Mycoprotein consumption has been shown to improve acute postprandial glycaemic control and decrease circulating cholesterol concentrations. We investigated the impact of incorporating mycoprotein into the diet on insulin sensitivity (IS), glycaemic control and plasma lipoprotein composition. Twenty healthy adults participated in a randomised, parallel-group trial in which they consumed a 7 d fully controlled diet where lunch and dinner contained either meat/fish (control group, CON) or mycoprotein (MYC) as the primary source of dietary protein. Oral glucose tolerance tests were performed pre- and post-intervention, and 24 h continuous blood glucose monitoring was applied throughout. Fasting plasma samples were obtained pre- and post-intervention and were analysed using quantitative, targeted NMR-based metabonomics. There were no changes within or between groups in blood glucose or serum insulin responses, nor in IS or 24 h glycaemic profiles. No differences between groups were found for 171 of the 224 metabonomic targets. Forty-five lipid concentrations of different lipoprotein fractions (VLDL, LDL, intermediate-density lipoprotein and HDL) remained unchanged in CON but showed a coordinated decrease (7–27 %; all P < 0·05) in MYC. Total plasma cholesterol, free cholesterol, LDL-cholesterol, HDL2-cholesterol, DHA and n-3 fatty acids decreased to a larger degree in MYC (14–19 %) compared with CON (3–11 %; P < 0·05). Substituting meat/fish for mycoprotein twice daily for 1 week did not modulate whole-body IS or glycaemic control but resulted in changes to plasma lipid composition, the latter primarily consisting of a coordinated reduction in circulating cholesterol-containing lipoproteins.

This study reports the validity of body fat percentage (BF%) estimates from several commonly employed techniques as compared with a five-component (5C) model criterion. Healthy adults (n 170) were assessed by dual-energy X-ray absorptiometry (DXA), air displacement plethysmography (ADP), multiple bioimpedance techniques and optical scanning. Output was also used to produce a criterion 5C model, multiple variants of three- and four-component models (3C; 4C) and anthropometry-based BF% estimates. Linear regression, Bland–Altman analysis and equivalence testing were performed alongside evaluation of the constant error (CE), total error (TE), se of the estimate (SEE) and coefficient of determination (R2). The major findings were (1) differences between 5C, 4C and 3C models utilising the same body volume (BV) and total body water (TBW) estimates are negligible (CE ≤ 0·2 %; SEE < 0·5 %; TE ≤ 0·5 %; R2 1·00; 95 % limits of agreement (LOA) ≤ 0·9 %); (2) moderate errors from alternate TBW or BV estimates in multi-component models were observed (CE ≤ 1·3 %; SEE ≤ 2·1 %; TE ≤ 2·2 %; R2 ≥ 0·95; 95 % LOA ≤ 4·2 %); (3) small differences between alternate DXA (i.e. tissue v. region) and ADP (i.e. Siri v. Brozek equations) estimates were observed, and both techniques generally performed well (CE < 3·0 %; SEE ≤ 2·3 %; TE ≤ 3·6 %; R2 ≥ 0·88; 95 % LOA ≤ 4·8 %); (4) bioimpedance technologies performed well but exhibited larger individual-level errors (CE < 1·0 %; SEE ≤ 3·1 %; TE ≤ 3·3 %; R2 ≥ 0·94; 95 % LOA ≤ 6·2 %) and (5) anthropometric equations generally performed poorly (CE 0·6– 5·7 %; SEE ≤ 5·1 %; TE ≤ 7·4 %; R2 ≥ 0·67; 95 % LOA ≤ 10·6 %). Collectively, the data presented in this manuscript can aid researchers and clinicians in selecting an appropriate body composition assessment method and understanding the associated errors when compared with a reference multi-component model.

