The influence of sweet taste sensitivity on food intake is not well understood. We investigated the involvement of salivary leptin and SNP of the sweet taste receptor genes (TAS1R2/TAS1R3) on sweet taste sensitivity, sensory-specific satiety (SSS) and macronutrient intake in healthy human adults. In all, nineteen high sweet sensitivity (HS) and eleven low sweet sensitivity (LS) subjects were classified based on the sweetness perception of one solution (9 mm sucrose) forced-choice triangle test. All participants completed a randomised crossover design experiment where they consumed one of three iso-energetic soup preloads differing in primary taste quality (sweet, non-sweet taste-control or no-taste energy-control). A period of 1 h after the preload, participants were offered a buffet meal consisting of foods varying in taste (sweet or non-sweet) and fat content. Subjective measures included hunger/fullness and SSS for sweetness. Saliva and buccal cells were collected to measure leptin level and to study the TAS1R2/TAS1R3 specific SNP, respectively. Salivary leptin concentrations were significantly higher in LS than HS participants (P<0·05). In addition, HS showed stronger sweet SSS compared with LH participants (P<0·05), and consumed less carbohydrate (% energy) and more non-sweet foods than LS (P<0·01 and P<0·05, respectively). Alleles from each TAS1R2 locus (GG compared with AA alleles of rs12033832, and CT/CC compared with TT alleles of rs35874116) were related to higher consumption of carbohydrates (% energy) and higher amount of sweet foods, respectively (P<0·05). In contrast, no associations were found for the TAS1R3 alleles. These results contribute to understand the links between taste sensitivity, macronutrient appetite and food consumption.

To compare the ability of a body shape index (ABSI) and body adiposity estimator (BAE) to BMI, waist circumference (WC) and waist:height ratio (WHtR) for predicting development of type 2 diabetes mellitus (T2DM) in rural adult Chinese. The prospective cohort study included 11 687 eligible participants who were free of T2DM at baseline. The risk of new-onset T2DM for ABSI, BAE, BMI, WC and WHtR quintiles was estimated by Cox proportional-hazards regression at follow-up. We also compared the power of ABSI and BAE to BMI, WC and WHtR for predicting the development of T2DM. With increasing ABSI, BAE, BMI, WC and WHtR, T2DM incidence was substantially increased (Ptrend<0·0001). After adjustment for multi-covariates, risk of T2DM was increased from the second to fifth quintile as compared with first quintile for ABSI (1·27; 95 % CI 0·95, 1·69; 1·35; 95 % CI 1·00, 1·82; 1·75; 95 % CI 1·33, 2·32 and 1·87; 95 % CI 1·40, 2·49; Ptrend<0·0001); BAE (1·82; 95 % CI 1·38, 2·41; 1·93; 95 % CI 1·38, 2·68; 2·73; 95 % CI 1·94, 3·84 and 4·18; 95 % CI 2·98, 5·87; Ptrend<0·0001); BMI (1·42; 95 % CI 1·03, 1·97; 1·62; 95 % CI 1·18, 2·23; 2·59; 95 % CI 1·92, 3·50 and 3·90; 95 % CI 2·90, 5·26; Ptrend<0·0001); WC (1·53; 95 % CI 1·08, 2·17; 1·66; 95 % CI 1·18, 2·33; 2·72; 1·97, 3·76 and 4·09; 95 % CI 2·97, 5·62; Ptrend<0·0001); and WHtR (1·40; 95 % CI 0·98, 1·99; 2·06; 95 % CI 1·47, 2·88; 2·90; 95 % CI 2·10, 4·01 and 4·22; 95 % CI 3·05, 5·85; Ptrend<0·0001). ABSI, BAE, BMI, WC and WHR were effective and comparable in discriminating cases from non-cases of T2DM. Risk of T2DM was increased with elevated ABSI and BAE, but the predictive ability for T2DM did not differ than that of BMI, WC and WHtR in a rural Chinese population.

