Habitual coffee consumption is associated with the prevention of type 2 diabetes, which often accompanies diabetic nephropathy. However, the relationship between coffee consumption and kidney function is unclear. Therefore, we investigated the associations between habitual coffee consumption and kidney function and damage assessed by the estimated glomerular filtration rate (eGFR) and proteinuria using dipstick urinalysis, respectively, in a cross-sectional study of 342 apparently healthy adults. Habitual coffee consumption was defined as drinking one or more cups of coffee per d. eGFR in coffee consumers (n 182; 80·1 (sd 15·0) ml/min per 1·73 m2) was significantly higher than that in non-coffee consumers (n 160; 76·9 (sd 12·6) ml/min per 1·73 m2) (P < 0·05). Multivariate logistic analysis showed that, compared with non-coffee consumption, coffee consumption was significantly associated with normal or increased eGFR (NIGFR) ( ≥ 90 ml/min per 1·73 m2), but not proteinuria, which was not attenuated, even after adjustment for age, sex, smoking, tea consumption and other cardiovascular risks (OR 2·91; 95 % CI 1·51, 5·61; P = 0·001). When we took into account eGFR measured 1 year before in a subgroup of the subjects (n 262), coffee consumption (n 142) had a significant relationship with eGFR, which was consistently higher with a difference of 4·0 ml/min per 1·73 m2 compared with non-coffee consumption (P = 0·01; two-way repeated ANOVA). Similar associations were observed in both sexes when data were reanalysed according to sex. In conclusion, our findings suggest that habitual coffee consumption is associated with NIGFR independently of clinical confounders. Further studies are needed to confirm this association and to explore whether the effect of coffee consumption on eGFR is beneficial for the kidney.

Disodium ascorbyl phytostanol phosphate (FM-VP4) is a synthetic compound derived from sitostanol and campestanol that has proved to be efficient as a cholesterol-lowering therapy in mice and human subjects. However, the mechanism of action of FM-VP4 remains unknown. The present study tests the ability of FM-VP4 to alter intestinal and liver cholesterol homeostasis in mice. Female C57BL/6J mice were fed either a control chow or a 2 % FM-VP4-enriched diet for 4 weeks. FM-VP4 reduced the in vivo net intestinal cholesterol absorption and plasma and liver cholesterol concentrations by 2·2-, 1·5- and 1·6-fold, respectively, compared with control mice. Furthermore, FM-VP4 also showed an impact on bile acid homeostasis. In FM-VP4 mice, liver and intestinal bile acid content was increased by 1·3- and 2·3-fold, respectively, whereas faecal bile acid output was 3·3-fold lower. FM-VP4 also increased the intestinal absorption of orally administered [3H]taurocholic acid to small intestine in vivo. Inhibition of intestinal cholesterol absorption by FM-VP4 was not mediated via transcriptional increases in intestine liver X receptor (LXR)-α, adenosine triphosphate-binding cassette transporter (ABC)-A1, ABCG5/G8 nor to decreases in intestinal Niemann-Pick C1-like 1 (NPC1L1) expression. In contrast, FM-VP4 up-regulated liver LXRα, ABCA1, ABCG5, scavenger receptor class BI (SR-BI) and hydroxymethylglutaryl coenzyme A reductase (HMGCoA-R) gene expression, whereas it down-regulated several farnesoid X receptor (FXR)-target genes such as cytochrome P450 family 7 subfamily A polypeptide 1 (CYP7A1) and Na+/taurocholate co-transporter polypeptide (NTCP). In conclusion, FM-VP4 reduced intestinal cholesterol absorption, plasma and liver cholesterol and affected bile acid homeostasis by inducing bile acid intestinal reabsorption and changed the liver expression of genes that play an essential role in cholesterol homeostasis. This is the first phytosterol or stanol that affects bile acid metabolism and lowers plasma cholesterol levels in normocholesterolaemic mice.