An 8-week feeding trial was conducted to evaluate the effects of dietary n-3 LC-PUFA levels on growth performance, tissue fatty acid profiles and relative expression of genes involved in the lipid metabolism of mud crab (Scylla paramamosain). Ten isonitrogenous diets were formulated to contain five n-3 LC-PUFA levels at 7 and 12 % dietary lipid levels. The highest weight gain and specific growth rate were observed in crabs fed the diets with 19·8 and 13·2 mg/g n-3 LC-PUFA at 7 and 12 % lipid, respectively. Moisture and lipid contents in hepatopancreas and muscle were significantly influenced by dietary n-3 LC-PUFA at the two lipid levels. The DHA, EPA, n-3 LC-PUFA contents and n-3:n-6 PUFA ratio in hepatopancreas and muscle significantly increased as dietary n-3 LC-PUFA levels increased at both lipid levels. The expression levels of -6 fatty acyl desaturase and acyl-CoA oxidase in hepatopancreas increased significantly, and expression levels of fatty acid synthase, carnitine palmitoyltransferase I and hormone-sensitive TAG lipase were down-regulated, with increased dietary n-3 LC-PUFA regardless of lipid level. Based on weight gain, n-3 LC-PUFA requirements of S. paramamosain were estimated to be 20·1 and 12·7 mg/g of diet at 7 and 12 % dietary lipid, respectively. Overall, dietary lipid level influenced lipid metabolism, and purified, high-lipid diets rich in palmitic acid reduced the n-3 LC-PUFA requirement of juvenile mud crab.

We evaluated whether early-life protein restriction alters structural parameters that affect β-cell mass on the 15th day and 20th day of gestation in control pregnant (CP), control non-pregnant (CNP), low-protein pregnant (LPP) and low-protein non-pregnant (LPNP) rats from the fetal to the adult life stage as well as in protein-restricted rats that recovered after weaning (recovered pregnant (RP) and recovered non-pregnant). On the 15th day of gestation, the CNP group had a higher proportion of smaller islets, whereas the CP group exhibited a higher proportion of islets larger than the median. The β-cell mass was lower in the low-protein group than that in the recovered and control groups. Gestation increased the β-cell mass, β-cell proliferation frequency and neogenesis frequency independently of the nutritional status. The apoptosis frequency was increased in the recovered groups compared with that in the other groups. On the 20th day of gestation, a higher proportion of islets smaller than the median was observed in the non-pregnant groups, whereas a higher proportion of islets larger than the median was observed in the RP, LPP and CP groups. β-Cell mass was lower in the low-protein group than that in the recovered and control groups, regardless of the physiological status. The β-cell proliferation frequency was lower, whereas the apoptosis rate was higher in recovered rats compared with those in the low-protein and control rats. Thus, protein malnutrition early in life did not alter the mass of β-cells, especially in the first two-thirds of gestation, despite the increase in apoptosis.

This trial was conducted to study the effects of dietary rapeseed cake (RSC) containing high glucosinolates (GLS) on rumen fermentation, nutrient digestion and the rumen microbial community in steers. Eight growing steers and four rations containing RSC (GLS 226·1 μmol/g DM) at 0·00, 2·65, 5·35 and 8·00 % DM were assigned in a replicate 4 × 4 Latin square design. The results indicated that increasing RSC levels increased the ruminal concentration of thiocyanate (SCN) (P < 0·01), decreased the ruminal concentration of ammonia nitrogen (NH3-N) and the molar proportion of isovalerate (P < 0·05), did not affect the ruminal concentration of total volatile fatty acids (P > 0·05), decreased the crude protein (CP) digestibility (P < 0·05) and increased the ether extract (EE) digestibility (P < 0·01). Increasing RSC levels tended to decrease the abundances of ruminal Ruminobacter amylophilus (P = 0·055) and Ruminococcus albus (P = 0·086) but did not affect methanogens, protozoa, fungi and other bacteria (P > 0·05). Increasing RSC levels in the ration did not affect the ruminal bacterial diversity (P > 0·05), but it increased the operational taxonomic units and the bacterial richness (P < 0·05) and affected the relative abundances of some bacteria at the phylum level and genus level (P < 0·05). In conclusion, RSC decreased the ruminal concentration of NH3-N and the CP digestibility, increased the EE digestibility and partly affected the ruminal bacterial community. SCN, as the metabolite of GLS, could be a major factor affecting these indices.