We previously found that guar gum (GG) and chickpea flour (CPF) added to flatbread wheat flour lowered postprandial blood glucose (PPG) and insulin responses dose dependently. However, rates of glucose influx cannot be determined from PPG, which integrates rates of influx, tissue disposal and hepatic glucose production. The objective was to quantify rates of glucose influx and related fluxes as contributors to changes in PPG with GG and CPF additions to wheat-based flatbreads. In a randomised cross-over design, twelve healthy males consumed each of three different 13C-enriched meals: control flatbreads (C), or C incorporating 15 % CPF with either 2 % (GG2) or 4 % (GG4) GG. A dual isotope technique was used to determine the time to reach 50 % absorption of exogenous glucose (T50 %abs, primary objective), rate of appearance of exogenous glucose (RaE), rate of appearance of total glucose (RaT), endogenous glucose production (EGP) and rate of disappearance of total glucose (RdT). Additional exploratory outcomes included PPG, insulin, glucose-dependent insulinotropic peptide and glucagon-like peptide 1, which were additionally measured over 4 h. Compared with C, GG2 and GG4 had no significant effect on T50 %abs. However, GG4 significantly reduced 4-h AUC values for RaE, RaT, RdT and EGP, by 11, 14, 14 and 64 %, respectively, whereas GG2 showed minor effects. Effect sizes over 2 and 4 h were similar except for significantly greater reduction in EGP for GG4 at 2 h. In conclusion, a soluble fibre mix added to flatbreads only slightly reduced rates of glucose influx, but more substantially affected rates of postprandial disposal and hepatic glucose production.

Perinatal maternal high-fat (HF) diet programmes offspring obesity. Obesity is associated with overactivation of the endocannabinoid system (ECS) in adult subjects, but the role of the ECS in the developmental origins of obesity is mostly unknown. The ECS consists of endocannabinoids, cannabinoid receptors (cannabinoid type-1 receptor (CB1) and cannabinoid type-2 receptor (CB2)) and metabolising enzymes. We hypothesised that perinatal maternal HF diet would alter the ECS in a sex-dependent manner in white and brown adipose tissue of rat offspring at weaning in parallel to obesity development. Female rats received standard diet (9 % energy content from fat) or HF diet (29 % energy content from fat) before mating, during pregnancy and lactation. At weaning, male and female offspring were killed for tissue harvest. Maternal HF diet induced early obesity, white adipocyte hypertrophy and increased lipid accumulation in brown adipose tissue associated with sex-specific changes of the ECS’s components in weanling rats. In male pups, maternal HF diet decreased CB1 and CB2 protein in subcutaneous adipose tissue. In female pups, maternal HF diet increased visceral and decreased subcutaneous CB1. In brown adipose tissue, maternal HF diet increased CB1 regardless of pup sex. In addition, maternal HF diet differentially changed oestrogen receptor across the adipose depots in male and female pups. The ECS and oestrogen signalling play an important role in lipogenesis, adipogenesis and thermogenesis, and we observed early changes in their targets in adipose depots of the offspring. The present findings provide insights into the involvement of the ECS in the developmental origins of metabolic disease induced by inadequate maternal nutrition in early life.

