Salt sensitivity is an independent CVD and mortality risk factor, which is present in both hypertensive and normotensive populations. It is genetically determined and it may affect the relationship between salt taste perception and salt intake. The aim of this study was to explore the genetic predisposition to salt sensitivity in a young and a middle-aged adult population and its effects on salt taste perception and salt intake. The effects of Na loading on blood pressure (BP) were investigated in twenty normotensive subjects and salt sensitivity defined as the change in BP after 7 d of low-Na (51·3 mmol Na/d) and 7 d of high-Na diet (307·8 mmol Na/d). Salt taste perception was identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011). Salt intake was assessed with a validated FFQ. DNA was genotyped for SNP in the SLC4A5, SCNN1B and TRPV1 genes. The subjects with AA genotype of the SLC4A5 rs7571842 exhibited the highest increase in BP (∆ systolic BP=7·75 mmHg, P=0·002, d=2·4; ∆ diastolic BP=6·25 mmHg, P=0·044, d=1·3; ∆ mean arterial pressure=6·5 mmHg, P=0·014, d=1·7). The SLC4A5 rs10177833 was associated with salt intake (P=0·037), and there was an association between salt taste perception and salt sensitivity (rs 0·551, P=0·041). In conclusion, there is a genetic predisposition to salt sensitivity and it is associated with salt taste perception. The association between salt taste perception and discretionary salt use suggests that preference for salty taste may be a driver of salt intake in a healthy population and warrants further investigation.

Keto analogues and amino acids (KAAA) supplementation can reduce blood ammonia concentrations in athletes undergoing high-intensity exercise under both ketogenic and thermoneutral conditions. This study evaluated the acute effects of KAAA supplementation on ammonia metabolism during extenuating endurance exercise in rats fed a ketogenic diet. In all, eighty male Fischer rats at 90 d of age were divided into eight groups, and some were trained using a swimming endurance protocol. A ketogenic diet supplemented with keto analogues was administered for 10 d. Administration of the ketogenic diet ended 3 d before the exhaustion test (extenuating endurance exercise). A ketogenic diet plus KAAA supplementation and extenuating endurance exercise (trained ketogenic diet supplemented with KAAA (TKKa)) increased blood ammonia concentrations by approximately 50 % compared with the control diet (trained control diet supplemented with KAAA (TCKa)) and similar training (effect size=1·33; statistical power=0·50). The KAAA supplementation reduced blood urea concentrations by 4 and 18 % in the control and ketogenic diet groups, respectively, compared with the groups fed the same diets without supplementation. The trained groups had 60 % lower blood urate concentrations after TCKa treatment than after TKKa treatment. Our results suggest that KAAA supplementation can reduce blood ammonia concentrations after extenuating endurance exercise in rats fed a balanced diet but not in rats fed a ketogenic diet.

Obesity increases the risk for developing kidney disease, and protection of kidneys through changes in diet should be investigated. Fish intake has been associated with reduced risk of developing kidney disease; therefore, we wanted to investigate whether cod protein intake could prevent or delay the development of kidney damage in an obese rat model that spontaneously develops proteinuria and focal segmental glomerulosclerosis. The aim of the study was to investigate any effects of cod protein intake on established markers of kidney function, amino acid composition, protein utilisation and growth in obese Zucker fa/fa rats in the early stage of decreased renal function. Male obese Zucker fa/fa rats (HsdOla:Zucker-Lepr) were fed cod muscle proteins in an amount corresponding to 25 % of dietary protein, with the remaining protein from a casein/whey mixture (COD diet). A control group was fed a diet with a casein/whey mixture as the only protein source (CAS diet). The intervention started when rats were 9–10 weeks old, and the rats were fed these diets for 4 weeks. At the end of the study, rats fed the COD diet had lower urine concentration of cystatin C, T-cell immunoglobulin mucin-1 (TIM-1), amino acids, carbamide, uric acid and ammonium and higher concentrations of creatine, trimethylamine N-oxide, 1-methylhistidine and 3-methylhistidine, lower kidney concentration of TIM-1 and showed better growth when compared with the CAS group. To conclude, cod protein may have the potential to delay the development of kidney damage in young obese Zucker rats and to improve protein utilisation and growth.

