Although studies show that the intake of ultra-processed products (UPP) has a negative impact on health, diet quality and dietary vitamin D, its influence on serum concentrations of this vitamin remains unknown; therefore, it is essential to verify the association between the UPP consumption and vitamin D deficiency. This is a cross-sectional, household, population-based study, carried out with 229 individuals aged 20 years or older, residents of the city of Teresina, Piauí, Brazil. Socio-demographic, lifestyle, food consumption and anthropometric data were collected. Food consumption was obtained using a 24-h food recall, and foods were grouped according to the NOVA classification. Plasma concentrations of calcidiol–25 (OH) D3 were determined by HPLC. Crude and adjusted binary logistic regression was applied to estimate the association between UPP consumption and vitamin D deficiency. Most individuals aged 20–39 years were vitamin D deficient (52·1 %). UPP contributed 19·9 % to the energetic intake of the participant’s diet. This contribution was higher for individuals with vitamin D deficiency (22·5 %, P = 0·04). In addition, a high intake of UPP was associated with twice the risk of vitamin D deficiency in comparison with low consumption of UPP (OR: 2·05; CI 1·06, 4·50; P: 0·04). Our results suggest that the consumption of UPP may have a negative impact on serum concentrations of vitamin D; more studies are needed.

This study investigated the effects of Lacticaseibacillus rhamnosus HN001 supplementation on the architecture and gene expression in small intestinal tissues of piglets used as an animal model for infant humans. Twenty-four 10-d-old entire male piglets (4·3 (sd 0·59) kg body weight) were fed an infant formula (IF) (control) or IF supplemented with 1·3 × 105 (low dose) or 7·9 × 106 (high dose) colony-forming units HN001 per ml of reconstituted formula (n 8 piglets/treatment). After 24 d, piglets were euthanised. Samples were collected to analyse the histology and gene expression (RNAseq and qPCR) in the jejunal and ileal tissues, blood cytokine concentrations, and blood and faecal calprotectin concentrations. HN001 consumption altered (false discovery rate < 0·05) gene expression (RNAseq) in jejunal tissues but not in ileal tissues. The number of ileal goblet cells and crypt surface area increased quadratically (P < 0·05) as dietary HN001 levels increased, but no increase was observed in the jejunal tissues. Similarly, blood plasma concentrations of IL-10 and calprotectin increased linearly (P < 0·05) as dietary HN001 levels increased. In conclusion, supplementation of IF with HN001 affected the architecture and gene expression of small intestine tissue, blood cytokine concentration and frequencies, and blood calprotectin concentrations, indicating that HN001 modulated small intestinal tissue maturation and immunity in the piglet model.

1. The compositions of the lipids in the atheromatous lesions of rabbits have been studied in an experiment in which two groups of rabbits (twelve/group) were given different atherogenic diets for a period of 38 weeks. One group of rabbits was given a diet in which 35% of the total calories was derived from butterfat and the other group was given a diet in which 48% of the total calories was derived from starch.

2. At the end of the feeding period the rabbits were killed and the atheromatous plaques were dissected out from the aortic intima of each rabbit. The lipid compositions of the aortic lesions were determined and the results compared with the compositions of the plasma lipids.

3. In the lipids of the aortic lesions in the rabbits given the high-butterfat diet, the proportions of cholesterol and cholesterol esters were higher and the proportion of triglycerides was lower than in the lipids of the aortic lesions in the rabbits given the high-starch diet. Irrespective of dietary treatment, free cholesterol constituted a higher proportion of the lesion lipids than it did of the plasma lipids.

4. In the rabbits on either dietary treatment, the lesion cholesterol esters contained higher concentrations of oleic acid and lower concentrations of linoleic acid than did the plasma cholesterol esters. In the lesion phospholipids there were higher concentrations of palmitic, palmitoleic, stearic and oleic acids and lower concentrations of linoleic and arachidonic acids than in the plasma phospholipids.

5. In both groups of rabbits the phospholipids of the aortic lesions contained higher proportions of cephalin and sphingomyelin and lower proportions of lecithin than did the plasma phospholipids.

6. The results of this investigation are discussed in relation to the possible origins of the lipids in the aortic lesions of the experimental rabbits.

1. The abomasal hydrolysis of lipids and the flow of endogenous (biliary) lipids was studied in two Friesian calves given four milk-substitute diets, by sampling the duodenal digesta. The diets were: reconstituted, mildly preheated, spray-dried skim-milk powder with (SKF) or without (SK) margarine fat or with 500 g/kg skim-milk powder in diet SKF replaced by soya-bean flour (ASKF) or fish-protein concentrate (BSKF) together with dried whey. The diets were given ad lib. twice daily from 13 to 37 d of age, each diet being given for six consecutive days. Collections of duodenal digesta from the re-entrant cannula situated caudal to the bile duct were made for 12 h after feeding the 6th and 12th meals for each diet. Samples from one collection only were subjected to detailed analysis of the lipid classes.

