled and double-blind trial, forty volunteers divided in two groups cleaned their teeth either with a placebo toothpaste or a retinyl palmitate-containing toothpaste (1 mg/g) for 56 d. Buccal mucosal cells samples were taken from the healthy volunteers during the retinyl palmitate application and the following wash-out phase to determine the concentration of retinyl palmitate and retinol by HPLC. Supplementary blood samples were taken from the volunteers on days 0 and 56 to investigate changes in plasma retinyl palmitate and retinol concentrations. Results from only thirty participants (sixteen placebo and fourteen treated subjects) were used in the statistical evaluation as the remaining sample results were spoiled by a technical defect during the HPLC analysis. A significant (P<0·05) uptake of retinyl palmitate in buccal mucosal cells after 7 d and a significant (P<0·05) increase of plasma retinol after 17 d was demonstrated in our present study. The uptake of retinyl palmitate and the following hydrolysis to retinol led to an enrichment of vitamin A in buccal mucosal cells.