Breast-fed infants are susceptible to vitamin D deficiency rickets. The current vitamin D ‘adequate intake’ (AI) for 0–6-month-old infants is 10 µg/d, corresponding with a human milk antirachitic activity (ARA) of 513 IU/l. We were particularly interested to see whether milk ARA of mothers with lifetime abundant sunlight exposure reaches the AI. We measured milk ARA of lactating mothers with different cultural backgrounds, living at different latitudes. Mature milk was derived from 181 lactating women in the Netherlands, Curaçao, Vietnam, Malaysia and Tanzania. Milk ARA and plasma 25-hydroxyvitamin D (25(OH)D) were analysed by liquid-chromatography-MS/MS; milk fatty acids were analysed by GC-flame ionisation detector (FID). None of the mothers reached the milk vitamin D AI. Milk ARA (n; median; range) were as follows: Netherlands (n 9; 46 IU/l; 3–51), Curaçao (n 10; 31 IU/l; 5–113), Vietnam: Halong Bay (n 20; 58 IU/l; 23–110), Phu Tho (n 22; 28 IU/l; 1–62), Tien Giang (n 20; 63 IU/l; 26–247), Ho-Chi-Minh-City (n 18; 49 IU/l; 24–116), Hanoi (n 21; 37 IU/l; 11–118), Malaysia–Kuala Lumpur (n 20; 14 IU/l; 1–46) and Tanzania-Ukerewe (n 21; 77 IU/l; 12–232) and Maasai (n 20; 88 IU/l; 43–189). We collected blood samples of these lactating women in Curaçao, Vietnam and from Tanzania–Ukerewe, and found that 33·3 % had plasma 25(OH)D levels between 80 and 249·9 nmol/l, 47·3 % between 50 and 79·9 nmol/l and 19·4 % between 25 and 49·9 nmol/l. Milk ARA correlated positively with maternal plasma 25(OH)D (range 27–132 nmol/l, r 0·40) and milk EPA+DHA (0·1–3·1 g%, r 0·20), and negatively with latitude (2°S-53°N, r −0·21). Milk ARA of mothers with lifetime abundant sunlight exposure is not even close to the vitamin D AI for 0–6-month-old infants. Our data may point at the importance of adequate fetal vitamin D stores.

With the association between increased carotenoid intake and lower risk of chronic diseases, the absorption of lutein from the diet becomes an important factor in its delivery and physiological action. The primary objective of this study was to gain an understanding of how a new formulation technology (mixture of mono- and diglycerides (MDG)), affected lutein absorption. Subjects (n 24) were randomised in a cross-over, double-blind study to receive a single dose of 6 mg lutein (FloraGLO 20 %) provided as capsules containing either high-oleic safflower (SAF) oil or a MDG oil. Subjects receiving a single dose of lutein in MDG showed a significantly greater change from baseline (0 h) to 4, 6, 8, 12, 24, 48 and 336 h (P<0·05) and baseline adjusted AUC for plasma lutein at 48 and 336 h (P<0·001) as compared with subjects given lutein in SAF. Analysis of the 48 h absorption kinetics of lutein showed that the time to peak level of lutein (12 h) was the same for SAF and MDG groups, but the change in plasma lutein at 12 and 48 h were 129 and 320 % higher, respectively, for MDG compared with SAF. This difference continued as the adjusted AUC 0–48 and 0–336 h for the MDG group was 232 and 900 % higher, respectively, v. SAF. The study data show that by changing the lipid that is combined with a lutein supplement results in significant increases in lutein absorption in healthy adults.

Underlying mechanisms responsible for the cholesterol-lowering effect of β-glucan have been proposed, yet have not been fully demonstrated. The primary aim of this study was to determine whether the consumption of barley β-glucan lowers cholesterol by affecting the cholesterol absorption, cholesterol synthesis or bile acid synthesis. In addition, this study was aimed to assess whether the underlying mechanisms are related to cholesterol 7α hydroxylase (CYP7A1) SNP rs3808607 as proposed by us earlier. In a controlled, randomised, cross-over study, participants with mild hypercholesterolaemia (n 30) were randomly assigned to receive breakfast containing 3 g high-molecular weight (HMW), 5 g low-molecular weight (LMW), 3 g LMW barley β-glucan or a control diet, each for 5 weeks. Cholesterol absorption was determined by assessing the enrichment of circulating 13C-cholesterol over 96 h following oral administration; fractional rate of synthesis for cholesterol was assessed by measuring the incorporation rate of 2H derived from deuterium oxide within the body water pool into the erythrocyte cholesterol pool over 24 h; bile acid synthesis was determined by measuring serum 7α-hydroxy-4-cholesten-3-one concentrations. Consumption of 3 g HMW β-glucan decreased total cholesterol (TC) levels (P=0·029), but did not affect cholesterol absorption (P=0·25) or cholesterol synthesis (P=0·14). Increased bile acid synthesis after consumption of 3 g HMW β-glucan was observed in all participants (P=0·049), and more pronounced in individuals carrying homozygous G of rs3808607 (P=0·033). In addition, a linear relationship between log (viscosity) of β-glucan and serum 7α-HC concentration was observed in homozygous G allele carriers. Results indicate that increased bile acid synthesis rather than inhibition of cholesterol absorption or synthesis may be responsible for the cholesterol-lowering effect of barley β-glucan. The pronounced TC reduction in G allele carriers of rs3808607 observed in the previous study may be due to enhanced bile acid synthesis in response to high-viscosity β-glucan consumption in those individuals.

