Epidemiological data indicate that there is a strong association between intake of trans-18 : 2 fatty acids (TFA) and sudden cardiac death. There is little known about the mechanisms by which TFA exert harmful effects on the cardiovascular system. The present in vitro study is the first to demonstrate the effects of membrane-incorporated C18 : 2 TFA on human aortic endothelial cell (HAEC) function. Trans-18 : 2 fatty acids were incorporated to a greater extent (2-fold) in the phospholipid fraction of endothelial cells than that of cis-18 : 2; furthermore, these fatty acids were enriched to a similar extent in the TAG fraction. Flow cytometric analysis indicated that TFA treatment of HAEC significantly increased the expression of endothelial adhesion molecules, including intercellular adhesion molecule-1 (CD54) and vitronectin receptor (CD51/CD61). Incorporation of TFA into membranes increased HAEC adhesion to fibronectin- or vitronectin-coated plates by 1·5- to 2-fold, respectively. Neutrophil and monocyte adhesion to HAEC monolayers was nearly proportional to adhesion molecule expression. TFA treatment also induced the release of monocyte chemoattractant protein-1 by nearly 3-fold in non-stimulated HAEC. Furthermore, we examined the role of TFA on in vitro angiogenic assays. Chemotactic migration of TFA-treated HAEC toward sphingosine-1-phosphate (SPP) was significantly increased compared with controls. Conversely, capillary morphogenesis of TFA-treated HAEC was significantly inhibited in response to SPP, suggesting that TFA incorporation suppresses endothelial cell differentiation. In conclusion, these in vitro studies demonstrated that TFA play a role in the induction of pro-inflammatory responses and endothelial cell dysfunction.

Bitter melon (Momordica charantia; BM) has been shown to ameliorate diet-induced obesity and insulin resistance. To examine the effect of BM supplementation on cell size and lipid metabolism in adipose tissues, three groups of rats were respectively fed a high-fat diet supplemented without (HF group) or with 5 % lyophilised BM powder (HFB group), or with 0·01 % thiazolidinedione (TZD) (HFT group). A group of rats fed a low-fat diet was also included as a normal control. Hyperinsulinaemia and glucose intolerance were observed in the HF group but not in HFT and HFB groups. Although the number of large adipocytes (>180 μm) of both the HFB and HFT groups was significantly lower than that of the HF group, the adipose tissue mass, TAG content and glycerol-3-phosphate dehydrogenase activity of the HFB group were significantly lower than those of the HFT group, implying that BM might reduce lipogenesis in adipose tissue. Experiment 2 was then conducted to examine the expression of lipogenic genes in adipose tissues of rats fed low-fat, HF or HFB diets. The HFB group showed significantly lower mRNA levels of fatty acid synthase, acetyl-CoA carboxylase-1, lipoprotein lipase and adipocyte fatty acid-binding protein than the HF group (P < 0·05). These results indicate BM can reduce insulin resistance as effective as the anti-diabetic drug TZD. Furthermore, BM can suppress the visceral fat accumulation and inhibit adipocyte hypertrophy, which may be associated with markedly down regulated expressions of lipogenic genes in the adipose.

Magnesium (Mg) is the fourth most abundant mineral in the body and the most abundant intracellular divalent cation, with essential roles in many physiological functions. Consequently, the assessment of Mg status is important for the study of diseases associated with chronic deficiency. In spite of intense research activities there is still no simple, rapid, and accurate laboratory test to determine total body Mg status in humans. However, serum Mg < 0·75 mmol/l is a useful measurement for severe deficiency, and for values between 0·75 and 0·85 mmol/l a loading test can identify deficient subjects. The loading test seems to be the gold standard for Mg status, but is unsuitable in patients with disturbed kidney and intestinal functions when administered orally. There is also a need to reach a consensus on a standardized protocol in order to compare results obtained in different clinical units. Other cellular Mg measurements, such as total or ionized Mg, frequently disagree and more research and systematic evaluations are needed. Muscle Mg appears to be a good marker, but biopsies limit its usefulness, as is the case with bone Mg, the most important but heterogeneous Mg compartment. The development of new and non invasive techniques such as nuclear magnetic resonance (NMR) may provide valuable tools for routinely analysing ionized Mg in tissues. With the development of molecular genetics techniques, the recent discovery of Transient Receptor Potential Melastatin channels offers new possibilities for the sensitive and rapid evaluation of Mg status in humans.

