Epidemiological studies on the association between the low carbohydrate diet (LCD) score and CVD risk factors have limited and inconsistent results. Data are from the baseline survey of Community-based Cohort Study on Nervous System Diseases. A total of 4609 adults aged ≥ 18 years were included in the study. Dietary data were assessed using a validated semi-quantitative FFQ. Multivariable logistic regression analyses were used to estimate relationships of three LCD scores with low HDL-cholesterol, high LDL-cholesterol, hypercholesterolaemia, hypertriacylglycerolaemia, impaired fasting glucose (IFG), high blood pressure and hyperuricaemia after adjusting for potential confounders. A higher LCD score was negatively associated with low HDL-cholesterol (OR: 0·65 (95 % CI 0·50, 0·83), P = 0·0001) and IFG (OR: 0·65 (95 % CI 0·51, 0·81), P = 0·001) after the final adjustment. However, there are sex differences in this result. Males in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of low HDL-cholesterol, and females in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of IFG than those in the lowest quintile of the LCD scores. These results suggest that sex differences should be considered when using LCD to treat dyslipidaemia and reduce fasting blood glucose.

The rates of utilization and oxidation of glutamine and glucose by oesophageal and duodenal tissues have been investigated in both rats and human subjects. In the rat, glutamine utilization by oesophageal tissue was 2–3-fold lower than that in the duodenum, and this substrate contributed less than 10 % to the total oxidative metabolism of the tissue, even when glutamine was the only substrate provided. In contrast, rat duodenal tissue derived about 34 % of the total CO2 production from glutamine-C, and this contribution was not suppressed by the addition of either glucose or a mixture of the other substrates. Rates of glucose utilization and oxidation by the duodenum were lower than those for glutamine, and were significantly (P<0·001) suppressed by addition of glutamine. In both oesophageal and duodenal tissues, less than 10 % of the glutamine-C utilized was fully oxidized, approximately 60–70 % was converted to glutamate, and 30–40 % to alanine. Results obtained using human biopsy tissue samples were similar to those observed in the rat. Glutamine oxidation contributed 34 (sd 4) % of the total CO2 production by the duodenal tissue, but only 8 (sd 4) % to oesophageal tissue oxidation. The findings suggest that glutamine is not an important or preferred fuel for oesophageal tissue, whereas it is for duodenal tissue. Thus, these tissues can be expected to respond differently to glutamine administration.

Most human intervention studies have examined the effects on a subset of risk factors, some of which may require long-term exposure. The plasma proteome may reflect the underlying changes in protein expression and activation, and this could be used to identify early risk markers. The aim of the present study was to evaluate the impact of regular fish intake on the plasma proteome. We recruited thirty healthy men aged 40 to 70 years, who were randomly allocated to a daily meal of chicken or trout raised on vegetable or marine feeds. Blood samples were collected before and after 8 weeks of intervention, and after the removal of the twelve most abundant proteins, plasma proteins were separated by two-dimensional gel electrophoresis. Protein spots < 66 kDa with a pI >4·3 visualised by silver staining were matched by two-dimensional imaging software. Within-subject changes in spots were compared between the treatment groups. Differentially affected spots were identified by matrix-assisted laser desorption ionisation-time of flight/time of flight MS and the human Swiss-Prot database. We found 23/681 abundant plasma protein spots, which were up- or down-regulated by the dietary treatment (P< 0·05, q< 0·30), and eighteen of these were identified. In each trout group, ten spots differed from those in subjects given the chicken meal, but only three of these were common, and only one spot differed between the two trout groups. In both groups, the affected plasma proteins were involved in biological processes such as regulation of vitamin A and haem transport, blood fibrinolysis and oxidative defence. Thus, regular fish intake affects the plasma proteome, and the changes may indicate novel mechanisms of effect.

