1. An experiment was performed to study the effect of sodium acetoacetate on urinary excretion of santhurenic acid and other tryptophan metabolites in male albino rats.

2. Animals were fed on a nicotinic acid-deficient diet for a period of 3 weeks. The animals were then divided into two groups and, after the basal urinary excretion of the tryptophan metabolites had been estimated, the rats of both the groups were force-fed with L-tryptophan (100 mg per rat), the rats of the second group being simultaneously injected intraperitoncally with acetoacetate (200 mg/kg body-weight), and the urine samples during the following 24 h were collected and analysed.

3. Acetoacetate-treated rats given tryptophan were found to excrete significantly greater amounts of kynurenine, hydroxykynurenine and xanthurenic acid than the corresponding control rats. There was no ditference between the amounts of kynurenic acid excreted by the animals in the two groups.

1. Newborn rabbits were overfed by encouraging them to suck from two lactating does. These double-fed rabbits were compared with single-fed litter-mate controls.

2. A standard set of fore- and hind-foot radiographs was obtained by taking daily radiographs from a normal litter and selecting the most representative film to act as a standard for that day.

3. Bone age was assessed in single- and double-fed rabbits at ages 7, 14, and 21 d by comparing radiographs taken at these ages with the standard films.

4. Double-feeding was associated with an increase in body-weight and an increase in bone age, although the former was increased to a much greater extent than the latter. The advance in bone age was proportional to an increase in bone length.

5. There is little information available on overnutrition and skeletal maturation in man, but what information is available suggests that height and skeletal maturation are increased in parallel. The present study with rabbits supports the concept that overnutrition increases growth rate but does not disturb the relation hetween bone growth and bone age.

6. Bone age can be assessed very sensitively in rabbits using the previously-described technique. It would therefore be a valuable technique for studying the endocrinology of skeletal maturation.

Female crabs enter a stage of rapid ovarian development after mating, and cholesterol is a substrate for steroid hormone synthesis. Therefore, in this experiment, an 8-week feeding trial was conducted to investigate the effects of mating treatments (mated crab and unmated crab) and three dietary cholesterol levels (0·09 %, 0·79 % and 1·40 %) on ovarian development, cholesterol metabolism and steroid hormones metabolism of adult female swimming crab (Portunus trituberculatus). The results indicated that crabs fed the diet with 0·79 % cholesterol significantly increased gonadosomatic index (GSI) and vitellogenin (VTG) content than other treatments in the same mating status. Moreover, mated crabs had markedly increased GSI and VTG content in the ovary and hepatopancreas than unmated crabs. The histological observation found that exogenous vitellogenic oocytes appeared in the mated crabs, while previtellogenic oocytes and endogenous vitellogenic oocytes were the primary oocytes in unmated crabs. The transmission electron microscopy analysis showed that when fed diet with 0·79 % cholesterol, the unmated crabs contained more rough endoplasmic reticulum and mated crabs had higher yolk content than other treatments. Furthermore, mating treatment and dietary 0·79 % cholesterol level both promoted cholesterol deposition by up-regulation of the mRNA and protein expression levels of class B scavenger receptors 1 (Srb1), while stimulating the secretion of steroid hormones by up-regulation of the mRNA and protein expression of steroidogenic acute regulatory protein (Star). Overall, the present results indicated that mating behaviour plays a leading role in promoting ovarian development, and dietary 0·79 % cholesterol level can further promote ovarian development after mating.

Our aim was to estimate associations of adolescent dietary patterns and meal habits with hypertensive disorders of pregnancy (HDP) and preterm birth. We used data from a prospective cohort study (Norwegian Young-HUNT1) where dietary information was collected during adolescence and pregnancy outcomes were obtained through record linkage to the Norwegian national birth registry. The outcomes were HDP, hypertension, pre-eclampsia/eclampsia, and preterm birth in the first pregnancy and in any pregnancy. Diet was self-reported from validated questionnaires, and exposures were dietary indexes (healthy; unhealthy; fruit and vegetable; fibre index) and meal habits. Recruitment took place in schools. Eligible participants were females aged 13–19 years at the time of dietary assessment with a subsequent singleton pregnancy (n 3622). Women who reported a higher fibre intake in adolescence had a lower risk of pre-eclampsia in the first pregnancy (Relative Risk: 0·84; 95 % CI 0·7, 1·0), although this was weaker in sensitivity analyses. Regular meal habits in mid-adolescence (aged 13–15 years), particularly breakfast and lunch, were weakly associated with a lower risk of hypertension in pregnancy. Our results are the first to indicate an association between aspects of diet and dietary behaviour in mid-adolescence and subsequent HDP. More evidence is needed from larger studies to replicate the results and from alternative study designs to disentangle causality.