7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the corresponding Picea abies extract (total extract P. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (−11 and −13 %) and fat mass (−11 and −18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and −12 % smaller and the liver was less steatotic (−62 and −65 %). Serum lipids decreased in TEP-treated mice (−11 % cholesterol, −23 % LDL and −15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genes PPARγ, C/EBPα and aP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1–6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptake in vitro.

Intra-uterine growth restriction (IUGR) is associated with adverse metabolic outcome later in life. Healthy mice challenged with a Western-style diet (WSD) accumulated less body fat when previously fed a diet containing large lipid globules (complex lipid matrix (CLM)). This study was designed to clarify whether an early-life CLM diet mitigates ‘programmed’ visceral adiposity and associated metabolic sequelae after IUGR. In rats, IUGR was induced either by bilateral uterine vessel ligation (LIG) or sham operation (i.e. intra-uterine stress) of the dam on gestational day 19. Offspring from non-operated (NOP) dams served as controls. Male offspring of all groups were either fed CLM or ‘normal matrix’ control diet (CTRL) from postnatal days (PND) 15 to 42. Thereafter, animals were challenged with a mild WSD until dissection (PND 98). Fat mass (micro computer-tomograph scan; weight of fat compartments), circulating metabolic markers and expression of ‘metabolic’ genes (quantitative real-time PCR) were assessed. CLM diet significantly reduced visceral fat mass in LIG at PND 40. At dissection, visceral fat mass, fasted blood glucose, TAG and leptin concentrations were significantly increased in LIG-CTRL v. NOP-CTRL, and significantly decreased in LIG-CLM v. LIG-CTRL. Gene expression levels of leptin (mesenteric fat) and insulin-like growth factor 1 (liver) were significantly reduced in LIG-CLM v. LIG-CTRL. In conclusion, early-life CLM diet mitigated the adverse metabolic phenotype after utero-placental insufficiency. The supramolecular structure of dietary lipids may be a novel aspect of nutrient quality that has to be considered in the context of primary prevention of obesity and metabolic disease in at-risk populations.

The source of starch may interfere with glycaemic control in dogs, but few studies have evaluated these aspects in diabetic dogs. This study compared the effects of two isonutrient diets with different starch sources, peas and barley (PB) v. maize (Mi), on diabetic dogs. The Mi diet was processed in order to generate a lower starch gelatinisation index. In all, fifteen adult diabetic dogs without other conditions were included. The animals were fed two dry extruded rations with moderate levels of fat and starch and high levels of protein and fibre using a random, double-blind cross-over design. Glycaemic curves over 48 h were developed via continuous glucose monitoring after 60 d on each diet and with the same neutral protamine Hagedorn (NPH) insulin dosage. The following were compared: fasting, mean, maximum and minimum blood glucose, maximum and minimum glycaemia difference, glycaemic increment, area under the glycaemic curve, area under the glycaemic increment curve and serum fructosamine concentration. Paired t tests or Wilcoxon signed-rank tests were used to compare the amount of food and nutrients ingested and the dietary effects on glycaemic variables between the diets. Dogs fed the PB diet presented a lower average mean interstitial glucose (P=0·01), longer mean hypoglycaemic time (P<0·01), shorter mean hyperglycaemic time (P<0·01) and smaller difference between maximum and minimum blood glucose levels (P=0·03). Thus, the processing applied to the Mi diet was not sufficient to achieve the same effects of PB on glycaemic control in diabetic dogs.

