Effects of protein intake on blood pressure, insulin sensitivity and blood lipids in children: a systematic review
Trudy Voortman, Anna Vitezova, Wichor M. Bramer, Charlotte L. Ars, Paula K. Bautista, Adriana Buitrago-Lopez, Janine F. Felix, Elisabeth T. M. Leermakers, Ayesha Sajjad, Sanaz Sedaghat, Anne Tharner, Oscar H. Franco, Edith H. van den Hooven
High protein intake in early childhood is associated with obesity, suggesting possible adverse effects on other cardiometabolic outcomes. However, studies in adults have suggested beneficial effects of protein intake on blood pressure (BP) and lipid profile. Whether dietary protein intake is associated with cardiovascular and metabolic health in children is unclear. Therefore, we aimed to systematically review the evidence on the associations of protein intake with BP, insulin sensitivity and blood lipids in children. We searched the databases Medline, Embase, Cochrane Central and PubMed for interventional and observational studies in healthy children up to the age of 18 years, in which associations of total, animal and/or vegetable protein intake with one or more of the following outcomes were reported: BP; measures of insulin sensitivity; cholesterol levels; or TAG levels. In the search, we identified 6636 abstracts, of which fifty-six studies met all selection criteria. In general, the quality of the included studies was low. Most studies were cross-sectional, and many did not control for potential confounders. No overall associations were observed between protein intake and insulin sensitivity or blood lipids. A few studies suggested an inverse association between dietary protein intake and BP, but evidence was inconclusive. Only four studies examined the effects of vegetable or animal protein intake, but with inconsistent results. In conclusion, the literature, to date provides insufficient evidence for effects of protein intake on BP, insulin sensitivity or blood lipids in children. Future studies could be improved by adequately adjusting for key confounders such as energy intake and obesity.
Full Papers
Betaine alleviates hepatic lipid accumulation via enhancing hepatic lipid export and fatty acid oxidation in rats fed with a high-fat diet
Li Xu, Danping Huang, Qiaolin Hu, Jing Wu, Yizhen Wang, Jie Feng
To assess the effects of betaine on hepatic lipid accumulation and investigate the underlying mechanism, thirty-two male Sprague–Dawley rats weighing 100 (sd 2·50) g were divided into four groups, and started on one of four treatments: basal diet, basal diet with betaine administration, high-fat diet and high-fat diet with betaine administration. The results showed that no significant difference of body weight was found among experimental groups. Compared with high-fat diet-fed rats, a betaine supplementation decreased (P< 0·05) hepatic TAG accumulation induced by high-fat diet, which was also supported by hepatic histology results. Additionally, hepatic betaine–homocysteine methyltransferase activity as well as its mRNA abundance and lecithin level were found increased (P< 0·05) by betaine supplementation in both basal diet-fed rats and high-fat diet-fed rats. Betaine administration in high-fat diet-fed rats exhibited a higher (P< 0·05) activity of hepatic carnitine palmitoyltransferase 1 (CPT1) compared with high-fat diet-fed rats. High-fat diet inhibited (P< 0·05) the gene expression of hepatic PPARα and CPT1. However, betaine administration in high-fat diet-fed rats elevated (P< 0·05) the gene expression of PPARα and CPT1. Moreover, concentration, gene and protein expressions of hepatic fibroblast growth factor 21 (FGF21) were increased (P< 0·05) in response to betaine administration in high-fat diet group; meanwhile the gene expression of hepatic AMP-activated protein kinase was increased (P< 0·05) as well. The results suggest that betaine administration enhanced hepatic lipid export and fatty acid oxidation in high-fat diet-fed rats, thus effectively alleviating fat accumulation in the liver.
