Intakes of micronutrient-rich foods are low among Indian women of reproductive age. We investigated whether consumption of a food-based micronutrient-rich snack increased markers of blood micronutrient concentrations when compared with a control snack. Non-pregnant women (n 222) aged 14–35 years living in a Mumbai slum were randomised to receive a treatment snack (containing green leafy vegetables, dried fruit and whole milk powder), or a control snack containing foods of low micronutrient content such as wheat flour, potato and tapioca. The snacks were consumed under observation 6 d per week for 12 weeks, compliance was recorded, and blood was collected at 0 and 12 weeks. Food-frequency data were collected at both time points. Compliance (defined as the proportion of women who consumed ≥ 3 snacks/week) was >85 % in both groups. We assessed the effects of group allocation on 12-week nutrient concentrations using ANCOVA models with respective 0-week concentrations, BMI, compliance, standard of living, fruit and green leafy vegetable consumption and use of synthetic nutrients as covariates. The treatment snack significantly increased β-carotene concentrations (treatment effect: 47·1 nmol/l, 95 % CI 6·5, 87·7). There was no effect of group allocation on concentrations of ferritin, retinol, ascorbate, folate or vitamin B12. The present study shows that locally sourced foods can be made into acceptable snacks that may increase serum β-carotene concentrations among women of reproductive age. However, no increase in circulating concentrations of the other nutrients measured was observed.

Ultraprocessed foods provide the majority of energy content in the American diet, yet little is known regarding consumption trends over time. We determined trends in diet processing level and diet quality from 1991 to 2008 within the prospective Framingham Offspring Cohort. Dietary intakes were collected by FFQ quadrennially 1991–2008 (total of four examinations). The analytical sample included 2893 adults with valid dietary data for ≥3 examinations (baseline mean age = 54 years). Based on the NOVA framework, we classified foods as: unprocessed/minimally processed foods; processed culinary ingredients (salt/sugar/fats/oils); and processed foods and ultraprocessed foods. We evaluated diet quality using the Dietary Guidelines for Americans Adherence Index (DGAI) 2010. Trends in consumption of foods within each processing level (servings/d) and diet quality over the four examinations were evaluated using mixed effects models with subject-specific random intercepts. Analyses were stratified by sex, BMI (<25 kg/m2, 25–29·9 kg/m2, ≥30 kg/m2) and smoking status. Over 17 years of follow-up, ultraprocessed food consumption decreased from 7·5 to 6·0 servings/d and minimally processed food consumption decreased from 11·9 to 11·3 servings/d (P trend < 0·001). Changes in intakes of processed foods, culinary ingredients and culinary preparations were minimal. Trends were similar by sex, BMI and smoking status. DGAI-2010 score increased from 60·1 to 61·5, P < 0·001. The current study uniquely describes trends in diet processing level in an ageing US population, highlighting the longstanding presence of ultraprocessed foods in the American diet. Given the poor nutritional quality of ultraprocessed foods, public health efforts should be designed to limit their consumption.

Evidence of couples’ BMI and its influence on birth weight is limited and contradictory. Therefore, this study aims to assess the association between couple’s preconception BMI and the risk of small for gestational age (SGA)/large for gestational age (LGA) infant, among over 4·7 million couples in a retrospective cohort study based on the National Free Pre-pregnancy Checkups Project between 1 December 2013 and 30 November 2016 in China. Among the live births, 256 718 (5·44 %) SGA events and 506 495 (10·73 %) LGA events were documented, respectively. After adjusting for confounders, underweight men had significantly higher risk (OR 1·17 (95 % CI 1·15, 1·19)) of SGA infants compared with men with normal BMI, while a significant and increased risk of LGA infants was obtained for overweight and obese men (OR 1·08 (95 % CI 1·06, 1·09); OR 1·19 (95 % CI 1·17, 1·20)), respectively. The restricted cubic spline result revealed a non-linear decreasing dose–response relationship of paternal BMI (less than 22·64) with SGA. Meanwhile, a non-linear increasing dose–response relationship of paternal BMI (more than 22·92) with LGA infants was observed. Moreover, similar results about the association between maternal preconception BMI and SGA/LGA infants were obtained. Abnormal preconception BMI in either women or men were associated with increased risk of SGA/LGA infants, respectively. Overall, couple’s abnormal weight before pregnancy may be an important preventable risk factor for SGA/LGA infants.