Fatty acids in milk are thought to play an important role in intestinal maturation and gene expression in the rat small intestine during the suckling–weaning period. In the present study, we determined the jejunal mRNA level of the cAMP-response-element-binding-protein-binding protein (CBP)/p300, which is one of the chromatin remodelling factors and regulates histone acetylation, during the postnatal period in rats. The mRNA level of CBP/p300 was high during the suckling and middle of the weaning period (day 5 to 20) and then declined sharply to a low level at the end of the weaning period and after weaning. In situ hybridisation also showed that CBP/p300 mRNA levels in the villus as well as the basal membrane clearly decreased after weaning. Rat pups at age 17 d, weaned to a high-fat diet, showed higher levels of CBP/p300 mRNA than those weaned to a low-fat diet. Oral administration of caprylic acid, oleic acid and linoleic acid, which are major fatty acid components in milk, induced jejunal CBP/p300 gene expression. The present results suggest that fatty acids in components of milk enhance expression of the CBP/p300 genes in the small intestine.

This article describes the principles and limitations of methods used to investigate reactive oxygen species (ROS) protective properties of dietary constituents and is aimed at providing a better understanding of the requirements for science based health claims of antioxidant (AO) effects of foods. A number of currently used biochemical measurements aimed of determining the total antioxidant capacity and oxidised lipids and proteins are carried out under unphysiologcial conditions and are prone to artefact formation. Probably the most reliable approaches are measurements of isoprostanes as a parameter of lipid peroxidation and determination of oxidative DNA damage. Also the design of the experimental models has a strong impact on the reliability of AO studies: the common strategy is the identification of AO by in vitro screening with cell lines. This approach is based on the assumption that protection towards ROS is due to scavenging, but recent findings indicate that activation of transcription factors which regulate genes involved in antioxidant defence plays a key role in the mode of action of AO. These processes are not adequately represented in cell lines. Another shortcoming of in vitro experiments is that AO are metabolised in vivo and that most cell lines are lacking enzymes which catalyse these reactions. Compounds with large molecular configurations (chlorophylls, anthocyans and polyphenolics) are potent AO in vitro, but weak or no effects were observed in animal/human studies with realistic doses as they are poorly absorbed. The development of -omics approaches will improve the scientific basis for health claims. The evaluation of results from microarray and proteomics studies shows that it is not possible to establish a general signature of alterations of transcription and protein patterns by AO. However, it was shown that alterations of gene expression and protein levels caused by experimentally induced oxidative stress and ROS related diseases can be normalised by dietary AO.

The mechanism that drives the growth of some colonic adenomas towards malignancy, while permitting others to remain for decades in quiescence, remains unknown. Diets can alter the growth rate of intestinal tumours but it is still unknown whether diets are able to alter the molecular biology of these adenomas in a way that predicts further outcome. To address this issue we fed Min/+ mice with two diets known to lead to different adenoma outcomes: a high-fat control diet (n 15) or a high-fat inulin-enriched (10 % w/w) diet (n 13). To study the effect of diet on cell signalling during adenoma growth, the adenomas of each Min/+ mouse were divided into three size-categories, and the levels of β-catenin, E-cadherin, cyclin D1 and matrix metalloproteinase-9, which are known to be involved in colon tumorigenesis, were determined. The growth-promoting inulin diet resulted in more large adenomas than the control feeding (P = 0·003) and doubled the total area of the adenomas (P = 0·008). The inulin diet increased the expression of nuclear β-catenin (P = 0·004) and its target cyclin D1 (P = 0·017) as the adenomas increased in size from small to large, indicating the presence of an accelerated cancerous process. Neither phenomenon was seen in the control group during adenoma growth. Our results suggest that in addition to the number, size, and growth rate of adenomatous polyps, the signalling pattern of the adenomas should also be considered when evaluating preventive dietary strategies.