Dietary effects on human gut microbiome diversity
Zhenjiang Xu, Rob Knight
Published online: 11 December 2014, pp. S1-S5
The human gut harbours diverse and abundant microbes, forming a complex ecological system that interacts with host and environmental factors. In this article, we summarise recent advances in microbiome studies across both Western and non-Western populations, either in cross-sectional or longitudinal surveys, and over various age groups, revealing a considerable diversity and variability in the human gut microbiome. Of all the exogenous factors affecting gut microbiome, a long-term diet appears to have the largest effect to date. Recent research on the effects of dietary interventions has shown that the gut microbiome can change dramatically with diet; however, the gut microbiome is generally resilient, and short-term dietary intervention is not typically successful in treating obesity and malnutrition. Understanding the dynamics of the gut microbiome under different conditions will help us diagnose and treat many diseases that are now known to be associated with microbial communities.
Invited Commentary
Assessing iodine intakes in pregnancy: why does this matter?
Elizabeth N. Pearce
Published online: 31 March 2015, pp. 1179-1181
Hydroxytyrosol improves mitochondrial function and reduces oxidative stress in the brain of db/db mice: role of AMP-activated protein kinase activation
Adi Zheng, Hao Li, Jie Xu, Ke Cao, Hua Li, Wenjun Pu, Ziqi Yang, Yunhua Peng, Jiangang Long, Jiankang Liu, Zhihui Feng
Hydroxytyrosol (HT) is a major polyphenolic compound found in olive oil with reported anti-cancer and anti-inflammatory activities. However, the neuroprotective effect of HT on type 2 diabetes remains unknown. In the present study, db/db mice and SH-SY-5Y neuroblastoma cells were used to evaluate the neuroprotective effects of HT. After 8 weeks of HT administration at doses of 10 and 50 mg/kg, expression levels of the mitochondrial respiratory chain complexes I/II/IV and the activity of complex I were significantly elevated in the brain of db/db mice. Likewise, targets of the antioxidative transcription factor nuclear factor erythroid 2 related factor 2 including p62 (sequestosome-1), haeme oxygenase 1 (HO-1), and superoxide dismutases 1 and 2 increased, and protein oxidation significantly decreased. HT treatment was also found to activate AMP-activated protein kinase (AMPK), sirtuin 1 and PPARγ coactivator-1α, which constitute an energy-sensing protein network known to regulate mitochondrial function and oxidative stress responses. Meanwhile, neuronal survival indicated by neuron marker expression levels including activity-regulated cytoskeleton-associated protein, N-methyl-d-aspartate receptor and nerve growth factor was significantly improved by HT administration. Additionally, in a high glucose-induced neuronal cell damage model, HT effectively increased mitochondrial complex IV and HO-1 expression through activating AMPK pathway, followed by the prevention of high glucose-induced production of reactive oxygen species and declines of cell viability and VO2 capacity. Our observations suggest that HT improves mitochondrial function and reduces oxidative stress potentially through activation of the AMPK pathway in the brain of db/db mice.
Effects of methionine supplementation on the expression of oxidative stress-related genes in acute heat stress-exposed broilers
The aim of the present study was to evaluate the effects of heat stress (HS) and methionine supplementation on the markers of stress and on the gene expression levels of uncoupling proteins (UCP), betaine–homocysteine methyltransferase (BHMT), cystathionine β-synthase (CBS), glutathione synthetase (GSS) and glutathione peroxidase 7 (GPx7). Broilers from 1 to 21 d and from 22 to 42 d of age were divided into three treatment groups related to methionine supplementation: without methionine supplementation (MD); recommended level of methionine supplementation (DL1); excess methionine supplementation (DL2). The broilers were either kept at a comfortable thermal temperature or exposed to HS (38°C for 24 h). During the starter period, we observed the effects of the interaction between diet and environment on the gene expression levels of UCP, BHMT and GSS. Higher gene expression levels of UCP and BHMT were observed in broilers that were maintained at thermal comfort conditions and received the MD diet. HS broilers fed the DL1 and DL2 diets had the highest expression level of GSS. The expression levels of the CBS and GPx7 genes were influenced by both the environment and methionine supplementation. During the grower period, the gene expression levels of BHMT, CBS, GSS and GPx7 were affected by the diet × environment interaction. A higher expression level of BHMT was observed in broilers maintained at thermal comfort conditions and on the MD diet. HS induced higher expression levels of CBS, GSS and GPx7 in broilers that received the DL1 and DL2 diets. The present results suggest that under HS conditions, methionine supplementation could mitigate the effects of stress, since methionine contributed to the increased expression levels of genes related to antioxidant activity.