The plasma lipid-lowering effect of PUFA, one of their main beneficial effects, is considered to be related to the regulation of lipid biosynthesis through transcription factors including sterol regulatory element binding proteins (SREBP). In the present study, we compared the effect of different PUFA on SREBP activity in HepG2 cells, using a sterol regulatory element–luciferase reporter construct as a probe. Supplementation with different fatty acids reduced SREBP activity in the order 20 : 5n-3 = 18 : 2n-6 = 20 : 4n-6≫18 : 3n-3 = 22 : 6n-3 = 22 : 5n-6≫18 : 1n-9. The suppression of SREBP activity greatly depended on the degree of incorporation of the supplemented PUFA into cellular lipids, and correlated positively with the unsaturation index (r 0·831; P < 0·01) of total cell lipids. Supplemented PUFA were also metabolised to longer and more unsaturated species. These processing activities were higher for n-3 than n-6 PUFA (P < 0·01). We studied the effect of PUFA on the intracellular distribution of non-esterified cholesterol, using filipin staining and fluorescence microscopy with or without the cholesterol traffic blocker U18666A. The data show that the incorporation of PUFA increases non-esterified cholesterol flow from the plasma membrane to intracellular membranes. We conclude that suppression of SREBP activity by PUFA depends on the degree of incorporation into cellular lipids, and is associated with increased flow of non-esterified cholesterol between the plasma membrane and intracellular membranes.

The dietary flavonoid epicatechin has been reported to exhibit a wide range of biological activities. The objective of the present study was to investigate the time-dependent regulation by epicatechin on the activity of the main transcription factors (NF-κB, activator protein-1 (AP-1) and nuclear transcription factor erythroid 2p45-related factor (Nrf2)) related to antioxidant defence and survival and proliferation pathways in HepG2 cells. Treatment of cells with 10 μm-epicatechin induced the NF-κB pathway in a time-dependent manner characterised by increased levels of IκB kinase (IKK) and phosphorylated inhibitor of κB subunit-α (p-IκBα) and proteolytic degradation of IκB, which was consistent with an up-regulation of the NF-κB-binding activity. Time-dependent activation of the AP-1 pathway, in concert with enhanced c-Jun nuclear levels and induction of Nrf2 translocation and phosphorylation were also demonstrated. Additionally, epicatechin-induced NF-κB and Nrf2 were connected to reactive oxygen species intracellular levels and to the activation of cell survival and proliferation pathways, being phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and extracellular regulated kinase (ERK) associated to Nrf2 modulation and ERK to NF-κB induction. These data suggest that the epicatechin-induced survival effect occurs by the induction of redox-sensitive transcription factors through a tight regulation of survival and proliferation pathways.

Protein from lupin is supposed to have anti-atherogenic effects due to its lipid-lowering properties in laboratory animals. It is further suggested that the amino acid cysteine plays a crucial role in this aspect. The objective of the present study was to compare the effects of lupin protein and cysteine-supplemented casein with those of casein on atherosclerotic lesion development in apoE-deficient mice. For that purpose, thirty mice were fed an egg albumin-based Western-type diet containing test protein (100 g/kg) for 4 months. ApoE-deficient mice fed the lupin protein or the cysteine-supplemented casein had more than 50 % less aortic calcification than mice fed casein (P < 0·05). The quantified lesion area as a percentage of the total surface area, as well as the collagen and fat content of the lesions were not different between the three groups of mice. The concentration of VLDL TAG was higher in mice fed the lupin protein and the cysteine-supplemented casein than in mice fed casein (P < 0·05). The cholesterol concentrations of VLDL, LDL and HDL from mice fed the lupin protein and cysteine-supplemented casein were not different compared with the mice fed casein. Also, the plasma concentrations of homocysteine, Ca, inorganic phosphate, and the activity of glutathione peroxidase in plasma and liver did not differ between the three groups of mice. The present study shows that lupin protein and cysteine-supplemented casein compared with casein reduce the calcification of atherosclerotic lesions in apoE-deficient mice. This effect seems not to be mediated by effects on plasma lipoproteins, homocysteine and circulating minerals.