PUFA might modulate inflammatory responses involved in the development of severe dengue. We aimed to examine whether serum PUFA concentrations in patients diagnosed with dengue fever (DF) were related to the risk of progression to dengue haemorrhagic fever/dengue shock syndrome (DHF/DSS). A secondary aim was to assess correlations between fatty acids (FA) and inflammatory biomarkers in patients with DF. We conducted a prospective case–control study nested within a cohort of patients who were diagnosed with DF and followed during the acute episode. We compared the distribution of individual FA (% of total FA) at onset of fever between 109 cases who progressed to DHF/DSS and 235 DF non-progressing controls using unconditional logistic regression. We estimated correlations between baseline FA and cytokine concentrations and compared FA concentrations between the acute episode and >1 year post-convalescence in a subgroup. DHA was positively related to progression to DHF/DSS (multivariable adjusted OR (AOR) for DHA in quintile 5 v. 1=5·34, 95 % CI 2·03, 14·1; Ptrend=0·007). Dihomo-γ-linolenic acid (DGLA) was inversely associated with progression (AOR for quintile 5 v. 1=0·30, 95 % CI 0·13, 0·69; Ptrend=0·007). Pentadecanoic acid concentrations were inversely related to DHF/DSS. Correlations of PUFA with cytokines at baseline were low. PUFA were lower during the acute episode than in a disease-free period. In conclusion, serum DHA in patients with DF predicts higher odds of progression to DHF/DSS whereas DGLA and pentadecanoic acid predict lower odds.

Air displacement plethysmography utilises a two-component model to assess body composition, which relies on assumptions regarding the density of fat-free mass (FFM). To date, there is no evidence as to whether Lohman’s or Wells et al.’s FFM density values are more accurate in young children. Therefore, the aims of this study were to compare total body fat percentage (TBF%) assessed using the BodPod with both Lohman’s and Wells et al.’s FFM density values with TBF% from the three-component (3C) model in forty healthy Swedish children aged 5·5 years. Average TBF% calculated using Lohman’s FFM density values underestimated TBF% in comparison with the corresponding value assessed using the 3C model (22·2 (sd 5·7) and 25·1 (sd 5·5) %, respectively; P<0·001). No statistically significant difference was observed between TBF% assessed using Wells et al.’s FFM density values and the 3C model (24·9 (sd 5·5) and 25·1 (sd 5·5) %, respectively; P=0·614). The Bland and Altman plots for TBF% using both Lohman’s and Wells et al.’s FFM density values did not show any bias across the range of body fatness (Lohman: r 0·056, P=0·733 and Wells et al.: r −0·006, P=0·970). These results indicate that Wells et al.’s FFM density values should be used when assessing body composition with the paediatric option for BodPod in 5-year-old children. However, future studies are needed to confirm these results in other populations, including a wider age range of children.

Evidence supports the role of vitamin D in various conditions of development and ageing. Serum 25-hydroxyvitamin D (25(OH)D) is the best indicator for current vitamin D status. However, the cost of its measurement can be prohibitive in epidemiological research. We developed and validated multivariable regression models that quantified the relationships between vitamin D determinants, measured through an in-person interview, and serum 25(OH)D concentrations. A total of 200 controls participating in a population-based case–control study in Montreal, Canada, provided a blood specimen and completed an in-person interview on socio-demographic, reproductive, medical and lifestyle characteristics and personal attributes. Serum 25(OH)D concentrations were quantified by liquid chromatography–tandem MS. Multivariable least squares regression was used to build models that predict 25(OH)D concentrations from interview responses. We assessed high-order effects, performed sensitivity analysis using the lasso method and conducted cross-validation of the prediction models. Prediction models were built for users and non-users of vitamin D supplements separately. Among users, alcohol intake, outdoor time, sun protection, dose of supplement use, menopausal status and recent vacation were predictive of 25(OH)D concentrations. Among non-users, BMI, sun sensitivity, season and recent vacation were predictive of 25(OH)D concentrations. In cross-validation, 46–47 % of the variation in 25(OH)D concentrations were explained by these predictors. In the absence of 25(OH)D measures, our study supports that predicted 25(OH)D scores may be used to assign exposure in epidemiological studies that examine vitamin D exposure.