Sugar-sweetened beverages and risk of hypertension and CVD: a dose–response meta-analysis
Bo Xi, Yubei Huang, Kathleen Heather Reilly, Shuangshuang Li, Ruolong Zheng, Maria T. Barrio-Lopez, Miguel A. Martinez-Gonzalez, Donghao Zhou
A number of prospective cohort studies have investigated the associations between consumption of sugar-sweetened beverages (SSB) and the risk of hypertension, CHD and stroke, but revealed mixed results. In the present study, we aimed to perform a dose–response meta-analysis of these prospective studies to clarify these associations. A systematic literature search was conducted using the PubMed and Embase databases up to 5 May 2014. Random- or fixed-effects models were used to calculate the pooled relative risks (RR) with 95 % CI for the highest compared with the lowest category of SSB consumption, and to conduct a dose–response analysis. A total of six prospective studies (240 726 participants and 80 411 incident cases of hypertension) from four publications on hypertension were identified. A total of four prospective studies (194 664 participants and 7396 incident cases of CHD) from four publications on CHD were identified. A total of four prospective studies (259 176 participants and 10 011 incident cases of stroke) from four publications on stroke were identified. The summary RR for incident hypertension was 1·08 (95 % CI 1·04, 1·12) for every additional one serving/d increase in SSB consumption. The summary RR for incident CHD was 1·17 (95 % CI 1·10, 1·24) for every serving/d increase in SSB consumption. There was no significant association between SSB consumption and total stroke (summary RR 1·06, 95 % CI 0·97, 1·15) for every serving/d increase in SSB consumption. The present meta-analysis suggested that a higher consumption of SSB was associated with a higher risk of hypertension and CHD, but not with a higher risk of stroke.
Nutritional Immunology
Impact of fish oils on the outcomes of a mouse model of acute Pseudomonas aeruginosa pulmonary infection
Pseudomonas aeruginosa is an opportunistic Gram-negative bacterium that causes pneumonia in immunocompromised humans and severe pulmonary damage in patients with cystic fibrosis. Imbalanced fatty acid incorporation in membranes, including increased arachidonic acid and decreased DHA concentrations, is known to play a critical role in chronic inflammation associated with bacterial infection. Other lipids, such as EPA and alkylglycerols, are also known to play a role in inflammation, particularly by stimulating the immune system, decreasing inflammation and inhibiting bacterial growth. In this context, the goal of the present study was to assess the effect of dietary DHA/EPA, in a 2:1 ratio, and alkylglycerols, as natural compounds extracted from oils of rays and chimeras, respectively, on the inflammatory reaction induced by P. aeruginosa pulmonary infection in mice. To this end, mice were fed with a control diet or isolipidic, isoenergetic diets prepared with oils enriched in DHA/EPA (2:1) or alkylglycerols for 5 weeks before the induction of acute P. aeruginosa lung infection by endotracheal instillation. In our model, DHA/EPA (2:1) significantly improved the survival of mice after infection, which was associated with the acceleration of bacterial clearance and the resolution of inflammation leading to the improvement of pulmonary injuries. By contrast, alkylglycerols did not affect the outcomes of P. aeruginosa infection. Our findings suggest that supplementation with ray oil enriched in DHA/EPA (2:1) can be considered as a preventive treatment for patients at risk for P. aeruginosa infection.