The effects of long-term dietary supplementation of fish oil (n-3 PUFA-rich) in adult male pigs on body condition as well as insulin sensitivity and secretion were examined. Fifteen Duroc boars aged 204·5 (sd 9·4) d (body weight 145·8 (sd 16·8) kg) received daily 2·5 kg basal diet with a supplement of: (1) 62 g hydrogenated animal fat (n 5); (2) 60 g menhaden oil containing 10·8 g DHA and 9·0 g EPA (n 6); (3) 60 g tuna oil containing 19·8 g DHA and 3·9 g EPA (n 4). Rations were balanced to be isoenergetic. After 7 months of treatments, oral glucose and meal tolerance tests were conducted after insertion of a catheter into the jugular vein. Dietary supplementation with n-3 PUFA altered the blood plasma profile: DHA and EPA increased whereas arachidonic acid decreased (P < 0·01). Plasma glucose, insulin and C-peptide responses to oral glucose and the test meal were not affected by treatments (P>0·34). For all animals, total body fat estimated from body weight and back fat thickness was correlated with both β-cell function (by homeostasis model assessment (HOMA); r+0·63) and insulin sensitivity (index of whole-body insulin sensitivity and by HOMA; r − 0·63 and r+0·66, respectively). In conclusion, long-term supplementation with dietary n-3 PUFA did not affect insulin metabolism in healthy adult male pigs. The relationship between body fat and insulin sensitivity, well documented in human subjects, suggests that the adult male pig could be a promising animal model for studies on insulin metabolism.

Genistein and daidzein are known to have both beneficial and adverse effects on human health due to their many biological actions at the cellular level. Both isoflavones have been shown to inhibit GLUT-mediated glucose transport across the plasma membrane of mammalian cells. Since lysosomal membrane transport is essential for maintaining cellular homeostasis, the present study examined the effects of genistein and daidzein on glucose and sulphate transport in isolated rat liver lysosomes. Both genistein and daidzein significantly inhibited lysosomal glucose uptake. Genistein was a more potent glucose transport inhibitor than daidzein, with a half-maximum inhibitory concentration (IC50) of 45 μmol/l compared with 71 μmol/l for daidzein. Uptake kinetics of d-glucose showed a significant decrease in Vmax (control:genistein treat = 1489 (sem 91):507 (sem 76) pmol/unit of β-hexosaminidase per 15 s) without a change in Km. The presence of 50 μm-genistein in the medium also reduced glucose efflux from lysosomes preloaded with 100 mm-d-glucose. Genistein also inhibited lysosomal sulphate transport. Similar to its effects on glucose uptake kinetics, genistein treatment caused a significant decrease in sulphate uptake Vmax (control:genistein treat = 87 (sem 4):59 (sem 5) pmol/unit of β-hexosaminidase per 30 s), while the Km was not affected. The evidence provided by the present study suggests that the most likely mechanism of lysosomal glucose transport inhibition by genistein is via direct interaction between genistein and the transporter, rather than mediation by tyrosine kinase inactivation. Genistein likely has a similar mechanism of directly inhibiting sulphate transporter.

The cytoplasmic serine/threonine ribosomal protein S6 kinase (S6K1) plays a critical role in controlling protein translation. There is evidence that amino acids regulate S6K1 and protein synthesis in avian species, but the effect of dietary protein level on the activation of S6K1 in neonatal chicks is unknown. Therefore, the aim of the present experiment was to investigate the effect of different protein levels, supplied during the first 5 d post-hatch, on body growth, breast muscle development and on the activation of S6K1 and its downstream target, the S6, in neonatal chicks. Chicks were fed a pre-starter diet during the first 5 d post-hatch containing low (19·6 % crude protein (CP); LP), medium (23·1 % CP; MP) or high (26·7 % CP) levels (HP) of protein. Weight gain of chicks fed the HP diet was higher (P < 0·05) compared with those fed the LP diet during day (d)3–d5 and the numerical advantage of this group was maintained from d2 to d7. On d2 and d3, greater levels of S6K1 and S6 phosphorylation and/or activity were observed in chicks receiving the HP diet compared with LP and MP diets, without differences between results of the latter two dietary treatments. In conclusion, the present results suggest that early protein nutrition impacts the development of broiler chicks.