Selenium (Se) deficiency among populations in Ethiopia is consistent with low concentrations of Se in soil and crops that could be addressed partly by Se-enriched fertilisers. This study examines the disease burden of Se deficiency in Ethiopia and evaluates the cost-effectiveness of Se agronomic biofortification. A disability-adjusted life years (DALY) framework was used, considering goiter, anaemia, and cognitive dysfunction among children and women. The potential efficiency of Se agronomic biofortification was calculated from baseline crop composition and response to Se fertilisers based on an application of 10 g/ha Se fertiliser under optimistic and pessimistic scenarios. The calculated cost per DALY was compared against gross domestic product (GDP; below 1–3 times national GDP) to consider as a cost-effective intervention. The existing national food basket supplies a total of 28·2 µg of Se for adults and 11·3 µg of Se for children, where the risk of inadequate dietary Se reaches 99·1 %–100 %. Cereals account for 61 % of the dietary Se supply. Human Se deficiency contributes to 0·164 million DALYs among children and women. Hence, 52 %, 43 %, and 5 % of the DALYs lost are attributed to anaemia, goiter, and cognitive dysfunction, respectively. Application of Se fertilisers to soils could avert an estimated 21·2–67·1 %, 26·6–67·5 % and 19·9–66·1 % of DALY via maize, teff and wheat at a cost of US$129·6–226·0, US$149·6–209·1 and US$99·3–181·6, respectively. Soil Se fertilisation of cereals could therefore be a cost-effective strategy to help alleviate Se deficiency in Ethiopia, with precedents in Finland.

Oxidative stress may be involved in the progression of hypothyroidism in patients with Hashimoto thyroiditis (HT). Vitamin C is a well-known powerful antioxidant. To our knowledge, whether vitamin C intake relates to hypothyroidism in patients with HT remains unclear. In this cross-sectional study based on the National Health and Nutrition Examination Survey, 2007–2012, we aimed to explore the relationship between total vitamin C intake and hypothyroidism in patients with HT, using multivariate logistic regression models and restricted cubic spline analyses. Our results showed a significant negative linear association between total vitamin C intake (log10-transformed data) and hypothyroidism in HT. Compared with those with the lowest quartile of total vitamin C intake (log10-transformed), participants with the highest quartile were at lower odds of having hypothyroidism (adjusted OR 0·40, 95 % CI: 0·18, 0·88, Ptrend = 0·027). This association was consistent in subgroups stratified by sex (Pfor interaction = 0·084) and age (≥ 60 years and < 60 years, Pfor interaction = 0·330). This study revealed that total vitamin C intake was inversely associated with hypothyroidism among individuals with HT, indicating that higher vitamin C intakes (4·57–1258·9 mg/d) may be associated with a lower likelihood of hypothyroidism among HT participants.

Linoleic acid (LA) transport in rats with experimental short-term and long-term renal failure (RF) was compared with that of sham-operated normal animals on liberal food intake and pair-fed animals. The perfusions in vivo and incubations in vitro were conducted using a micellar solution containing a wide range of LA concentrations. Both absorption in vivo and uptake in vitro of LA were significantly reduced in animals with short-term RF. Lipid extraction and separation by thin-layer chromatography revealed a marked LA trapping as trilinolein (TL) in the perfused intestinal tissue in the short-term RF group. The esterification process, as defined by the rate of LA incorporation into TL, was moderately reduced in short-term RF animals. The thickness of the unstirred water layer showed no significant difference among the groups studied. In contrast, animals with long-term RF exhibited normal absorption of LA in vivo at all concentrations tested. In conclusion, LA absorption is reduced in short-term RF and restored in long-term RF. Several steps including LA transport into and TL transport out of the enterocyte and the esterification process were impaired in short-term RF. These changes are not due to alteration in the unstirred water layer, anorexia, weight loss or a rapid effect of uraemic chemical environment or circulatory factors.