Dietary l-carnitine (LC) is a nutritional factor that reduces liver lipid content. However, whether dietary LC can improve lipid metabolism via simultaneous activation of mitochondrial fatty acid (FA) β-oxidation and suppression of endoplasmic reticulum (ER) stress is still unknown. Large yellow croaker were fed with a high-fat diet (HFD) supplemented with dietary LC at 0, 1·2 or 2·4 ‰ for 10 weeks. The results indicated that a HFD supplemented with LC reduced the liver total lipid and TAG content and improved serum lipid profiles. LC supplementation administered to this fish increased the liver antioxidant capacity by decreasing serum and liver malondialdehyde levels and enhancing the liver antioxidant capacity, which then relieved the liver damage. Dietary LC increased the ATP dynamic process and mitochondrial number, decreased mitochondrial DNA damage and enhanced the protein expression of mitochondrial β-oxidation, biogenesis and mitophagy. Furthermore, dietary LC supplementation increased the expression of genes and proteins related to peroxisomal β-oxidation and biogenesis. Interestingly, feeding fish with LC-enriched diets decreased the protein levels indicative of ER stress, such as glucose-regulated protein 78, p-eukaryotic translational initiation factor 2a and activating transcription factor 6. Dietary LC supplementation downregulated mRNA expression relative to FA synthesis, reduced liver lipid and relieved liver damage through regulating β-oxidation and biogenesis of mitochondria and peroxisomes, as well as the ER stress pathway in fish fed with HFD. The present study provides the first evidence that dietary LC can improve lipid metabolism via simultaneously promoting FA β-oxidation capability and suppressing the ER stress pathway in fish.

Decreasing sodium intake has been associated with improvements in blood pressure (BP) and proteinuria, two important risk factors for CVD and chronic kidney disease (CKD) progression. We aimed to investigate the role of sodium intake by examining the effect of changes in sodium intake over 1 year on BP and proteinuria in people with early stage CKD. From thirty-two general practices, 1607 patients with previous estimated glomerular filtration rate of 59–30 ml/min per 1·73 m2 and mean age of 72·9 (sd 9·0) years were recruited. Clinical assessment, urine and serum biochemistry testing were performed at baseline and after 1 year. Sodium intake was estimated from early morning urine specimens using an equation validated for this study population. We found that compared with people who increased their sodium intake from ≤100 to >100 mmol/d over 1 year, people who decreased their intake from >100 to ≤100 mmol/d evidenced a greater decrease in all BP variables (Δmean arterial pressure (ΔMAP)=–7·44 (sd 10·1) v. –0·23 (sd 10·4) mmHg; P<0·001) as well as in pulse wave velocity (ΔPWV=–0·47 (sd 1·3) v. 0·08 (sd 1·88) m/s; P<0·05). Albuminuria improved only in albuminuric patients who decreased their sodium intake. BP improved in people who maintained low sodium intake at both times and in those with persistent high intake, but the number of anti-hypertensive increased only in the higher sodium intake group, and PWV improved only in participants with lower sodium intake. Decreasing sodium intake was an independent determinant of ΔMAP. Although more evidence is needed, our results support the benefits of reducing and maintaining sodium intake below 100 mmol/d (2·3–2·4 g/d) in people with early stages of CKD.

Obesity and particularly central obesity are the main risk factors of colon cancer. All intestinal cell populations including stem cells, their progenitors and differentiated colonocytes seem to be the origin of colorectal cancer. However, recent data support the role of differentiated cells as cancer origin especially during inflammation. Based on Yamanaka’s seminal work, re-expression of few transcription factors in terminally differentiated cells creates stemness properti'es. Although these transcription factors are involved in tumorigenesis, they are epigenetically repressed in adult tissues. We proposed that obesity might regulate methylation of stemness genes in colonocytes via inflammatory signalling. Obesity-associated inflammation was analysed using Western blot analysis of phospho-IκB (inhibitor of NF-κB). Methylation-sensitive high-resolution melting analysis was performed on colonic mucosal samples of twenty obese and twenty normal-weight men to analyse promoter methylation of POU5F1 (OCT4), NANOG, MYC and CDKN2A. TNF-treated HT-29 cells were used to recapitulate the effect of NF-κB activation on stemness genes methylation. Our results showed that colonic phosphorylation of IκB, as a signal of NF-κB activation, was higher in obese subjects compared with their normal-weight counterparts. Moreover, promoter methylation of NANOG was likely to be lower in obese subjects and correlated with central obesity. HT-29 cells incubated by TNF-α showed hypomethylation of POU5F1 and MYC genes in addition to the NANOG. These results suggest that obesity-induced inflammation might be involved in the regulation of DNA methylation of oncogenic genes such as NANOG in differentiated colonocytes and thus predispose them to later oncogenic alterations.