Traditional plant treatments have been used throughout the world for the therapy of diabetes mellitus. The aim of the present study was to investigate the efficacy and mode of action of Terminalia bellirica used traditionally for the treatment of diabetes in India. T. bellirica aqueous extract stimulated basal insulin output and potentiated glucose-stimulated insulin secretion concentration-dependently in the clonal pancreatic β-cell line, BRIN-BD11 (P < 0·001). The insulin-secretory activity of the plant extract was abolished in the absence of extracellular Ca2+ and by inhibitors of cellular Ca2+ uptake, diazoxide and verapamil (P < 0·001; n 8). Furthermore, the extract did not increase insulin secretion in depolarised cells and did not further augment insulin secretion triggered by tolbutamide or glibenclamide. T. bellirica extract also displayed insulin-mimetic activity and enhanced insulin-stimulated glucose uptake in 3T3-L1 adipocytes by 300 %. At higher concentrations, the extract also produced a 10–50 % (P < 0·001) decrease in starch digestion in vitro and inhibited protein glycation (P < 0·001). The present study has revealed that components in T. bellirica extract stimulate insulin secretion, enhance insulin action and inhibit both protein glycation and starch digestion. The former actions are dependent on the active principle(s) in the plant being absorbed intact. Future work assessing the use of T. bellirica as a dietary adjunct or as a source of active anti-diabetic agents may provide new opportunities for the treatment of diabetes.

Our preliminary clinical trial showed that consumption of cooked rice of a Japanese common cultivar Yukihikari improved atopic dermatitis associated with a suspected rice allergy, although the underlying mechanisms remain unclear. We hypothesised that the ameliorating effect of Yukihikari on atopic dermatitis is associated with the gut microbiota. BALB/c mice were fed a synthetic diet supplemented with uncooked and polished white rice powder prepared from one of four different cultivars: Yukihikari, rice A (common rice), rice B (brewery rice) and rice C (waxy rice). Denaturing gradient gel electrophoresis of PCR-amplified 16S rRNA gene fragments showed that the composition of faecal microbiota was different between mice fed Yukihikari and those fed rice A. Analysis of the 16S rRNA clone library and species-specific real-time PCR showed that the abundance of Akkermansia muciniphila, a mucin degrader, tended to be lower in mice fed Yukihikari. The incidence of allergic diarrhoea induced by oral administration of ovalbumin in systemically immunised mice was lower in mice fed Yukihikari, albeit with no difference in serum antibodies specific to ovalbumin. In a separate experiment, serum antibody levels specific to orally administered ovalbumin were lower in mice fed Yukihikari. Additionally, the translocation of horseradish peroxidase in isolated segments of ileum and colon tended to be lower in mice fed Yukihikari, suggesting a reduction in gut permeability in mice fed Yukihikari. These data indicate that changes in the gut microbiota of mice fed Yukihikari could be advantageous in the prevention of food allergy.

Ageing has been suggested to cause changes in the intestinal microbial community. In the present study, the microbiota of a previously well-defined group of elderly subjects aged between 70 and 85 years, both non-steroidal anti-inflammatory drugs (NSAID) users (n 9) and non-users (n 9), were further compared with young adults (n 14) with a mean age of 28 years, by two DNA-based techniques: percentage guanine+cytosine (%G+C) profiling and 16S rDNA sequencing. Remarkable changes in microbiota were described with both methods: compared with young adults a significant reduction in overall numbers of microbes in both elderly groups was measured. Moreover, the total number of microbes in elderly NSAID users was higher than in elderly without NSAID. In 16S rDNA sequencing, shifts in all major microbial phyla, such as lower numbers of Firmicutes and an increase in numbers of Bacteroidetes in the elderly were monitored. On the genus level an interesting link between reductions in the proportion of known butyrate producers belonging to Clostridium cluster XIVa, such as Roseburia and Ruminococcus, could be demonstrated in the elderly. Moreover, in the Actinobacteria group, lower numbers of Collinsella spp. were evident in the elderly subjects with NSAID compared both with young adults and the elderly without NSAID, suggesting that the use of NSAID along with age may also influence the composition of intestinal microbiota. Furthermore, relatively high numbers of Lactobacillus appeared only in the elderly subjects without NSAID. In general, the lowered numbers of microbial members in the major phyla, Firmicutes, together with changes in the epithelial layer functions can have a significant effect on the colon health of the elderly.