We aimed to examine whether baseline neutrophil counts affected the risk of new-onset proteinuria in hypertensive patients, and, if so, whether folic acid treatment is particularly effective in proteinuria prevention in such a setting. A total of 8208 eligible participants without proteinuria at baseline were analysed from the renal substudy of the China Stroke Primary Prevention Trial. Participants were randomised to receive a double-blind daily treatment of 10 mg of enalapril and 0·8 mg of folic acid (n 4101) or 10 mg of enalapril only (n 4107). The primary outcome was new-onset proteinuria, defined as a urine dipstick reading of ≥1+ at the exit visit. The mean age of the participants was 59·5 (sd, 7·4) years, 3088 (37·6 %) of the participants were male. The median treatment duration was 4·4 years. In the enalapril-only group, a significantly higher risk of new-onset proteinuria was found among participants with higher neutrophil counts (quintile 5; ≥4·8 × 109/l, OR 1·44; 95 % CI 1·00, 2·06), compared with those in quintiles 1–4. For those with enalapril and folic acid treatment, compared with the enalapril-only group, the new-onset proteinuria risk was reduced from 5·2 to 2·8 % (OR 0·49; 95 % CI 0·29, 0·82) among participants with higher neutrophil counts (≥4·8 × 109/l), whereas there was no significant effect among those with neutrophil counts <4·8 × 109/l. In summary, among hypertensive patients, those with higher neutrophil counts had increased risk of new-onset proteinuria, and this risk was reduced by 51 % with folic acid treatment.

1. Studies were performed with female rats to examine the effect of various levels of orally administered oxytetracycline on body-weight, weight of various portions of the intestinal tract, weight of mesenteric lymph nodes, distribution pattern of the tissue elements in the terminal portion of the ileum, and on the susceptibility to invasion by Salmonella typhi-murium.

2. There was no growth promotion resulting from any antibiotic treatment. A consistent finding was the decrease in the wet weight of mesenteric lymph nodes in the rats given antibiotic.

3. In the bacteriological test, no differences between antibiotic-fed and control groups were observed in isolations from the liver, spleen or intestinal tissue. It was concluded that there were no effects of oxytetracycline administration on invasive capacity of orally administered S. typhi-murium.

Treatment of lactating rats with the anti-progestin Mifepristone or Onapristone adversely affects growth of their litters. The present studies aimed to elucidate the underlying mechanism. The treatment did not interfere with the behavioural interactions between mothers and pups, which are required for normal litter growth. Treatment with the antagonists had a stimulatory action on ovarian oestrogen production. However, ovarian hormones did not play a role in litter growth impairment, as this also occurred with lactating ovariectomized rats. Treatment with anti-progestins did not affect the concentrations of the macronutrients in milk (protein, lactose and lipid), nor did it change the fatty acid composition of lipid. Reduced litter growth was not related to a possible direct effect of exposure of the suckling young to the drugs via the milk. Direct injections into them unequivocally affected adrenal gland and testicular development, but did not affect their body-weight development. Milk secretion, as measured by the milk weight accumulating during 6 or 24 h following sudden removal of litters in advanced lactation, was not impaired by the treatments. However, the ingestion of food and water by dams treated with Mifepristone was significantly below that of control animals. It is concluded that litter growth impairment during treatment of lactating rats with anti-progestin results from the reduction of the intake of food and water by the mother.

In this study, we aimed to examine the relationship between energy-adjusted dietary inflammatory index (E-DII) and a comprehensive profile of malnutrition in Iranian haemodialysis (HD) patients. In this cross-sectional study, 291 participants on HD for at least 6 months before enrollment were included. The current dietary intakes of participants were assessed using a 4-d diet diary-assisted recall, including 2 non-dialysis days and 2 dialysis days to calculate E-DII. To determine the malnutrition status of HD patients, BMI, subjective global assessment (SGA), dialysis malnutrition score (DMS) and malnutrition inflammation score (MIS) were used. Overall, 291 HD patients comprised our study population. After controlling for potential confounders, E-DII was associated with a higher risk of malnutrition, as evidenced by SGA (OR = 2·23; 95 % CI: 1·11, 4·49), DMS (OR = 2·31; 95 % CI: 1·16, 4·60) and MIS (OR = 2·50; 95 % CI: 1·28, 4·88). No significant association was detected between E-DII and BMI either before (OR = 1·78; 95 % CI: 0·83, 3·81) or after adjustment for possible confounders (OR = 1·43; 95 % CI: 0·58, 3·54). This study showed that E-DII was significantly associated with reliable malnutrition markers including SGA, DMS and MIS in HD patients. However, further longitudinal studies are warranted to infer a cause-and-effect relationship between DII and malnutrition.

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.