Disturbances in lipid metabolism are at the core of several health issues facing modern society, including fatty liver and obesity. The sterol regulatory element-binding protein 1 (SREBP-1) is one important transcription factor regulating lipid metabolism, but the relevant mechanism still remains unknown. The present study determined the transcriptional regulation of SREBP-1 and its target genes (including acetyl-CoA carboxylase α (accα), fatty acid synthase (fas) and stearoyl-CoA desaturase 1 (scd1)) in a freshwater teleost, grass carp Ctenopharyngodon idella. We cloned and characterised the 1988 bp, 2043 bp, 1632 bp and 1889 bp sequences of srebp-1, accα, scd1 and fas promoters, respectively. A cluster of putative binding sites of transcription factors, such as specific protein, yin yang 1, nuclear factor Y, sterol response elements (SRE) and enhancer box (E-box) element, were predicted on their promoter regions. Overexpression of nSREBP-1 reduced srebp-1 promoter activity, increased scd1 and fas promoter activity but did not influence accα promoter activity. The site-mutation and electrophoretic mobility shift assay analysis indicated that srebp-1, fas and scd1 promoters, but not accα promoter, possessed SRE. In Ctenopharyngodon idella kidney (CIK) cells of grass carp, nSREBP-1 overexpression significantly reduced srebp-1 mRNA expression and up-regulated miR-29 mRNA expression. The 3′UTR of srebp-1 possessed the potential miR-29 binding site and miR-29 up-regulated the luciferase activity of srebp-1 3′UTR and srebp-1 mRNA expression, implying a self-activating loop of SREBP-1 and miR-29 in grass carp. Based on the above-mentioned results, we found two novel transcriptional mechanisms for SREBP-1 in grass carp: (1) the auto-regulation sited on the SREBP-1 promoter regions was suppressive and (2) there was a self-activating loop of SREBP-1 and miR-29.

Fatty acid taste (FAT) perception is involved in the regulation of dietary fat intake, where impaired FAT is associated with increased fatty food intake. There are a number of FAT receptors identified on human taste cells that are potentially responsible for FAT perception. Manipulating dietary fat intake, and in turn FAT perception, would elucidate the receptors that are associated with long-term regulation of FAT perception. The present study aimed to assess associations between diet-mediated changes to FAT receptors and FAT perception in humans. A co-twin randomised controlled trial was conducted, where each matching twin within a pair were randomly allocated to either an 8-week low-fat (LF; <20 % energy fat) or an 8-week high-fat (HF; >35 % energy fat) diet. At baseline and week 8, fungiform papillae were biopsied in the fasted state and FAT receptor gene expressions (cluster of differentiation 36 (CD36), free fatty acid receptor 2 (FFAR2), FFAR4, G protein-coupled receptor 84 (GPR84) and a delayed rectifying K+ channel (K+ voltage-gated channel subfamily A member 2; KCNA2)) were measured using RT-PCR; and FAT threshold (FATT) was assessed using three-alternate forced choice methodology. Linear mixed models were fitted, adjusting for correlation between co-twins. Intake was compliant with the study design, with the LF and HF groups consuming 14·8 and 39·9 % energy from fat, respectively. Expression of FFAR4 increased by 38 % in the LF group (P = 0·023; time–diet interaction P = 0·063). ΔFFAR4 (Δ, week 8–baseline) was associated with Δfat intake (g) ( = −159·4; P < 0·001) and ΔFATT ( = −8·8; P = 0·016). In summary, FFAR4 is involved in long-term diet-mediated changes to FAT perception. Manipulating dietary fat intake, and therefore FFAR4 expression, might aid in reducing taste-mediated passive overconsumption of fatty foods.