DHA and arachidonic acid (AA) are important for neurodevelopment. A traditional neonatal neurological examination and the evaluation of general movement quality are sensitive techniques for assessing neurodevelopment in young infants. Mildly abnormal general movements at 3 months have been associated with a non-optimal current brain condition. We investigated whether supplementation of DHA during pregnancy and lactation influences the infant's brain development and whether additional AA modulates this effect. Healthy women were randomly assigned to DHA (220 mg/d, n 42), DHA+AA (220 mg each/d, n 41) or control (n 36), from about week 17 (range 14–20 weeks) of pregnancy until 12 weeks postpartum. The control and the DHA+AA groups had approximately comparable dietary DHA/AA ratios. The standardised neonatal neurological examination was carried out at 2 weeks. General movement quality was assessed at 2 and 12 weeks. Neither DHA alone nor DHA+AA influenced outcomes in the traditional examination. General movement quality of infants in the DHA group was lower than that of infants in the other two groups, especially at 12 weeks: 61 % of the infants in the DHA group showed mildly abnormal general movements compared with 31 % in the control group (P = 0·008) and 34 % in the DHA+AA group (P = 0·015). We conclude that general movement quality at 12 weeks is sensitive to the maternal dietary DHA/AA balance.

Heart rate (HR) variability and large arterial compliance can be improved using fish oils. DHA, a component of fish oil, has cardiovascular health benefits, but its effect on HR variability (HRV) and arterial compliance is yet to be quantified. Sixty-seven overweight or obese adults (thirty-six males and thirty-one females; 53 (sem 2) year; BMI 31·7 (sem 1·1) kg/m2) were randomly allocated to consume either 6 g/d sunola oil (control; n 17), fish oil (260 mg DHA+60 mg EPA per g) at doses of 2 g/d (n 16), 4 g/d (n 17) or 6 g/d (n 17). Blood pressure, HR and compliance of large and small arteries were measured while supine at baseline and after 12 weeks in all participants, and HRV was assessed in a subgroup of forty-six participants. There was no effect of fish oil on blood pressure, small artery compliance or HR. However, the low frequency:high frequency ratio of HRV decreased with increasing doses of fish oil (r − 0·34, P = 0·02), while large artery compliance increased (r 0·34, P = 0·006). Moreover, the changes in these biomarkers were significantly correlated (r − 0·31, P = 0·04) and may reflect fish oil-induced improvements in arterial function and cardiac autonomic regulation.

Epidemiological studies suggest that a diet high in flavonoids protects against chronic diseases such as CVD and cancer. The objective of the present study was to evaluate the relationship between the intake of quercetin, kaempferol, isorhamnetin, apigenin and luteolin and their corresponding plasma concentrations, and further to explore whether these flavonoids can serve as biomarkers of their intake. Flavonoid intake and their plasma concentrations were analysed in ninety-two subjects consuming their habitual diet. Flavonoid intake was estimated with 7-d dietary records using available data on the flavonoid content of food. Plasma flavonoid concentrations were quantified by HPLC. In addition, we undertook a dietary intervention study to investigate plasma apigenin concentration after the consumption of celery leaf. The mean intake estimates of quercetin, kaempferol, isorhamnetin, apigenin and luteolin amounted to 13·58, 14·97, 12·31, 4·23 and 8·08 mg/d, respectively. The corresponding mean plasma concentrations were 80·23, 57·86, 39·94, 10·62 and 99·90 nmol/l. The mean 7 d intake of five flavonoids was positively correlated to their corresponding plasma concentrations, with correlation coefficients ranging from 0·33 to 0·51 (P < 0·05). In the dietary intervention study, the plasma apigenin concentration rose after celery leaf ingestion, and fell within 28 h to below the limit of detection (2·32 nmol/l). The present results suggest that quercetin, kaempferol, isorhamnetin, apigenin and luteolin are bioavailable from the diet. The levels of fasting plasma flavonoids seem to be suitable biomarkers of short-term intake. The combination of plasma flavonoids with their intake may prove useful when the possible health-protective effects of flavonoids are studied.