High-fat diet decreases energy expenditure and expression of genes controlling lipid metabolism, mitochondrial function and skeletal system development in the adipose tissue, along with increased expression of extracellular matrix remodelling- and inflammation-related genes
Myung-Sook Choi, Young-Je Kim, Eun-Young Kwon, Jae Young Ryoo, Sang Ryong Kim, Un Ju Jung
The aim of the present study was to identify the genes differentially expressed in the visceral adipose tissue in a well-characterised mouse model of high-fat diet (HFD)-induced obesity. Male C57BL/6J mice (n 20) were fed either HFD (189 % of energy from fat) or low-fat diet (LFD, 42 % of energy from fat) for 16 weeks. HFD-fed mice exhibited obesity, insulin resistance, dyslipidaemia and adipose collagen accumulation, along with higher levels of plasma leptin, resistin and plasminogen activator inhibitor type 1, although there were no significant differences in plasma cytokine levels. Energy intake was similar in the two diet groups owing to lower food intake in the HFD group; however, energy expenditure was also lower in the HFD group than in the LFD group. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation–reduction, insulin sensitivity and skeletal system development were down-regulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodelling and inflammation were up-regulated. The top ten up- or down-regulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1 and Gpnmb, whose roles in the deterioration of obesity-associated adipose tissue are poorly understood. In conclusion, the genes identified here provide new therapeutic opportunities for prevention and treatment of diet-induced obesity.
Diet, nutrients and metabolism: cogs in the wheel driving Alzheimer's disease pathology?
Rhona Creegan, Wendy Hunt, Alexandra McManus, Stephanie R. Rainey-Smith
Alzheimer's disease (AD), the most common form of dementia, is a chronic, progressive neurodegenerative disease that manifests clinically as a slow global decline in cognitive function, including deterioration of memory, reasoning, abstraction, language and emotional stability, culminating in a patient with end-stage disease, totally dependent on custodial care. With a global ageing population, it is predicted that there will be a marked increase in the number of people diagnosed with AD in the coming decades, making this a significant challenge to socio-economic policy and aged care. Global estimates put a direct cost for treating and caring for people with dementia at $US604 billion, an estimate that is expected to increase markedly. According to recent global statistics, there are 35·6 million dementia sufferers, the number of which is predicted to double every 20 years, unless strategies are implemented to reduce this burden. Currently, there is no cure for AD; while current therapies may temporarily ameliorate symptoms, death usually occurs approximately 8 years after diagnosis. A greater understanding of AD pathophysiology is paramount, and attention is now being directed to the discovery of biomarkers that may not only facilitate pre-symptomatic diagnosis, but also provide an insight into aberrant biochemical pathways that may reveal potential therapeutic targets, including nutritional ones. AD pathogenesis develops over many years before clinical symptoms appear, providing the opportunity to develop therapy that could slow or stop disease progression well before any clinical manifestation develops.
Dietary calcium concentration and cereals differentially affect mineral balance and tight junction proteins expression in jejunum of weaned pigs
Barbara U. Metzler-Zebeli, Evelyne Mann, Reinhard Ertl, Stephan Schmitz-Esser, Martin Wagner, Dieter Klein, Mathias Ritzmann, Qendrim Zebeli
Ca plays an essential role in bone development; however, little is known about its effect on intestinal gene expression in juvenile animals. In the present study, thirty-two weaned pigs (9·5 (sem 0·11) kg) were assigned to four diets that differed in Ca concentration (adequate v. high) and cereal composition (wheat–barley v. maize) to assess the jejunal and colonic gene expression of nutrient transporters, tight junction proteins, cytokines and pathogen-associated molecular patterns, nutrient digestibility, Ca balance and serum acute-phase response. To estimate the impact of mucosal bacteria on colonic gene expression, Spearman's correlations between colonic gene expression and bacterial abundance were computed. Faecal Ca excretion indicated that more Ca was available along the intestinal tract of the pigs fed high Ca diets as compared to the pigs fed adequate Ca diets (P< 0·05). High Ca diets decreased jejunal zonula occludens 1 (ZO1) and occludin (OCLN) expression, up-regulated jejunal expression of toll-like receptor 2 (TLR2) and down-regulated colonic GLUT2 expression as compared to the adequate Ca diets (P< 0·05). Dietary cereal composition up-regulated jejunal TLR2 expression and interacted (P= 0·021) with dietary Ca on colonic IL1B expression; high Ca concentration up-regulated IL1B expression with wheat–barley diets and down-regulated it with maize diets. Spearman's correlations (r>0·35; P< 0·05) indicated an association between operational taxonomic units assigned to the phyla Bacteroidetes, Firmicutes and Proteobacteria and bacterial metabolites and mucosal gene expression in the colon. The present results indicate that high Ca diets have the potential to modify the jejunal and colonic mucosal gene expression response which, in turn, interacts with the composition of the basal diet and mucosa-associated bacteria in weaned pigs.