The major facilitator superfamily domain 2a protein was identified recently as a lysophosphatidylcholine (LPC) symporter with high affinity for LPC species enriched with DHA (LPC-DHA). To test the hypothesis that reproductive state and choline intake influence plasma LPC-DHA, we performed a post hoc analysis of samples available through 10 weeks of a previously conducted feeding study, which provided two doses of choline (480 and 930 mg/d) to non-pregnant (n 21), third-trimester pregnant (n 26), and lactating (n 24) women; all participants consumed 200 mg of supplemental DHA and 22 % of their daily choline intake as 2H-labelled choline. The effects of reproductive state and choline intake on total LPC-DHA (expressed as a percentage of LPC) and plasma enrichments of labelled LPC and LPC-DHA were assessed using mixed and generalised linear models. Reproductive state interacted with time (P = 0·001) to influence total LPC-DHA, which significantly increased by week 10 in non-pregnant women, but not in pregnant or lactating women. Contrary to total LPC-DHA, patterns of labelled LPC-DHA enrichments were discordant between pregnant and lactating women (P < 0·05), suggestive of unique, reproductive state-specific mechanisms that result in reduced production and/or enhanced clearance of LPC-DHA during pregnancy and lactation. Regardless of the reproductive state, women consuming 930 v. 480 mg choline per d exhibited no change in total LPC-DHA but higher d3-LPC-DHA (P = 0·02), indicating that higher choline intakes favour the production of LPC-DHA from the phosphatidylethanolamine N-methyltransferase pathway of phosphatidylcholine biosynthesis. Our results warrant further investigation into the effect of reproductive state and dietary choline on LPC-DHA dynamics and its contribution to DHA status.

Chinese sturgeon (Acipenser sinensis) is an endangered species, listed as a grade I protected animal in China. The females rarely successfully develop their gonads from stage II to III in captivity, which handicaps the propagation of cultured Chinese sturgeon. The present study aimed to understand the effects of dietary lipid level on the ovarian development and the related regulation mechanism in female Chinese sturgeon. A 24-month feeding trial was conducted with 10-year-old Chinese sturgeons with ovaries at the developmental stage II, with three experimental diets containing 10, 14 and 18 % lipids. Ovary, muscle and serum samples were collected at four time points (6, 12, 18 and 24 months) for further analyses. Serum metabolomics and ovary transcriptomics analyses were conducted at 18 months. Results showed that only the 18 % lipid diet promoted ovary development to stage IV. Oocytes at stage II in this group also exhibited higher diameter and more lipid droplets. Serum TAG content in the 18 % group was significantly higher than in 10 and 14 % groups (both at 12 and 18 months). Oestradiol content in the 14 % group was significantly higher than in 10 and 18 % groups, except at 24 months. Metabolomic and transcriptomic results indirectly indicated that 14 % of dietary lipids benefited steroid hormone synthesis, while 18 % lipid facilitated arachidonic acid metabolism, cholesterol biosynthesis and vitellogenesis, although serum cholesterol content did not vary with dietary lipid level. In conclusion, 18 % dietary lipid is the optimal level for improving gonad development of female Chinese sturgeon.

Physicochemical properties of diets are believed to play a major role in the regulation of digesta transit in the gastrointestinal tract. Starch, being the dominant nutrient in pig diets, strongly influences these properties. We studied transport of digesta solids and liquids through the upper gastrointestinal tract of ninety pigs in a 3 × 3 factorial arrangement. Dietary treatments varied in starch source (barley, maize and high-amylose maize) and form (isolated starch, ground cereal and extruded cereal). Mean retention times (MRT) of digesta solids ranged 129–225 min for the stomach and 86–124 min for the small intestine (SI). The MRT of solids consistently exceeded that of liquids in the stomach, but not in the SI. Solid digesta of pigs fed extruded cereals remained 29–75 min shorter in the stomach compared with pigs fed ground cereals (P < 0·001). Shear stress of whole digesta positively correlated with solid digesta MRT in the stomach (r 0·33, P < 0·001), but not in the SI. The saturation ratio (SR), the actual amount of water in stomach digesta as a fraction of the theoretical maximum held by the digesta matrix, explained more variation in digesta MRT than shear stress. The predictability of SR was hampered by the accumulation of large particles in the stomach. In addition, the water-holding capacity of gelatinised starch leads to a decreased SR of diets, but not of stomach digesta, which was caused by gastric hydrolysis of starch. Both of these phenomena hinder the predictability of gastric retention times based on feed properties.