Oxidative stress is a physiological condition that is associated with atherosclerosis, and it can be influenced by diet. Our objective was to group fifty-seven individuals with dyslipidaemia controlled by statins according to four oxidative biomarkers, and to evaluate the diet pattern and blood biochemistry differences between these groups. Blood samples were collected and the following parameters were evaluated: diet intake; plasma fatty acids; lipoprotein concentration; glucose; oxidised LDL (oxLDL); malondialdehyde (MDA); total antioxidant activity by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ferric reducing ability power assays. Individuals were separated into five groups by cluster analysis. All groups showed a difference with respect to at least one of the four oxidative stress biomarkers. The separation of individuals in the first axis was based upon their total antioxidant activity. Clusters located on the right side showed higher total antioxidant activity, higher myristic fatty acid and lower arachidonic fatty acid proportions than clusters located on the left side. A negative correlation was observed between DPPH and the peroxidability index. The second axis showed differences in oxidation status as measured by MDA and oxLDL concentrations. Clusters located on the upper side showed higher oxidative status and lower HDL cholesterol concentration than clusters located on the lower side. There were no differences in diet among the five clusters. Therefore, fatty acid synthesis and HDL cholesterol concentration seem to exert a more significant effect on the oxidative conditions of the individuals with dyslipidaemia controlled by statins than does their food intake.

The evidence of the effect of the age at introduction of new foods during infancy on the development of asthma and allergic rhinitis is inconsistent and scarce. We set out to study these associations. A prospective birth cohort of infants with increased HLA-DQB1-conferred risk for type 1 diabetes was recruited in 1996–2000. The families completed at home a record on the age at introduction of new foods. Persistent asthma and allergic rhinitis were assessed at the age of 5 years with an International Study of Asthma and Allergies in Childhood-type questionnaire. The Cox proportional hazards regression analyses were adjusted for parental asthma and allergic diseases, and several perinatal and sociodemographical factors. Out of the 1293 children, 77 (6·0 %) developed persistent asthma; and out of the 1288 children, 185 (14·4 %) developed allergic rhinitis by the age of 5 years. Early age at introduction of oats was associated with a reduced risk of persistent asthma (hazard ratio (HR; 95 % CI) for the first and mid-tertiles compared with the latest tertile was 0·36 (0·15, 0·85) and 0·37 (0·22, 0·62), respectively, P < 0·001). Early age at introduction of fish was dose dependently associated with a decreased risk of allergic rhinitis (HR (95 % CI) for the first and mid-tertiles compared with the latest tertile was 0·34 (0·22, 0·54) and 0·45 (0·28, 0·70), respectively, P < 0·001). The present finding that age at introduction of oats is inversely and independently associated with development of persistent asthma is novel. We confirmed the earlier observation that the age at introduction of fish is inversely related to the risk of allergic rhinitis. Clinical implications remain to be determined.

An investigation was carried out to determine whether there were significant changes in the intake of dietary fibre (NSP) and phytate of adult men and women in the UK from 1982 (aged 36 years) to 1999 (aged 53 years). The 1253 subjects studied were members of the Medical Research Council National Survey of Health and Development; a longitudinal study of a nationally representative cohort of births in 1946. Food intake was recorded in a 5 d diary at age 36 years in 1982, 43 years in 1989 and 53 years in 1999. The food composition database was amended with revised values for phytate. Outcome measures were mean intakes of total NSP and phytate by year, sex and food source. There were significant changes in total NSP and phytate intake over the three time points. Intakes of NSP rose significantly between 1982 and 1999 for men and women but phytate intakes rose significantly only between 1989 and 1999. Cereal foods were the most important source of both NSP and phytate. Between 1989 and 1999 there was a significant increase in the contribution from pasta, rice and other grains. The present study shows that an increase in dietary fibre that is in accordance with dietary guidelines would almost inevitably be accompanied by a rise in phytate. The increased dietary phytate is discussed in relation to its recognised inhibition of mineral absorption and its merits with regard to protection against some cancers and other diseases of an ageing population.