The serum albumin level is a widely accepted indicator of nutritional status in healthy adults and elderly individuals. However, there are few data regarding the distribution and correlates of serum albumin levels in individuals with intellectual and/or motor disabilities. We conducted a cross-sectional study at a public facility for individuals with intellectual and/or motor disabilities in Ibaraki prefecture, Japan. Health check-up data obtained in 2001 from 477 individuals with intellectual disability (286 males, average age 40·6 (sd 12·3) years; 191 females, average age 45·1 (sd 11·6) years) were retrospectively reviewed. With the exception of men with cerebral palsy, the serum albumin level was nearly normally distributed. The mean was 44 (sd 3·6) g/l for males and 44 (sd 3·6) g/l for females with intellectual disability, 43 (sd 3·2) g/l in males and 44 (sd 2·6) g/l for females with cerebral palsy, 41 (sd 2·7) g/l for males and 42 (sd 3·7) g/l for females with Down's syndrome, and 42 (sd 4·5) g/l for males and 41 (sd 3·2) g/l for females with severe motor and intellectual disabilities. Only six of 474 individuals (1·3 %) had a serum albumin ≤ 35 g/l. Low serum albumin was related to age, use of anticonvulsants and/or major tranquilisers, use of other medications, high C-reactive protein (CRP), high zinc sulfate turbidity test (ZTT), low serum Hb and low serum Fe among men; among women, high CRP and high ZTT were related to low serum albumin. The present study found an unexpectedly low incidence of low serum albumin among institutionalised individuals with intellectual and/or motor disabilities. Low serum albumin was associated with age, medications and inflammation in men, as well as inflammation in women.

An extension of the previously proposed model of Mg metabolism (Robson et al. 1997) has been developed to consider the transactions of Mg that are associated with cerebrospinal fluid (CSF) and bone. The representation of the CSF as a single Mg compartment with uptake from the plasma described by Michaelis–Menten kinetics gives very good agreement with published experiments. Analysis of the available information on resorption of Mg from adult bone indicates that this process makes a negligible contribution to Mg homeostasis and can be omitted from the model.

1. Using a double-lumen tube jejunal perfusion system, the rate of glycine absorption from a glycylglycine solution (50 mmol/l) was measured in three groups of Zambian African subjects: in fifteen subjects there was no evidence of an infection (normal group); in eleven there was acute bacterial pneumonia and five had a chronic systemic infection.

2. Differences between the mean absorption rates for the three groups were not significant.

3. Glycine absorption rate has been shown previously to be increased in subjects with acute bacterial pneumonia. The present result provides further evidence that glycine and glycylglycine use separate transfer mechanisms in man, and suggests that dipeptide absorption rate is influenced to a lesser extent than that for free amino acids by systemic stimuli.

The present study assessed the prevalence of vitamin D deficiency in an urban south Indian population in individuals with different grades of glucose tolerance. A total of 1500 individuals (900 normal glucose tolerance (NGT), 300 prediabetes and 300 with type 2 diabetes mellitus (T2DM)) who were not on vitamin D supplementation were randomly selected from the Chennai Urban Rural Epidemiological Study follow-up study. Anthropometric, clinical examination and biochemical investigations (25-hydroxyvitamin D (25(OH)D), insulin, glycated Hb (HbA1c) and serum lipids) were measured. Vitamin D deficiency was defined as serum 25(OH)D < 20·0 ng/ml, insufficiency as 20–29·9 ng/ml and sufficiency as ≥30 ng/ml. Of the 1500 individuals studied, 45 % were males and the mean age was 46 (sd 12) years. Vitamin D levels lowered with increasing degrees of glucose tolerance (NGT: 21 (sd 11); prediabetes: 19 (sd 10); T2DM: 18 (sd 11) ng/ml, P < 0·001). The overall prevalence of vitamin D deficiency was 55 % and was significantly higher among individuals with T2DM (63 %) followed by prediabetes (58 %) and NGT (51 %) (Pfor trend < 0·001). Women had 1·6 times the risk of vitamin D deficiency compared with men (unadjusted OR 1·6 (95 % CI 1·3, 2·0) and adjusted OR 1·6 (95 % CI 1·2, 1·9)). However, there was no increasing trend observed with increasing age. The prevalence of abdominal obesity (66 v. 49 %), generalised obesity (80 v. 64 %), the metabolic syndrome (45 v. 37 %) and insulin resistance (38 v. 27 %) was significantly higher in those with vitamin D deficiency compared with those without. This study shows that vitamin D deficiency is highly prevalent in this urban south Indian population and was higher among individuals with T2DM and prediabetes compared with those with NGT.