Based on the potential benefits of cis-9, trans-11-conjugated linoleic acid (CLA) for human health there is interest in developing sustainable nutritional strategies for enhancing the concentration of this fatty acid in ruminant-derived foods. Most evidence to date suggests that endogenous synthesis is the major source of cis-9, trans-11 in milk fat and ruminal outflow is limited and largely independent of dietary 18 : 2n-6 supply. Four lactating cows fitted with a rumen cannula were used in a 4 × 4 Latin square with 14 d experimental periods to examine the effects of sunflower-seed oil (SFO) as a source of 18 : 2n-6 on ruminal lipid metabolism. Cows were offered grass silage-based diets supplemented with 0, 250, 500 or 750 g SFO/d. Supplements of SFO had no effect on DM intake, milk fat or protein secretion, but increased linearly (P < 0·01) milk yield and milk lactose output and shifted (P < 0·001) rumen fermentation towards propionate at the expense of acetate. SFO supplements increased linearly (P < 0·05) the flow of 18 : 0, 18 : 1, 18 : 2n-6 and total CLA at the omasum and enhanced ruminal cis-9-18 : 1, 18 : 2n-6 and 18 : 3n-3 metabolism. Flows of all-trans- (Δ4–16) and cis- (Δ9–16) 18 : 1 isomers were elevated, while increases in ruminal CLA outflow were confined to trans-8, trans-10 and geometric 9,11 and 10,12 isomers. It is concluded that supplementing grass silage-based diets with plant oils rich in 18 : 2n-6 enhances ruminal outflow of trans-11-18 : 1 and cis-9, trans-11-CLA in lactating cows.

Lower CVD incidence is reported in Asian populations consuming soya-containing food. As polymorphonuclear leukocytes (PMN) are involved in the risk of CVD, we investigated the modulatory effect of soya isoflavones on several PMN functions and their molecular mechanisms in vitro. PMN, isolated from blood from healthy subjects, were tested upon activation with 1 μm- n-formyl-methyl-leucyl-phenylalanine (fMLP) for superoxide anion production (ferric cytochrome c reduction) and released elastase (chromogenic test). PMN homotypic aggregates stimulated by fMLP or P-selectin in dynamic conditions were detected by optical microscopy. PMN, mixed with thrombin-activated, washed platelets, formed cell aggregates, measured by flow cytometry. Phosphorylation of Pyk2, a focal adhesion kinase, was studied by immunoprecipitation and immunoblotting with specific antibodies. Genistein, daidzein and equol inhibited superoxide anion production (IC50 0·25 (sem 0·1), 21·0 (sem 4·2) and 13·0 (sem 2·8) μm, respectively); the release of elastase was prevented by genistein (IC50 63 (sem 17) μm). PMN homotypic aggregates, stimulated by fMLP, were significantly reduced (24 (sem 12) and 51 (sem 14) % of control) by 100 μm genistein and equol. P-selectin-induced aggregates were reduced to 19 (sem 6), 44 (sem 10) and 28 (sem 9) % of control by 100 μm genistein, daidzein and equol, respectively. Genistein, daidzein and equol also significantly reduced mixed platelet-PMN aggregates (IC50 4·0 (sem 0·9), 57 (sem 6) and 66 (sem 23) μm, respectively). In PMN challenged by fMLP or P-selectin, activation of Pyk2 was prevented by isoflavones. The cardioprotective effect of soya-containing food might be linked to reduction of PMN activation and PMN-platelet interaction, novel targets for the biological effects of soya isoflavones.