This study aimed to assess how Bacillus subtilis and Enterococcus faecium co-fermented feed (FF) affects the antioxidant capacity, muscle fibre types and muscle lipid profiles of finishing pigs. In this study, a total of 144 Duroc × Berkshire × Jiaxing Black finishing pigs were randomly assigned into three groups with four replicates (twelve pigs per replication). The three treatments were a basal diet (0 % FF), basal diet + 5 % FF and basal diet + 10 % FF, respectively. The experiment lasted 38 d after 4 d of acclimation. The study revealed that 10 % FF significantly increased the activity of superoxide dismutase (SOD) and catalase (CAT) compared with 0 % FF group, with mRNA levels of up-regulated antioxidant-related genes (GPX1, SOD1, SOD2 and CAT) in 10 % FF group. 10 % FF also significantly up-regulated the percentage of slow-twitch fibre and the mRNA expression of MyHC I, MyHC IIa and MyHC IIx, and slow MyHC protein expression while reducing MyHC IIb mRNA expression. Lipidomics analysis showed that 5 % FF and 10 % FF altered lipid profiles in longissimus thoracis. 10 % FF particularly led to an increase in the percentage of TAG. The Pearson correlation analysis indicated that certain molecular markers such as phosphatidic acid (PA) (49:4), Hex2Cer (d50:6), cardiolipin (CL) (72:8) and phosphatidylcholine (PC) (33:0e) could be used to indicate the characteristics of muscle fibres and were closely related to meat quality. Together, our findings suggest that 10 % FF improved antioxidant capacity, enhanced slow-twitch fibre percentage and altered muscle lipid profiles in finishing pigs.

We aimed to investigate the association of metabolic obesity phenotypes with all-cause mortality risk in a rural Chinese population. This prospective cohort study enrolled 15 704 Chinese adults (38·86 % men) with a median age of 51·00 (interquartile range: 41·00–60·00) at baseline (2007–2008) and followed up during 2013–2014. Obesity was defined by waist circumference (WC: ≥ 90 cm for men and ≥ 80 cm for women) or waist-to-height ratio (WHtR: ≥ 0·5). The hazard ratio (HR) and 95 % CI for the risk of all-cause mortality related to metabolic obesity phenotypes were calculated using the Cox hazards regression model. During a median follow-up of 6·01 years, 864 deaths were identified. When obesity was defined by WC, the prevalence of participants with metabolically healthy non-obesity (MHNO), metabolically healthy obesity (MHO), metabolically unhealthy non-obesity (MUNO) and metabolically unhealthy obesity (MUO) at baseline was 12·12 %, 2·80 %, 41·93 % and 43·15 %, respectively. After adjusting for age, sex, alcohol drinking, smoking, physical activity and education, the risk of all-cause mortality was higher with both MUNO (HR = 1·20, 95 % CI 1·14, 1·26) and MUO (HR = 1·20, 95 % CI 1·13, 1·27) v. MHNO, but the risk was not statistically significant with MHO (HR = 0·99, 95 % CI 0·89, 1·10). This result remained consistent when stratified by sex. Defining obesity by WHtR gave similar results. MHO does not suggest a greater risk of all-cause mortality compared to MHNO, but participants with metabolic abnormality, with or without obesity, have a higher risk of all-cause mortality. These results should be cautiously interpreted as the representation of MHO is small.