The prevalence of impaired fasting glucose (IFG) and diabetes mellitus (DM) has reportedly increased significantly among Chinese children and adolescents. We aimed to examine the prevalence of IFG and DM, the disparities in sex and region and related risk factors among Chinese children and adolescents. A total of 16 434 Chinese children aged 6–17 years were selected from a national cross-sectional survey, and fasting glucose was measured for all participants. Overall, mean fasting plasma glucose (FPG) concentration was (4·64 (sd 0·51)) mmol/l, and the prevalence of DM and IFG was 0·10 and 1·89 %, respectively. Compared with girls, boys had higher FPG concentration (4·69 v. 4·58 mmol/l, r 0·107, P<0·001) and IFG prevalence (2·67 v. 1·07 %, rφ 0·059, P<0·001). Compared with rural children and adolescents, urban children and adolescent had higher FPG concentration (4·65 v. 4·62 mmol/l, r 0·029, P<0·001) and DM prevalence (0·15 v. 0·05 %, rφ 0·016, P<0·01). In addition, self-reported fried foods intake and overweight/obesity were positively associated with IFG, and the proportion of consuming fried foods more than or equal to once per week and overweight/obesity prevalence in boys and urban children and adolescents were significantly higher than girls and rural children and adolescents, respectively (P<0·05). Although the prevalence of IFG and DM was relatively low in Chinese children and adolescents, sex and region disparities were observed, which may be associated with differences in overweight/obesity prevalence and dietary factors.

High protein intake in young children is associated with excess gains in weight and body fat, but the specific role of different protein sources has yet to be described. The study aimed to investigate the role of different types of protein in the post-weaning stage on weight, BMI and overweight/obesity at 60 months. Intakes of animal, dairy and plant protein and a dietary pattern characterising variation in protein types at 21 months of age were estimated using a 3-d diet diary in a cohort of 2154 twins; weight and height were recorded every 3 months from birth to 60 months. Longitudinal mixed-effect models investigated the associations between sources of protein intake or dietary pattern scores and BMI, weight and overweight/obesity from 21 months up to 60 months. Adjusting for confounders, dairy protein intake at 21 months was positively associated with greater weight (46 (95 % CI 21, 71) g and BMI up to 60 months (0·04 (95 % CI 0·004, 0·070) kg/m2) and the odds of overweight/obesity at 3 years (OR 1·12; 95 % CI 1·00, 1·24). Milk showed associations of similar magnitude. A dietary pattern low in dairy protein and high in plant protein was associated with lower weight gain up to 60 months, but not overweight/obesity. Intake of dairy products in early childhood is most strongly associated with weight gain, compared with other protein sources. A dietary pattern characterised by lower protein intake and greater protein source diversity at 2 years may confer a lower risk of excess weight gain.

There is a paucity of data examining the effect of cutlery size on the microstructure of within-meal eating behaviour or food intake. Therefore, the present studies examined how manipulation of spoon size influenced these eating behaviour measures in lean young men. In study one, subjects ate a semi-solid porridge breakfast ad libitum, until satiation. In study two, subjects ate a standardised amount of porridge, with mean bite size and mean eating rate covertly measured by observation through a one-way mirror. Both studies involved subjects completing a familiarisation visit and two experimental visits, where they ate with a teaspoon (SMALL) or dessert spoon (LARGE), in randomised order. Subjective appetite measures (hunger, fullness, desire to eat and satisfaction) were made before and after meals. In study one, subjects ate 8 % less food when they ate with the SMALL spoon (SMALL 532 (SD 189) g; LARGE 575 (SD 227) g; P=0·006). In study two, mean bite size (SMALL 10·5 (SD 1·3) g; LARGE 13·7 (SD 2·6) g; P<0·001) and eating rate (SMALL 92 (SD 25) g/min; LARGE 108 (SD 29) g/min; P<0·001) were reduced in the SMALL condition. There were no condition or interaction effects for subjective appetite measures. These results suggest that eating with a small spoon decreases ad libitum food intake, possibly via a cascade of effects on within-meal eating microstructure. A small spoon might be a practical strategy for decreasing bite size and eating rate, likely increasing oral processing, and subsequently decreasing food intake, at least in lean young men.