PPARγ is obligatory for fat mass generation and is thought to determine the amount of TAG stored per fat cell. We investigated whether ligand availability for PPARγ is rate limiting in fat mass generation and substrate metabolism. Twenty healthy men (20–29 years) were randomly assigned to receive the PPARγ ligand rosiglitazone (RSG) (8 mg/d) (n 10) or a placebo (n 10) during a stay of 7 d in a respiration chamber. Food intake was ad libitum, resulting in positive energy balances of 32·2 MJ (placebo) and 44·7 MJ (RSG). Fat cell size and expression of PPARγ, adipocyte fatty acid-binding protein (aP2), adipsin, adiponectin and fasting-induced adipose factor (FIAF) were determined in subcutaneous abdominal fat biopsies. The total amount of fat stored and the amount of TAG per fat cell were not different between groups. For the entire group, fat cell size was decreased after overeating (P = 0·02). FIAF mRNA levels were decreased after overeating in the RSG group (P = 0·01), with a trend towards a decrease in the placebo group. Unexpectedly, RSG treatment did not influence the expression levels of PPARγ and of the PPARγ responsive genes aP2, adiponectin and adipsin. In addition, RSG resulted in a larger increase in plasma TAG during overeating than placebo treatment. These results suggest that in healthy, non-obese males the PPARγ ligand RSG influences TAG metabolism, independent of its PPARγ transcriptional activity in the subcutaneous adipose tissue.

Several studies have reported differing data on the effect of exogenous nucleosides and nucleotides on the proliferation and differentiation in various intestinal cell lines and explants. To study whether exogenous nucleosides modulate intestinal cell differentiation, IEC-6 cells were differentiated in the presence or absence of a nucleoside mixture (cytidine, uridine, guanosine and inosine, 30 μm each), and the concentrations of nucleoside derivatives were determined by HPLC. Cell differentiation was assessed by electron microscopy, alkaline phosphatase activity and Rnd3 gene expression. The present results showed that uridine, guanosine and inosine were cleared from culture media (up to 32, 63 and 100 % in proliferating cells, and 31, 80 and 94 % in differentiated cells, respectively) whereas cytidine concentrations increased. Differentiation of IEC-6 cells was associated with a significant increase in intracellular nucleotide concentrations. Clearance of nucleosides correlated with a significant increase in the intracellular nucleotide pool in proliferating and differentiated IEC-6 cells. Intracellular guanosine nucleotides increased 2·5- and 5-fold in nucleoside-supplemented proliferating and differentiated cells, respectively. At 24 h, nucleoside-supplemented differentiated IEC-6 cells had significantly higher energy charge and GTP levels than non-supplemented ones. These modifications paralleled changes in cell differentiation as indicated by increased alkaline phosphatase activity, prolonged microvilli formation and accelerated down-regulation of Rnd3 gene expression. The present findings suggest that exogenous nucleosides were selectively taken up by IEC-6 cells, increased the intracellular nucleotide pool, GTP and energy charge, and favoured cell morphological and functional changes during differentiation.

Cancers of the gastrointestinal tract are amongst the most common causes of death from cancer, but there is substantial variation in incidence across populations. This is consistent with a major causative role for diet. There is convincing evidence that fruits and vegetables protect against cancers of the upper alimentary tract and the large bowel, and this has focused attention on biologically active phytochemicals, and on flavonoids in particular. Many flavonoids exert anticarcinogenic effects in vitro and in animals, and many of these effects occur via signalling pathways known to be important in the pathogenesis of colorectal, gastric and oesophageal cancers. However dietary flavonoid intakes are generally low and their metabolism in humans is extremely complex. The advent of new post-genomic technologies will do much to address these problems by making it possible to monitor patterns of gene expression in humans to provide essential molecular biomarkers of early disease. By combining such data with knowledge of the dietary exposure and bioavailability of the most effective compounds it will be possible to predict the most effective dietary sources and to properly evaluate the potential role of flavonoids in clinical nutrition.