The objective of the present study was to document the food, energy and macronutrient contribution of out-of-home prepared foods in school-going adolescents in Cotonou (Benin) and compare the food, energy and macronutrient intakes of low and high out-of-home consumers. We used a cross-sectional study with 24 h dietary recalls on two non-consecutive school days to collect food intake data. Low and high consumers were defined respectively as subjects whose percentage of daily energy intake from out-of-home foods was in the first and the third terciles of the sample distribution. The setting was twelve secondary schools in Cotonou with 656 adolescents aged 13–19 years. Out-of-home prepared foods contributed more than 40 % of the daily energy, fat, protein, carbohydrate and fibre intakes and of the daily weight of food in the adolescents. They were highly present at breakfast and as afternoon snacks in high consumers, providing respectively 94 and 82 % of the energy intake of high consumers at breakfast and as afternoon snacks. Low consumers ate more fruit and vegetables and cereal grain products than high consumers whereas high consumers consumed more sweet energy-dense foods. Both categories had a diet poor in fruit and vegetables (hardly one-fourth of the recommended 400 g) and high in fat. We concluded that out-of-home foods are important in the diet of urban school adolescents in Benin. Therefore, they should be investigated in depth and taken into account in the development of interventions to promote healthy diet and lifestyles in adolescents.

Although anthropometric parameters have been extensively studied regarding their relationship to physical function status, the association between these parameters and the activity of daily living (ADL) function remains controversial. We investigated whether BMI or mid-upper arm circumference (AC) is an indication of variation in the physical functioning of the frail elderly. The present study was a prospective cohort analysis of 543 community-dwelling frail elderly. Data included the participants' demographic characteristics, basic ADL, comorbidity and anthropometric measurements at baseline and at 2-year follow-up. Logistic regression models were used to investigate the association between ADL status and anthropometric measurements during the study period. Among the 543 participants, 418 maintained or improved their ADL status, while 125 showed an ADL decline during the study period. Multivariate logistic regression analysis showed that BMI and AC levels or ADL status at baseline were not independent predictors of the loss of ADL function or the decline in these anthropometric measurements during the study period, respectively. However, the decline in BMI and AC levels and the loss of ADL function were associated with each other during the study period. There is an association between the negative changes in anthropometric measurements during the follow-up period and the decline in ADL function during a 2-year follow-up in community-dwelling frail elderly.

Glycaemic responses to foods reflect the balance between glucose loading into, and its clearance from, the blood. Current in vitro methods for glycaemic analysis do not take into account the key role of glucose disposal. The present study aimed to develop a food intake-sensitive method for measuring the glycaemic impact of food quantities usually consumed, as the difference between release of glucose equivalents (GGE) from food during in vitro digestion and a corresponding estimate of clearance of them from the blood. Five foods – white bread, fruit bread, muesli bar, mashed potato and chickpeas – were consumed on three occasions by twenty volunteers to provide blood glucose response (BGR) curves. GGE release during in vitro digestion of the foods was also plotted. Glucose disposal rates estimated from downward slopes of the BGR curves allowed GGE dose-dependent cumulative glucose disposal to be calculated. By subtracting cumulative glucose disposal from cumulative in vitro GGE release, accuracy in predicting the in vivo glycaemic effect from in vitro GGE values was greatly improved. GGEin vivo = 0·99GGEin vitro+0·75 (R2 0·88). Furthermore, the difference between the curves of cumulative GGE release and disposal closely mimicked in vivo incremental BGR curves. We conclude that valid measurement of the glycaemic impact of foods may be obtained in vitro, and expressed as grams of glucose equivalents per food quantity, by taking account not only of GGE release from food during in vitro digestion, but also of blood glucose clearance in response to the food quantity.