2. The inclusion of non-milk protein (ASKF and BSKF) not only increased the rate of passage of lipid through the abomasum but also the proportion of the lipid present as triglyceride particularly, in the first 2 h after feeding.

3. In a 12 h period, 2·3–6·3 g ‘polar’ lipids (mainly biliary phospholipids) were estimated to have been secreted. The rate of flow was high during the first hour after feeding and constant thereafter. The quantity of ‘polar’ lipid was not related to the type of milk fed or the duodenal flow of lipid.

4. When diet SK was fed, the small amounts of lipid present were extensively hydrolysed so that free fatty acids represented 700 g/kg lipid of dietary origin passing through the duodenum. When margarine fat was included in the diets (SKF, ASKF and BSKF), the free fatty acids represented only 210 g/kg lipid of dietary origin.

5. The quantities of lipid and nitrogen passing through the duodenum were poorly related to the quantities ingested at the beginning of the 12 h experimental period but were closely related to each other.

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.

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.

Inadequate protein intake and lack of micronutrients may affect neurodevelopment in infants. This randomised controlled trial was conducted to measure the effect of two milk–cereal mixes with modest and high amounts of protein and enriched with multiple micronutrients, given between 6 and 12 months, on cognitive, language, motor and behavioural scores at 12 and 24 months of age, compared with no-supplementation. The two supplements were also compared with each other. The study was conducted in urban Delhi, India, and the infants were randomised in a 1:1:1 ratio to the three study groups. At 12 and 24 months of age, 1134 and 1214 children were available, respectively. At 12 months of age, compared with no-supplement group, an increase in the motor scores (mean difference, MD 1·52, 95 % CI: 0·28, 2·75) and a decrease in the infant temperament scores (MD − 2·76, 95 % CI: −4·23, −1·29) in the modest-protein group was observed. Those in the high-protein group had lower socio-emotional scores (MD − 1·40, 95 % CI: −2·43, −0·37) and higher scores on Infant Temperament Scale (MD 2·05, 95 % CI: 0·62, 3·48) when compared with modest-protein group. At 24 months, no significant differences in any of the neurodevelopment scores between the three study groups was found. In conclusion, supplementation with modest amount of protein and multiple micronutrients may lead to short-term small improvements in motor function and infant temperament. There appears no advantage of supplementing with high protein, rather negative effects on infant behaviour were observed

1. Protein-deficient weanling rats fed on a 30 g casein/kg diet for 3 weeks lost albumin but maintained the level of serum α-1-antitrypsin, the most abundant protease inhibitor in blood.

2.α-1-Antitrypsins from malnourished rats and control rats (given 250 g casein/kg diet) differed; the protease inhibitor from protein-deficient animals: (1) was more acidic, (2) appeared slightly larger (57400 v. 56000 daltons) on sodium dodecyl sulphate (SDS)-polyacrylamide gels, (3) had a more acidic Pi type and increased anodal mobility at pH 8.9, (4) bound more concanavalin-A and contained more carbohydrate, specifically two to three extra sialic acid residues. The amino sugar and neutral sugar contents of both preparations of α-1-antitrypsin were the same.

3. Analysis of the products of cyanogen-bromide cleavage revealed that α-1-antitrypsin preparations from protein-deficient rats contain an extra glycopeptide that was not present in α-1-antitrypsin from control animals.

4. In vivo studies showed that the increased sialic acid content of α-1-antitrypsin of protein-deficient rats did not alter the half-life of the molecule in the blood of control rats. However, the fractional catabolic rate of α-1-antitrypsin from either well-nourished or protein-deficient rats was significantly (P < 0.01) lower in protein- deficient rats than in control rats (0.0247/h v. 0.0406/h).

5. The decreased fractional catabolic rate could not be explained by changes in hepatic mannosyl-, galactosyl- or N-acetylhexosaminyl receptors since liver perfusion studies showed that bovine serum albumin, when covalently modified separately with each of these ligands, was extracted from the perfusion medium as rapidly or more rapidly by livers from malnourished animals.

6. Perfused livers from protein-deficient rats secrete three times more α-1-antitrypsin than do livers from well-nourished animals.

7. The decreased fractional catabolic rate and increased rate of biosynthesis and secretion of the glycoprotein by livers from protein-deficient animals may account for the maintenance of α-1-antitrypsin levels during protein malnutrition.