The increasing prevalence of obesity during growth and development is significantly related to the education of children, and also to that of parents who influence food intake and physical activity from the beginning of life. The effect of maternal level of education has been shown in regular anthropometric surveys in 10-year intervals since 1951. This concerns the mother's own nutrition and physical activity regimen as well as the child's nutrition since birth, including the duration of breast-feeding. Children of parents with overweight and obesity were shown more often to be obese, as was the case for children from families with the lowest level of education, or from smaller communities where the level of education is usually lower than in larger cities. The composition of the mother's diet during pregnancy had, for example, an effect on the blood lipids of newborns. During preschool age, less body fat, a higher level of HDL, and higher levels of cardiorespiratory fitness, skill and physical performance were found in active children. In school-age children, when obesity increases, a number of prevention programmes using diet, exercise and behavioural intervention have been developed for schools, communities, churches, and/or have been organized by special institutions and medical centres, which were most efficient in family groups. The greatest reduction of weight, BMI and fatness, and improvement of functional capacity, and hormonal and metabolic parameters were achieved in summer camps or spas, with consistent and monitored nutrition, exercise and behavioural treatment. Fluctuation of positive outcomes occurred due to the interruption of the educational process during the school year, and repeated long-lasting interventions have been always necessary for permanent desirable results.

Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 ± 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 ± 14 μg/d. Plasma Se concentrations averaged 1·13 ± 0·16 μmol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.

Altered fatty acid (FA) composition is related to insulin resistance and CVD. One possible mediator may be inflammation, but longitudinal data relating FA composition to inflammation taking insulin resistance into account are limited. We investigated the long-term association between FA composition and C-reactive protein (CRP) concentrations in a large population-based cohort study in 767 men followed for 20 years. The association between FA composition in serum cholesteryl esters at age 50 and CRP concentrations at age 70 was investigated using linear regression. In addition, desaturase activities (stearoyl-CoA desaturase-1 (SCD-1), Δ5- and Δ6-desaturase) were estimated using FA product-to-precursor ratios. Insulin resistance was measured directly at follow-up by euglycaemic clamp. After adjusting for confounders (smoking, physical activity, alcohol intake, obesity and erythrocyte sedimentation rate) CRP concentrations were inversely associated with the proportion of 18 : 2n-6 (P = 0·002) and positively associated with 16 : 1n-7 (P = 0·008), 18 : 1n-9 (P = 0·0003), 20 : 5n-3 (P = 0·04) and estimated SCD-1 (P = 0·005) and Δ6-desaturase (P = 0·02) activities. After adding insulin resistance to the model, 18 : 1n-9, 18 : 2n-6 and SCD-1 remained significant predictors of CRP. A FA composition indicating low intake of 18 : 2n-6, high intake of SFA and high SCD-1 activity is, in a Swedish population of middle-aged men, associated with CRP concentrations 20 years later, even independently of obesity and insulin resistance.

Hyperuricaemia is one of the components of metabolic syndrome. Both oxidative stress and hyperinsulinism are important variables in the genesis of this syndrome and have a close association with uric acid (UA). We evaluated the effect of an oral glucose challenge on UA concentrations. The study included 656 persons aged 18 to 65 years. Glycaemia, insulin, UA and plasma proteins were measured at baseline and 120 min after an oral glucose tolerance test (OGTT). The baseline sample also included measurements of total cholesterol, triacylglycerol (TAG) and HDL-cholesterol. Insulin resistance was calculated with the homeostasis model assessment. UA levels were significantly lower after the OGTT (281·93 (sd 92·19) v. 267·48 (sd 90·40) μmol/l; P < 0·0001). Subjects with a drop in UA concentrations >40·86 μmol/l (>75th percentile) had higher plasma TAG levels (P = 0·0001), baseline insulin (P = 0·02) and greater insulin resistance (P = 0·034). Women with a difference in plasma concentrations of UA above the 75th percentile had higher baseline insulin levels (P = 0·019), concentration of plasma TAG (P = 0·0001) and a greater insulin resistance index (P = 0·029), whereas the only significant difference in men was the level of TAG. Multiple regression analysis showed that the basal TAG levels, insulin at 120 min, glycaemia at 120 min and waist:hip ratio significantly predicted the variance in the UA difference (r2 0·077). Levels of UA were significantly lower after the OGTT and the individuals with the greatest decrease in UA levels are those who have greater insulin resistance and higher TAG levels.