Obesity phenotypes can be regarded as an indicator of CVD risk factors. The aim of the present study was to determine the prevalence of adolescents with different obesity phenotypes and the role of obesity phenotypes in prediction of the metabolic syndrome (MetS) in adults. For this population-based cohort study, 2159 adolescents aged 11–18 years were included. Subjects were divided into four obesity phenotype groups: metabolically healthy normal weight (MHNW), metabolically healthy obese (MHO), metabolically unhealthy normal weight (MUNW) and metabolically unhealthy obese (MUO). Cox proportional hazard modelling was used to estimate the incidence of the MetS in adults after a median follow-up of 11·3 years. The incidence rate of the MetS in early adulthood was 111·6 (95 % CI 98·7, 126·3) per 10 000 person-years, with higher values in boys (210·1 (95 % CI 183·0, 241·3)), compared with girls (39·7 (95 % CI 30·2, 52·1)). In the age- and adult BMI-adjusted model, the hazard ratio of the MetS in adulthood for boys was 3·33 (95 % CI 2·08, 5·32) among MUO phenotype followed less than 6 years, 1·71 (95 % CI 1·01, 2·90) among MHO, and 2·52 (95 % CI 1·72, 3·68) among MUNW. All associations were attenuated in girls except for MUO phenotype followed less than 6 years (5·72 (95 % CI 2·14, 15·3)). In conclusion, MUNW and MHO phenotypes in boys, but not in girls, and MUO phenotype in both sexes with less than 6 years of follow-up increased the risk of adult MetS compared with MHNW. It seems that lack of obesity at least in boys does not protect them from MetS development in adulthood.

Little is known about the association between dietary choline intake and mortality. We evaluated the link between choline consumption and overall as well as cause-specific mortality by using both individual data and pooling prospective studies by meta-analysis and systematic review. Furthermore, adjusted means of cardiometabolic risk factors across choline intake quartiles were calculated. Data from the National Health and Nutrition Examination Survey (1999–2010) were collected. Adjusted Cox regression was performed to determine the risk ratio (RR) and 95 % CI, as well as random-effects models and generic inverse variance methods to synthesise quantitative and pooling data, followed by a leave-one-out method for sensitivity analysis. After adjustments, we found that individuals consuming more choline had worse lipid profile and glucose homeostasis, but lower C-reactive protein levels (P < 0·001 for all comparisons) with no significant differences in anthropometric parameters and blood pressure. Multivariable Cox regression models revealed that individuals in the highest quartile (Q4) of choline consumption had a greater risk of total (23 %), CVD (33 %) and stroke (30 %) mortality compared with the first quartile (Q1) (P < 0·001 for all comparison). These results were confirmed in a meta-analysis, showing that choline intake was positively and significantly associated with overall (RR 1·12, 95 % CI 1·08, 1·17, I2 = 2·9) and CVD (RR 1·28, 95 % CI 1·17, 1·39, I2 = 9·6) mortality risk. In contrast, the positive association between choline consumption and stroke mortality became non-significant (RR 1·18, 95 % CI 0·97, 1·43, P = 0·092, I2 = 1·1). Our findings shed light on the potential adverse effects of choline intake on selected cardiometabolic risk factors and mortality risk.

Anecdotal evidence suggests the use of bolus tube feeding is increasing in the long-term home enteral tube feed (HETF) patients. A cross-sectional survey to assess the prevalence of bolus tube feeding and to characterise these patients was undertaken. Dietitians from ten centres across the UK collected data on all adult HETF patients on the dietetic caseload receiving bolus tube feeding (n 604, 60 % male, age 58 years). Demographic data, reasons for tube and bolus feeding, tube and equipment types, feeding method and patients’ complete tube feeding regimens were recorded. Over a third of patients receiving HETF used bolus feeding (37 %). Patients were long-term tube fed (4·1 years tube feeding, 3·5 years bolus tube feeding), living at home (71 %) and sedentary (70 %). The majority were head and neck cancer patients (22 %) who were significantly more active (79 %) and lived at home (97 %), while those with cerebral palsy (12 %) were typically younger (age 31 years) but sedentary (94 %). Most patients used bolus feeding as their sole feeding method (46 %), because it was quick and easy to use, as a top-up to oral diet or to mimic mealtimes. Importantly, oral nutritional supplements (ONS) were used for bolus feeding in 85 % of patients, with 51 % of these being compact-style ONS (2·4 kcal (10·0 kJ)/ml, 125 ml). This survey shows that bolus tube feeding is common among UK HETF patients, is used by a wide variety of patient groups and can be adapted to meet the needs of a variety of patients, clinical conditions, nutritional requirements and lifestyles.

There exists an ever-increasing number of systematic reviews, with or without meta-analysis, in the field of nutrition. Concomitant with this increase is the increased use of such to guide future research as well as both practice and policy-based decisions. Given this increased production and consumption, a need exists to educate both producers and consumers of systematic reviews, with or without meta-analysis, on how to conduct and evaluate high-quality reviews of this nature in nutrition. The purpose of this paper is to try and address this gap. In the present manuscript, the different types of systematic reviews, with or without meta-analyses, are described as well as the description of the major elements, including methodology and interpretation, with a focus on nutrition. It is hoped that this non-technical information will be helpful to producers, reviewers and consumers of systematic reviews, with or without meta-analysis, in the field of nutrition.