The effects of resistant starch on glycaemic control are controversial. In this study, a systematic review and meta-analysis of results from nineteen randomised controlled trials (RCT) was performed to illustrate the effects of resistant starch on glycaemic control. A literature search was conducted on PubMed, Scopus and Cochrane electronic databases for related publications from inception to 6 April 2020. Key inclusion criteria were: RCT; resistant starch as intervention substances and reporting glucose- and insulin-related endpoints. Exclusion criteria were: using type I resistant starch or a mixture of resistant starch and other functional food ingredients as intervention; using substances other than digestible starch as controls. The effect of resistant starch on fasting plasma glucose was significant (effect size (ES) –0·09 (95 % CI –0·13, −0·04) mmol/l, P = 0·001) compared with digestible starch. Subgroup analyses revealed that the ES was larger when the dosage of resistant starch was more than 28 g/d (ES –0·16 (95 % CI –0·24, –0·08) mmol/l, P < 0·001) or the intervention period was more than 8 weeks (ES –0·12 (95 % CI –0·18, –0·06) mmol/l, P < 0·001). The effect on homoeostatic model assessment (HOMA)-insulin resistance (IR) was significant (ES –0·33 (95 % CI –0·51, –0·14), P = 0·001). However, the effects on other insulin-related endpoints were not significant, including fasting plasma insulin, four endpoints from the frequently sampled intravenous glucose tolerance test (insulin sensitivity index, acute insulin response, disposition index and glucose effectiveness) and HOMA-β. The current study indicated moderate effects of resistant starch on improving glycaemic control.

Although glucose is the best-known nutrient to stimulate glucagon-like peptide-1 (GLP-1) secretion, dietary peptides also potently stimulate GLP-1 secretion. Certain peptide fragments derived from dietary proteins possess dipeptidyl peptidase-4 (DPP-4) inhibitory activity in vitro. Hence, we hypothesised that dietary peptides protect GLP-1 from degradation through attenuating DPP-4 activity in vivo. Here, we compared GLP-1 responses with dietary proteins, a carbohydrate and a lipid (Intralipos) in rats having or not having plasma DPP-4 activity. Plasma GLP-1 concentrations clearly increased by oral administration of whey protein (2–4 g/kg), but not by that of dextrin (2–4 g/kg), in control rats (untreated Sprague–Dawley rats and F344/Jcl rats), having DPP-4 activity. In contrast, dextrin administration increased the plasma GLP-1 concentrations as the whey protein administration did, in rats having reduced or no DPP-4 activity (a DPP-4 inhibitor, sitagliptin-treated Sprague–Dawley rats or DPP-4-deficient F344/DuCrl/Crlj rats). DPP-4 inhibition by sitagliptin treatment also enhanced GLP-1 response to Intralipos, and casein, but the treatment did not further enhance GLP-1 response to whey protein. Intestinal GLP-1 content and gastric emptying rate were not associated with differences in GLP-1 responses to test nutrients. The luminal contents from rats administered whey protein decreased DPP-4 activity in vitro. These results suggest that GLP-1 released by dextrin, Intralipos and casein was immediately degraded by DPP-4, while GLP-1 released by whey protein was less degraded. Our study provides novel in vivo evidence supporting the hypothesis that dietary peptides not only stimulate GLP-1 secretion but also inhibit DPP-4 activity to potentiate GLP-1 response.

In December 2019, a novel human-infecting coronavirus, named Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2), was recognised to cause a pneumonia epidemic outbreak with different degrees of severity in Wuhan, Hubei Province in China. Since then, this epidemic has spread worldwide; in Europe, Italy has been involved. Effective preventive and therapeutic strategies are absolutely required to block this serious public health concern. Unfortunately, few studies about SARS-CoV-2 concerning its immunopathogenesis and treatment are available. On the basis of the assumption that the SARS-CoV-2 is genetically related to SARS-CoV (about 82 % of genome homology) and that its characteristics, like the modality of transmission or the type of the immune response it may stimulate, are still poorly known, a literature search was performed to identify the reports assessing these elements in patients with SARS-CoV-induced infection. Therefore, we have analysed: (1) the structure of SARS-CoV-2 and SARS-CoV; (2) the clinical signs and symptoms and pathogenic mechanisms observed during the development of acute respiratory syndrome and the cytokine release syndrome; (3) the modification of the cell microRNome and of the immune response in patients with SARS infection; and (4) the possible role of some fat-soluble compounds (such as vitamins A, D and E) in modulating directly or indirectly the replication ability of SARS-CoV-2 and host immune response.