This study was designed to determine whether (1) protein type and (2) the dietary carbohydrate to lipid content affected daily energy intake, body weight and adiposity in rats receiving high-protein diets ad libitum over a 25 d period. Each of the ten groups (n 8) consumed ad libitum one of the diets described below. A normal protein diet (P14C56L30, containing whole milk protein) and nine high-protein diets were used. The composition of the high-protein diets varied in terms of two parameters: macronutrient composition and protein type. Three macronutrient compositions (P55C35L10, P55C15L30 and P55L45) combined with three protein types (Milk, Whey and βLac) allowed us to test nine diets. The results show that both protein type (βLac > Whey > Milk) and the carbohydrate to lipid ratio (P55L45>P55C35L10 or P55C15L30) modulated reductions in energy intake, body weight and adiposity in rats receiving high-protein diets ad libitum, when compared with rats fed a normal diet under the same conditions. By contrast, blood lipid profiles were mainly influenced by the carbohydrate to lipid ratio (P55C15L30>P55L45 or P55C35L10). Moreover, βLac protein was also the most efficient in tending to preserve lean body mass at the expense of fat mass, and improve blood metabolism hormones (insulin, leptin). Taken together, the present results show that whey-derived protein sources, and particularly β-lactoglobulin-enriched fraction, are of considerable value because of their ability to reduce both body weight gain and the adiposity index.

Numerous mechanisms have been proposed to explain the anti-carcinogenic effects of Se, among them altered carcinogen metabolism. We investigated the effect of Se supplementation on activities of glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione S-transferase (GST) in different blood compartments, and expression of selected phase 1 and phase 2 genes in leucocytes (GPX1, γ-glutamylcysteine ligase catalytic subunit (GCLC), AP-1 transcription factor Fos-related antigen 1 (Fra1), NAD(P)H:quinone oxidoreductase (NQO1), and aryl hydrocarbon receptor repressor (AhRR)). Healthy elderly Danes (n 105; age 71·3 (sd 4·26) years; 36 % reporting use of multivitamin/mineral supplements) participated and were supplemented daily for 5 years with placebo, 100 μg, 200 μg or 300 μg Se as Se-enriched yeast (SelenoPrecise®). Blood samples were collected after 5 years of intervention. When all four groups were compared we found no effect of Se supplementation on plasma GPX or GR, on erythrocyte GPX, GR or GST, or on thrombocyte GR or GST. We found increased thrombocyte GPX activity at the two highest dosage levels in women only, but not in men. No effects on GPX1, NQO1 or AhRR gene expression were found. When all Se-supplemented groups were pooled we found significant down regulation of the expression of some phase 2 genes (GCLC, Fra1). A significant increase in AhRR gene expression with smoking was found but was independent of Se supplementation. Down regulation of phase 2 genes could increase the risk of cancer. However, further studies are needed to establish whether the observed effect in leucocytes reflects a similar expression pattern in target tissues.