Choline plays a crucial role in hepatic lipid homeostasis by acting as a major methyl-group donor. However, despite this well-accepted fact, no study has yet explored how choline’s methyl-donor function contributes to preventing hepatic lipid dysregulation. Moreover, the potential regulatory role of Ire-1α, an ER-transmembrane transducer for the unfolded protein response (UPRer), in choline-mediated hepatic lipid homeostasis remains unexplored. Thus, this study investigated the mechanism by which choline prevents hepatic lipid dysregulation, focusing on its role as a methyl-donor and the involvement of Ire-1α in this process. To this end, a model animal for lipid metabolism, yellow catfish (Pelteobagrus fulvidraco) were fed two different diets (adequate or deficient choline diets) in vivo for 10 weeks. The key findings of studies are as follows: 1. Dietary choline, upregulated selected lipolytic and fatty acid β-oxidation transcripts promoting hepatic lipid homeostasis. 2. Dietary choline ameliorated UPRer and prevented hepatic lipid dysregulation mainly through ire-1α signalling, not perk or atf-6α signalling. 3. Choline inhibited the transcriptional expression level of ire-1α by activating site-specific DNA methylations in the promoter of ire-1α. 4. Choline-mediated ire-1α methylations reduced Ire-1α/Fas interactions, thereby further inhibiting Fas activity and reducing lipid droplet deposition. These results offer a novel insight into the direct and indirect regulation of choline on lipid metabolism genes and suggests a potential crosstalk between ire-1α signalling and choline-deficiency-induced hepatic lipid dysregulation, highlighting the critical contribution of choline as a methyl-donor in maintaining hepatic lipid homeostasis.

Vitamin D deficiency in infants is widely prevalent. Most paediatric professional associations recommend routine vitamin D prophylaxis for infants. However, the optimal dose and duration of supplementation are still debated. We aimed to compare the efficacy and safety of different vitamin D supplementation regimens in term and late preterm neonates. For this systematic review and network meta-analysis, we searched MEDLINE, the Cochrane Central Register of Controlled Trials and Embase. Randomised and quasi-randomised clinical trials that evaluated any enteral vitamin D supplementation regimen initiated within 6 weeks of life were included. Two researchers independently extracted data on study characteristics and outcomes and assessed quality of included studies. A network meta-analysis with a Bayesian random-effects model was used for data synthesis. Certainty of evidence (CoE) was assessed using GRADE. Primary outcomes were mean serum vitamin D concentrations and the proportion of infants with vitamin D insufficiency (VDI). We included twenty-nine trials that evaluated fourteen different regimens of vitamin D supplementation. While all dosage regimens of ≥400 IU/d increased the mean 25(OH)D levels compared with no treatment, supplementation of ≤250 IU/d and 1400 IU/week did not. The CoE varied from very low to high. Low CoE indicated that 1600 IU/d, compared with lower dosages, reduced the proportion of infants with VDI. However, our results indicated that any dosage of ≥800 IU/d increased the risk of hypervitaminosis D and hypercalcaemia. Data on major clinical outcomes were sparse. Vitamin D supplementation of 400–600 IU/d may be the most effective and safest in infants.

The purpose of the present study was to compare next-morning responses of RMR and appetite to pre-sleep consumption of casein protein (CP) in pre- and postmenopausal women. The study was a randomised, crossover, double-blind, placebo-controlled trial. Seven sedentary premenopausal (age: 19·9 (sd 1·2) years; BMI: 23·1 (sd 2·6) kg/m2) and seven sedentary postmenopausal (age: 56·4 (sd 4·9) years; BMI: 26·3 (sd 3·5) kg/m2) women participated. During visit one, anthropometrics and body composition were measured. Following visit one, subjects consumed either CP (25 g) or placebo (PL) ≥2 h after their last meal and ≤30 min prior to sleep on the night before visits two and three. Visits two and three occurred ≥1 week after visit one and were 48 h apart. During visits two and three, RMR (VO2), RER and appetite were measured via indirect calorimetry and visual analogue scale, respectively. Anthropometrics and body composition were analysed by one-way ANOVA. RMR and measures of appetite were analysed using a 2 × 2 (menopause status × CP/PL) repeated-measures ANOVA. Significance was accepted at P ≤ 0·05. RMR was significantly lower in postmenopausal compared with premenopausal women under both conditions (P = 0·003). When consumed pre-sleep CP did not alter RMR, RER or appetite compared with PL when assessed next morning in pre- and postmenopausal women. These data contribute to growing evidence that pre-sleep consumption of protein is not harmful to next-morning metabolism or appetite. In addition, these data demonstrate that menopause may not alter next-morning RMR, RER or appetite after pre-sleep consumption of CP.