Inflammation confounds the interpretation of several micronutrient biomarkers resulting in estimates that may not reflect the true burden of deficiency. We aimed to assess and compare the micronutrient status of a cohort of Indonesian infants (n 230) at aged 6, 9 and 12 months by ignoring inflammation (unadjusted) and adjusting four micronutrient biomarkers for inflammation with C-reactive protein (CRP) and α-1-glycoprotein (AGP) using the following methods: (1) arithmetic correction factors with the use of a four-stage inflammation model; and (2) regression modelling. Prevalence of infants with any inflammation (CRP>5 mg/l and/or AGP>1 g/l) was about 25% at each age. Compared with unadjusted values, regression adjustment at 6, 9 and 12 months generated the lowest (P<0·001) geometric mean (GM) for serum ferritin (26·5, 14·7, 10·8 μg/l) and the highest GM for serum retinol-binding protein (0·95, 1·00, 1·01 μmol/l) and Zn (11·8, 11·0, 11·5 μmol/l). As a consequence, at 6, 9 and 12 months regression adjustment yielded the highest prevalence of Fe deficiency (20·3, 37·8, 59·5 %) and the lowest prevalence of vitamin A (26·4,16·6, 17·3 %) and Zn (16·9, 20·6, 11·0 %) deficiency, respectively. For serum Se, irrespective of adjustment, GM were low (regression: 0·73, 0·78, 0·81 μmol/l) with prevalence of deficiency >50 % across all ages. In conclusion, without inflammation adjustment, Fe deficiency was grossly under-estimated and vitamin A and Zn deficiency over-estimated, highlighting the importance of correcting for the influence of such, before implementing programmes to alleviate micronutrient malnutrition. However, further work is needed to validate the proposed approaches with a particular focus on assessing the influence of varying degrees of inflammation (i.e. recurrent acute infections and low-grade chronic inflammation) on each affected nutrient biomarker.

As a key indicator of childhood malnutrition, few studies have focused on stunting in relation to various socio-economic factors in which disadvantaged groups face in China. We conducted a community-based cross-sectional study incorporating forty-two rural counties in seven western provinces of China in 2011. In total, 5196 children aged 6–23 months were included. We used Poisson regression to examine risk factors for inadequate minimum dietary diversity (MDD) and stunting status, respectively. Overall, the proportion of children not meeting MDD was 44·5 %. Children aged 6–11 months (adjusted risk ratio (ARR)=1·39; 95 % CI 1·31, 1·49), with two siblings (ARR=1·09; 95 % CI 1·02, 1·17), delivered at home (ARR=1·30; 95 % CI 1·20, 1·41), within Yi (ARR=1·15; 95 % CI 1·04, 1·28) or Uighur groups (ARR=1·52; 95 % CI 1·36, 1·71), with an illiterate caregiver (ARR=2·12; 95 % CI 1·52, 2·96), receiving lowest income (ARR=1·32; 95 % CI 1·17, 1·50), and with breast-feeding in the last day (ARR=1·55; 95 % CI 1·44, 1·66) were more likely to have inadequate MDD. Moreover, inadequate MDD was positively associated with stunting (ARR=1·15; 95 % CI 1·01, 1·31). Other determinants for stunting were age, sex, place of delivery, minority group and income. The stunting prevalence and proportion of inadequate MDD remained high in Western China; to reduce stunting rates of ethnic minorities, further efforts addressing appropriate dietary feeding practices are needed, especially within these groups.