The pathogenesis of congenital diaphragmatic hernia (CDH) is largely unknown; however, vitamin A seems to play a role in diaphragmatic development. Previous case–control studies reported that maternal dietary vitamin A intake was inversely associated with the risk of CDH. To our knowledge, however, there is no prospective evidence regarding this association. Our aim was to examine whether maternal intake of vitamin A was associated with CDH occurrence. Baseline data, from the Japan nationwide birth cohort study (2011–2014) of 89 658 mothers (mean age at delivery = 31·2 years) who delivered singleton live births, were analysed. We assessed dietary habits using an FFQ focused on the first trimester and estimated the daily intake of total vitamin A (retinol activity equivalents), retinol, provitamin A carotenoids and vegetables. The occurrence of CDH was ascertained from medical records. A total of forty cases of CDH were documented. The adjusted OR of CDH occurrence for the high total vitamin A intake category (median = 468 μg/d) was 0·6 (95 % CI 0·3, 1·2) with reference to the low intake category (230 μg/d). When we restricted to mothers with a prepregnancy BMI of 18·5–24·9 kg/m2, vitamin A intake was inversely associated with the risk of their children being born with CDH (OR 0·5, 95 % CI 0·2, 1·0). Even given the limited number of cases in the study, our findings provide additional evidence to link vitamin A with CDH.

Consumption of sugar-sweetened beverages (SSB) by infants and young children are less explored in Asian populations. The Growing Up in Singapore Towards healthy Outcomes cohort study examined associations between SSB intake at 18 months and 5 years of age, with adiposity measures at 6 years of age. We studied Singaporean infants/children with SSB intake assessed by FFQ at 18 months of age (n 555) and 5 years of age (n 767). The median for SSB intakes is 28 (interquartile range 5·5–98) ml at 18 months of age and 111 (interquartile range 57–198) ml at 5 years of age. Association between SSB intake (100 ml/d increments and tertile categories) and adiposity measures (BMI standard deviation scores (sd units), sum of skinfolds (SSF)) and overweight/obesity status were examined using multivariable linear and Poisson regression models, respectively. After adjusting for confounders and additionally for energy intake, SSB intake at age 18 months were not significantly associated with later adiposity measures and overweight/obesity outcomes. In contrast, at age 5 years, SSB intake when modelled as 100 ml/d increments were associated with higher BMI by 0·09 (95 % CI 0·02, 0·16) sd units, higher SSF thickness by 0·68 (95 % CI 0·06, 1·44) mm and increased risk of overweight/obesity by 1·2 (95 % CI 1·07, 1·23) times at age 6 years. Trends were consistent with SSB intake modelled as categorical tertiles. In summary, SSB intake in young childhood is associated with higher risks of adiposity and overweight/obesity. Public health policies working to reduce SSB consumption need to focus on prevention programmes targeted at young children.

The present study examined whether the combination of medium-chain TAG (MCT) along with exercise suppresses energy intake to a greater extent compared with either intervention alone. Twelve participants consumed a porridge breakfast containing 692·9 kJ of either vegetable or MCT oil on two separate occasions: one followed by rest for 240 min and another followed by rest broken up with 1 h of cycling at 65 % $\dot V$O2peak starting at 120 min. At 240 min, participants consumed a buffet lunch to satiation and recorded their food intake for the rest of the day. Expired air samples (for calculation of energy expenditure (EE)) and subjective ratings of appetite on visual analogue scales were taken every 30 min, and gastric emptying (GE) breath samples were taken every 15 min. No effect of either breakfast or exercise condition was observed on energy intake at any time point (P > 0·05) or no effect was observed on subjective appetite ratings (P > 0·05). Exercise trials resulted in significantly higher EE compared with resting trials (2960·6 kJ, 95 % CI 2528·9, 3392·2; P < 0·001), and MCT increased resting EE over 4 h compared with long-chain TAG (LCT) (124·8 kJ, 95 % CI 13·5, 236·0; P = 0·031). GE was accelerated by exercise, regardless of the breakfast consumed, but delayed by MCT in both resting and exercise trials. The results show that exercise causes energy deficits via increased EE without promoting dietary compensation. MCT has no effect on energy intake or satiety but increases EE under resting conditions. There is no additive effect of MCT and exercise on EE, intake or appetite ratings.