The aim of the present study was to examine the effects of cobalamin (Cbl) on the activity and expression of l-methylmalonyl-CoA mutase (MCM) in rat liver and cultured COS-7 cells. The MCM holoenzyme activity was less than 5 % of the total (holoenzyme+apoenzyme) activity in the liver although rats were fed a diet containing sufficient Cbl. When weanling rats were maintained on a Cbl-deficient diet, the holo-MCM activity became almost undetectable at the age of 10 weeks. In contrast, a marked increase in the total-MCM activity occurred under the Cbl-deficient conditions, and at the age of 20 weeks it was about 3-fold higher in the deficient rats than in the controls (108 (sd 14·5) v. 35 (sd 8·5) nmol/mg protein per min (n 5); P < 0·05). Western blot analysis confirmed that the MCM protein level increased significantly in the Cbl-deficient rats. However, the MCM mRNA level, determined by real-time PCR, was rather decreased. When COS-7 cells were cultured in a medium in which 10 % fetal bovine serum was the sole source of Cbl, holo-MCM activity was barely detected. The supplementation of Cbl resulted in a large increase in the holo-MCM activity in the cells, but the activity did not exceed 30 % of the total-MCM activity even in the presence of Cbl at 10 μmol/l. In contrast, the total-MCM activity was significantly decreased by the Cbl supplementation, indicating that Cbl deficiency results in an increase in the MCM protein level in COS-7 cells as well as in rat liver.

The present study evaluates the evidence about the principal sources of fat in the Australian diet from the national per capita food supply data (apparent consumption; AC) and the national dietary survey of 6255 adults aged 25 to 64 years (NDSA). The AC and the NDSA data were converted to, and expressed on, an equivalent food basis to allow appropriate comparisons of foods consumed, and food sources of dietary fat. The AC figures showed that the principal sources of fat nationally were meat, edible fats, fat spreads and oils, and milk and milk products. As an estimate of adult food consumption the AC underestimated beef and veal, lamb, total meat, and poultry consumption by 41, 10, 29 and 13% respectively, and overestimated offal, milk and milk products, and fats and oils by 15, 61, 20, and 29% respectively. The AC data rated fat spreads and cooking fats as providing more of the fat in the adult diet than did the NDSA, both in terms of total fat and fat as a percentage of energy. Conversely, on this same basis, the AC underrated meats as sources of fat in the adult diet. Other foods were of similar importance as sources of dietary fat in both sets of data. The AC markedly underestimated adult fat intake at 32% of energy compared with the NDSA result of 37%. These results have implications for epidemiological research and for the development of food and nutrition policy and programmes in Australia and similar countries.

1. The contractile properties of soleus and extensor digitorum longus muscles from animals at 12 months of age whose mothers had been undernourished during pregnancy and lactation (PU rats) have been compared with those of muscles from age-matched controls.

2. Body-weight and muscle wet weight of PU rats was significantly reduced. Muscle: body-weight values were, however, no different from controls.

3. No significant alterations in whole muscle speeds of contraction or relaxation could be delected when compared with those of age-matched controls.

4. Twitch and tetanic forces of both SOL and EDL were greater per unit weight of muscle in PU rats. Apart from SOL twitch these differences were significant. The tetanus:twitch values were, however, not different.

The effects of dietary supplementation with fat of different fatty acid profile and chronic intermittent hypoxia (CIH) on the fatty acid composition of serum and heart lipids were analysed. Adult male Wistar rats were fed a standard non-fat diet enriched with 10 % of lard, fish oil (n-3 PUFA) or maize oil (n-6 PUFA) for 10 weeks. After 4 weeks on the diets, each group was divided in two subgroups, either exposed to CIH in a barochamber (7000 m, twenty-five exposures) or kept at normoxia. In normoxic rats, the fish oil diet increased the level of conjugated dienes. The n-6:n-3 PUFA ratio in serum TAG, phospholipids (PL), cholesteryl esters (CE) and heart TAG, PL and diacylglycerols (DAG) followed the ratio in the fed diet (in the sequence maize oil>lard>fish oil). In heart TAG, PL and DAG, 20 : 4n-6 and 18 : 2n-6 were replaced by 22 : 6n-3 in the fish oil group. The main fatty acid in CE was 20 : 4n-6 in the lard and maize oil groups whereas in the fish oil group, half of 20 : 4n-6 was replaced by 20 : 5n-3. CIH further increased 20 : 5n-3 in CE in the fish oil group. CIH decreased the n-6:n-3 PUFA ratio in serum CE, heart TAG, PL and DAG in all dietary groups and stimulated the activity of catalase in the maize and fish oil groups. In conclusion, PUFA diets and CIH, both interventions considered to be cardioprotective, distinctly modified the fatty acid profile in serum and heart lipids with specific effects on conjugated diene production and catalase activity.