Dietary choline, which is converted to phosphatidylcholine (PC) in intestinal enterocytes, may benefit inflammatory bowel disease patients who typically have reduced intestinal choline and PC. The present study investigated the effect of dietary choline supplementation on colitis severity and intestinal mucosal homoeostasis using a Citrobacter rodentium-induced colitis model. C57BL/6J mice were fed three isoenergetic diets differing in choline level: choline-deficient (CD), choline-sufficient (CS) and choline-excess (CE) for 3 weeks prior to infection with C. rodentium. The effect of dietary choline levels on the gut microbiota was also characterised in the absence of infection using 16S rRNA gene amplicon sequencing. At 7 d following infection, the levels of C. rodentium in CD mice were significantly greater than that in CS or CE groups (P < 0·05). CD mice exhibited greater damage to the surface epithelium and goblet cell loss than the CS or CE mice, which was consistent with elevated pro-inflammatory cytokine and chemokine levels in the colon. In addition, CD group exhibited decreased concentrations of PC in the colon after C. rodentium infection, although the decrease was not observed in the absence of challenge. Select genera, including Allobaculum and Turicibacter, were enriched in response to dietary choline deficiency; however, there was minimal impact on the total bacterial abundance or the overall structure of the gut microbiota. Our results suggest that insufficient dietary choline intake aggravates the severity of colitis and demonstrates an essential role of choline in maintaining intestinal homoeostasis.

Protein supplementation may be beneficial for patients with chronic liver disease (CLD). This study compared the effects of whey protein isolate (WP) and casein (CA) supplementation on nutritional status and immune parameters of CLD patients who were randomly assigned to take 20 g of WP or CA twice per d as a supplement for 15 d. Body composition, muscle functionality and plasmatic immunomarkers were assessed before and after supplementation. Patients were also classified according to the model for end-stage liver disease (MELD) into less (MELD < 15) and more (MELD ≥ 15) severe disease groups. Malnutrition, determined by the Subjective Global Assessment at baseline, was observed in 57·4 % and 54·2 % of patients in the WP and CA groups, respectively (P = 0·649). Protein intake was lower at baseline in the WP group than in the CA group (P = 0·035), with no difference after supplementation (P = 0·410). Both the WP and CA MELD < 15 groups increased protein intake after supplementation according to the intragroup analysis. No differences were observed in body composition, muscle functionality, most plasma cytokines (TNF, IL-6, IL-1β and interferon-γ), immunomodulatory proteins (sTNFR1, sTNFR2, brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor) or immunomodulatory hormones (adiponectin, insulin and leptin) after supplementation in the WP groups at the two assessed moments. WP supplementation increased the levels of interferon-γ-induced protein-10/CXCL10 (P = 0·022), eotaxin-1/CCL11 (P = 0·031) and monocyte chemoattractant protein-1/CCL2 (P = 0·018) and decreased IL-5 (P = 0·027), including among those in the MELD ≥ 15 group, for whom IL-10 was also increased (P = 0·008). Thus, WP consumption by patients with CLD impacted the immunomodulatory responses when compared with CA with no impact on nutritional status.