This study examined the influence of different resistant starch (RS) varieties and conventional fibres on the efficiency of nutrient utilisation and intestinal fermentation in pigs. Thirty-six pigs (30 kg) were fed poultry meal-based diets supplemented with 10 % granular resistant corn starch (GCS), granular resistant potato starch (GPS), retrograded resistant corn starch (RCS), guar gum (GG) or cellulose for 36 d according to a completely randomised block design. Distal ileal and total tract recoveries were similar (P>0·05) among the RS varieties. Distal ileal starch recovery was higher (P < 0·05) in pigs consuming the RS diets (27–42 %) as compared with the control group (0·64 %). Consumption of GCS reduced (P < 0·05) apparent total tract digestibility and whole-body retention of crude protein in comparison with the control group. Consumption of GPS reduced (P < 0·05) total tract Ca digestibility and whole-body retention of Ca and P compared with the control group. However, consumption of RCS increased (P < 0·05) total tract Ca digestibility compared with the control group. Caecal butyrate concentration was increased (P < 0·05) following consumption of RCS and GG in comparison with the control group. Consumption of all the RS varieties reduced (P < 0·05) caecal indole concentrations compared with the control. Caecal butyrate concentrations were positively correlated (P < 0·05; r 0·63–0·83) with thermal properties among the RS varieties. We conclude that nutrient utilisation and intestinal fermentation are differentially affected by the consumption of different RS varieties and types of fibres. Thermal properties associated with different RS varieties may be useful markers for developing RS varieties with specific functionality.

Fructus Ligustri Lucidi (FLL), a kidney-tonifying Chinese herb, was shown to regulate Ca balance in ovariectomized (OVX) rats in our previous study. This study investigated whether it could improve bone properties in aged normal and OVX rats and increase osteoblastic differentiation in rat osteoblast-like UMR-106 cells. Ten-month-old aged rats underwent sham-operation or ovariectomy, were orally administered with FLL extracts or its vehicle and fed with diets containing different levels of Ca (LCD, 0·1 % Ca; MCD, 0·6 % Ca; HCD, 1·2 % Ca) for 12 weeks. Ovariectomy induced bone loss at multiple-sites of both tibia and femur in all rats being studied. FLL extract increased bone mineral density and bone mineral content at both tibial and femoral diaphysis as well as the lumbar vertebra (LV-2) in rats fed either LCD or MCD. In addition, FLL increased biomechanical strength of the tibial diaphysis in these rats. Combination of FLL and high-Ca diet significantly improved bone mass of cortical and trabecular bone at appendicular bones and LV-2 and decreased bone loss associated with ovarietomy and low-Ca feeding. Treatment of UMR-106 cells with FLL extracts accelerated the formation of calcified matrix and increased extracellular Ca and P depositions in time- and dose-dependent manner. The level of mineralization reached a maximum by 6 d incubation at the dosage of 10 μg FLL extract/ml. Our study indicated that FLL extract could improve bone properties in aged rats possibly via its direct action on osteoblastic cells by enhancement of the mineralization process.

Folate and the metabolically related B-vitamins, vitamin B12 and riboflavin, have attracted much scientific and public health interest in recent years. Apart from a well established role in preventing neural tube defects (NTDs), evidence is emerging to support other potential roles for folate and/or related B-vitamins in protecting against cardiovascular disease (especially stroke), certain cancers, cognitive impairment and osteoporosis. However, typical folate intakes are sub-optimal, in that although adequate in preventing clinical folate deficiency (i.e. megaloblastic anaemia) in most people, they are generally insufficient to achieve a folate status associated with the lowest risk of NTDs. Natural food folates have a limited ability to enhance folate status as a result of their poor stability under typical cooking conditions and incomplete bioavailability when compared with the synthetic vitamin, folic acid (as found in supplements and fortified foods). Current folate recommendations to prevent NTDs (based primarily on folic acid supplementation) have been found to be ineffective in several European countries. In contrast, in North America and Chile, the policy of mandatory folic acid-fortification has proven itself in terms of lowering the prevalence of NTD, but remains controversial because of concerns regarding potential risks of chronic exposure to high-dose folic acid. In the case of vitamin B12, the achievement of an optimal status is particularly difficult for many older people because of the common problem of food-bound B12 malabsorption. Finally, there is evidence that riboflavin status is generally low in the UK population, and particularly so in younger women; this warrants further investigation.