Approximately 8–20 % of reproductive-aged women experience premenstrual syndrome (PMS), substantially impacting quality of life. Women with PMS are encouraged to reduce fat intake to alleviate symptoms; however, its role in PMS development is unclear. We evaluated the association between dietary fat intake and PMS development among a subset of the prospective Nurses’ Health Study II cohort. We compared 1257 women reporting clinician-diagnosed PMS, confirmed by premenstrual symptom questionnaire and 2463 matched controls with no or minimal premenstrual symptoms. Intakes of total fat, subtypes and fatty acids were assessed via FFQ. After adjustment for age, BMI, smoking, Ca and other factors, intakes of total fat, MUFA, PUFA and trans-fat measured 2–4 years before were not associated with PMS. High SFA intake was associated with lower PMS risk (relative risk (RR) quintile 5 (median=28·1 g/d) v. quintile 1 (median=15·1 g/d)=0·75; 95 % CI 0·58, 0·98; P trend=0·07). This association was largely attributable to stearic acid intake, with women in the highest quintile (median=7·4 g/d) having a RR of 0·75 v. those with the lowest intake (median=3·7 g/d) (95 % CI 0·57, 0·97; P trend=0·03). Individual PUFA and MUFA, including n-3 fatty acids, were not associated with risk. Overall, fat intake was not associated with higher PMS risk. High intake of stearic acid may be associated with a lower risk of developing PMS. Additional prospective research is needed to confirm this finding.

Quantification of lean body mass and fat mass can provide important insight into epidemiological research. However, there is no consensus on generalisable anthropometric prediction equations to validly estimate body composition. We aimed to develop and validate practical anthropometric prediction equations for lean body mass, fat mass and percent fat in adults (men, n 7531; women, n 6534) from the National Health and Nutrition Examination Survey 1999–2006. Using a prediction sample, we predicted each of dual-energy X-ray absorptiometry (DXA)-measured lean body mass, fat mass and percent fat based on different combinations of anthropometric measures. The proposed equations were validated using a validation sample and obesity-related biomarkers. The practical equation including age, race, height, weight and waist circumference had high predictive ability for lean body mass (men: R 2=0·91, standard error of estimate (SEE)=2·6 kg; women: R 2=0·85, SEE=2·4 kg) and fat mass (men: R 2=0·90, SEE=2·6 kg; women: R 2=0·93, SEE=2·4 kg). Waist circumference was a strong predictor in men only. Addition of other circumference and skinfold measures slightly improved the prediction model. For percent fat, R 2 were generally lower but the trend in variation explained was similar. Our validation tests showed robust and consistent results with no evidence of substantial bias. Additional validation using biomarkers demonstrated comparable abilities to predict obesity-related biomarkers between direct DXA measurements and predicted scores. Moreover, predicted fat mass and percent fat had significantly stronger associations with obesity-related biomarkers than BMI did. Our findings suggest the potential application of the proposed equations in various epidemiological settings.

The aim of this study was to develop a purified diet that mimics the characteristics of the Japanese diet using readily available materials with a simpler composition and a focus on quality, with the goal of facilitating performance of studies on the Japanese diet worldwide. The utility of the new diet was examined as a mimic of the standard Japanese diet for use in animal experiments. We examined whether a key characteristic of the Japanese diet of being less likely to cause obesity could be reproduced. The mimic diet had a balance of protein, fat and carbohydrate based on the 1975 Japanese diet, which is the least likely to cause obesity, and materials chosen with reference to the National Health and Nutrition Survey (NHNS). To examine similarities of the mimic diet with the model 1975 Japanese diet, we created a menu of the 1975 diet based on the NHNS and prepared the freeze-dried and powdered diet. The mimic diet, the 1975 Japanese diet, a control AIN-93G diet and a Western diet were fed to mice for 4 weeks. As a result, the mimic diet and the 1975 diet resulted in less accumulation of visceral fat and liver fat. Mice given these two diets showed similar effects. This indicates that the mimic diet used in this study has characteristics of the 1975 Japanese diet and could be used as a standard Japanese diet in animal experiments.