Casein glycomacropeptide (CGMP) is a bioactive milk-derived peptide with potential anti-inflammatory effects. Animal studies suggest that CGMP may work by altering gut microbiota composition and enhancing butyrate production. Its effects on intestinal homoeostasis, microbiota and metabolites in humans are unknown. The aim of the present study was to assess both the intestinal and systemic immunomodulatory effects of orally ingested CGMP. We hypothesised that daily oral CGMP intake would reduce high-sensitive C-reactive protein (hsCRP) in healthy adults. In a single-centre limited but randomised, double-blinded, reference-controlled study, we compared the effects of a 4-week intervention of either 25 g of oral powder-based chocolate-flavoured CGMP or a reference drink. We included twenty-four healthy adults who all completed the study. CGMP had no systemic or intestinal immunomodulatory effects compared with a reference drink, with regard to either hsCRP or faecal calprotectin level, faecal microbiota composition or faecal SCFA content. CGMP ingestion did not affect satiety or body weight, and it caused no severe adverse events. The palatability of CGMP was acceptable, and adherence was high. CGMP did not induce or change gastrointestinal symptoms. In conclusion, we found no immunomodulatory effects of CGMP in healthy adults. In a minor group of healthy adults, oral ingestion of 25 g of CGMP during 4 weeks was safe, well tolerated, had acceptable palatability and was without any effects on body weight.

Oral nutritional supplements are widely recommended to head-and-neck cancer patients undergoing anti-cancer treatment; however, their effects on the outcomes of most importance to patients are unclear. This study aimed to systematically review the evidence of effect of oral nutritional supplements on mortality, treatment tolerance, quality of life, functional status, body weight and adverse effects. We searched PubMed, Embase, CENTRAL, LILACS, Web of Science, CINAHL, two trial registry platforms, three sources of grey literature and reference lists of included studies. We assessed the risk of bias using the revised Cochrane risk-of-bias tool (RoB 2), and certainty of evidence using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) approach. We used random-effects models with Hartung–Knapp correction for the meta-analyses. We included fifteen trials, of which five were ongoing or unpublished, providing evidence in four comparisons. We found very low to low certainty evidence for the effect of oral nutritional supplements on mortality, treatment tolerance, quality of life, functional status and adverse effects. When compared with nutritional counselling alone, nutritional counselling plus oral nutritional supplements probably increased body weight slightly. We also found adverse events relating to supplements use such as nausea, vomiting and feeling of fullness. Possible increases in mortality, treatment tolerance and quality of life besides a possible decrease in functional status are worthy of further investigation. Future research could attempt to address the clinical importance of a probable increase in body weight. Possible adverse effects of the use of oral nutritional supplements should not be overlooked.

Studies have revealed that the timing of macronutrient ingestion may influence body weight and glucose tolerance. We aimed to examine the effect of high protein v. high carbohydrate intake at the evening meal on metabolic parameters of patients with type 2 diabetes. This is a single-blinded, parallel, randomised controlled trial. Ninety-six patients with type 2 diabetes, aged 32–65 years with a mean BMI of 28·5 (sd 3·4) kg/m2, were randomly assigned into one of these three groups: standard evening meal (ST), high-carbohydrate evening meal (HC) and high-protein evening meal (HP). Then, the patients were followed for 10 weeks. HbA1c, fasting blood glucose, fasting insulin, insulin resistance, TAG, LDL-cholesterol, VLDL-cholesterol, diastolic blood pressure, body weight, body fat percentage and waist circumference decreased significantly in all three groups (P < 0·05). HbA1c showed more improvement in the ST compared with the HP group (–0·45 (sd 0·36) v. –0·26 (sd 0·36)). Reductions in BMI and body weight were significantly higher in the ST compared with the HP group (P < 0·05). Reductions in total cholesterol, non-HDL-cholesterol and systolic blood pressure were significant in all groups, except for the HP group. Non-HDL-cholesterol:HDL-cholesterol remained unchanged in all groups. The results of the present study revealed that even distribution of carbohydrates and protein among meals compared with reducing carbohydrates and increasing protein at dinner may have a more beneficial effect on glycaemic control of patients with type 2 diabetes.

Food pantries provide free food to individuals at nutritional risk given lack of available foods. Frequent use of food pantries is associated with higher dietary quality; however, neither the nutrient contributions of food pantries to participant diets nor their relationship with household food security are known. This cross-sectional analysis used secondary data from rural food pantry participants, including sociodemographic characteristics, household food security and 24-h recalls. Mean intakes of selected food groups and nutrients from food pantries, supermarkets, other stores and restaurants, and other were compared by one-way ANCOVA. Interaction effects of household food security with food sources were evaluated by two-way ANCOVA. About 40 % of participants’ dietary intake came from food pantries. Mean intakes of fibre (P < 0·0001), Na (P < 0·0001), fruit (P < 0·0001), grains (P < 0·0001) and oils (P < 0·0001) were higher from food pantries compared with all other sources, as were Ca (P = 0·004), vitamin D (P < 0·0001) and K (P < 0·0001) from food pantries compared with two other sources. Percentage total energy intake (%TEI) from added sugars (P < 0·0001) and saturated fat (P < 0·0001) was higher from supermarkets than most other sources. Significant interaction effects were observed between food sources and household food security for vegetables (P = 0·01), Na (P = 0·01) and %TEI from saturated fat (P = 0·004), with food-insecure participants having significantly higher intakes from food pantries and/or supermarkets compared with all other sources. Future interventions may incorporate these findings by providing education on purchasing and preparing healthy meals on limited budgets, to complement foods received from pantries, and by reducing Na in pantry environments.

Anthocyanins and bromelain have gained significant attention due to their antioxidative and anti-inflammatory properties. Both have been shown to improve endothelial function, blood pressure (BP) and oxygen utility capacity in humans; however, the combination of these two and the impacts on endothelial function, BP, total antioxidant capacity (TAC) and oxygen utility capacity have not been previously investigated. The purpose of this study was to investigate the impacts of a combined anthocyanins and bromelain supplement (BE) on endothelial function, BP, TAC, oxygen utility capacity and fatigability in healthy adults. Healthy adults (n 18, age 24 (sd 4) years) received BE or placebo in a randomised crossover design. Brachial artery flow-mediated dilation (FMD), BP, TAC, resting heart rate, oxygen utility capacity and fatigability were measured pre- and post-BE and placebo intake. The BE group showed significantly increased FMD, reduced systolic BP and improved oxygen utility capacity compared with the placebo group (P < 0·05). Tissue saturation and oxygenated Hb significantly increased following BE intake, while deoxygenated Hb significantly decreased (P < 0·05) during exercise. Additionally, TAC was significantly increased following BE intake (P < 0·05). There were no significant differences for resting heart rate, diastolic BP or fatigability index. These results suggest that BE intake is an effective nutritional therapy for improving endothelial function, BP, TAC and oxygen utility capacity, which may be beneficial to support vascular health in humans.

The major complication of end jejunostomy is excessive fluid and electrolyte loss through the stoma, leading to hypovolaemia and dyselectrolytaemia within days and malnutrition within weeks. The aim was to compare the results of two nutritional approaches: unrestricted and restricted oral intake in patients with end jejunostomy commencing home parenteral nutrition (HPN) in terms of liver and renal biochemical markers and time to reconstructive bowel surgery with correlation to stoma output. Twenty patients with stabilised high output end-jejunostomy were divided into two groups. Group A consisted of ten patients with oral intake restricted to keep stomal output under 1000 ml. Group B consisted of ten patients with unrestricted oral intake. The following parameters were evaluated over 6 months: stomal output, self-estimation of general condition, body weight gain, plasma bilirubin and creatinine, number of hospitalisations prior to reconstructive surgery, the frequency of ostomy bag emptying, feelings of hunger and thirst in the daytime, and the time to reconstructive surgery. Stoma losses were compensated by parenteral supply. In group B, lower quality of life was observed, reflected by weakness, permanent feelings of hunger and thirst and the need for night-time emptying of the stoma bag. Patients in group B developed more complications and required more time to prepare for surgery. One death occurred in group B due to renal insufficiency followed by septic complications. Restricted oral intake seems to be more effective for prevention of HPN-related complications and shortening of time to surgery. Unrestricted oral intake appears to provoke uncontrolled losses of energy and protein, inhibiting weight gain.