Lorenzo M. Donini, Lluis Serra-Majem, Mònica Bulló, Ángel Gil, Jordi Salas-Salvadó
Published online: 07 July 2015, pp. S1-S3
Oligosaccharides in infant formula: more evidence to validate the role of prebiotics
Yvan Vandenplas, Irina Zakharova, Yulia Dmitrieva
The gastrointestinal (GI) microbiota differs between breast-fed and classic infant formula-fed infants. Breast milk is rich in prebiotic oligosaccharides (OS) and may also contain some probiotics, but scientific societies do not recommend the addition of prebiotic OS or probiotics to standard infant formula. Nevertheless, many infant formula companies often add one or the other or both. Different types of prebiotic OS are used in infant formula, including galacto-oligosaccharide, fructo-oligosaccharide, polydextrose and mixtures of these OS, but none adds human milk OS. There is evidence that the addition of prebiotics to infant formula brings the GI microbiota of formula-fed infants closer to that of breast-fed infants. Prebiotics change gut metabolic activity (by decreasing stool pH and increasing SCFA), have a bifidogenic effect and bring stool consistency and defecation frequency closer to those of breast-fed infants. Although there is only limited evidence that these changes in GI microbiota induce a significant clinical benefit for the immune system, interesting positive trends have been observed in some markers. Additionally, adverse effects are extremely seldom. Prebiotics are added to infant formula because breast milk contains human milk OS. Because most studies suggest a trend of beneficial effects and because these ingredients are very safe, prebiotics bring infant formula one step closer to the golden standard of breast milk.
Effects of the Dietary Approach to Stop Hypertension (DASH) diet on cardiovascular risk factors: a systematic review and meta-analysis
Mario Siervo, Jose Lara, Shakir Chowdhury, Ammar Ashor, Clio Oggioni, John C. Mathers
The Dietary Approach to Stop Hypertension (DASH) is recommended to lower blood pressure (BP), but its effects on cardiometabolic biomarkers are unclear. A systematic review and meta-analysis of randomised controlled trials (RCT) was conducted to determine the effects of the DASH diet on cardiovascular risk factors. Medline, Embase and Scopus databases were searched from inception to December 2013. Inclusion criteria were as follows: (1) DASH diet; (2) RCT; (3) risk factors including systolic and diastolic BP and glucose, HDL, LDL, TAG and total cholesterol concentrations; (4) control group. Random-effects models were used to determine the pooled effect sizes. Meta-regression analyses were carried out to examine the association between effect sizes, baseline values of the risk factors, BMI, age, quality of trials, salt intake and study duration. A total of twenty articles reporting data for 1917 participants were included in the meta-analysis. The duration of interventions ranged from 2 to 24 weeks. The DASH diet was found to result in significant decreases in systolic BP ( − 5·2 mmHg, 95 % CI − 7·0, − 3·4; P< 0·001) and diastolic BP ( − 2·6 mmHg, 95 % CI − 3·5, − 1·7; P< 0·001) and in the concentrations of total cholesterol ( − 0·20 mmol/l, 95 % CI − 0·31, − 0·10; P< 0·001) and LDL ( − 0·10 mmol/l, 95 % CI − 0·20, − 0·01; P= 0·03). Changes in both systolic and diastolic BP were greater in participants with higher baseline BP or BMI. These changes predicted a reduction of approximately 13 % in the 10-year Framingham risk score for CVD. The DASH diet improved cardiovascular risk factors and appeared to have greater beneficial effects in subjects with an increased cardiometabolic risk. The DASH diet is an effective nutritional strategy to prevent CVD.
Huan-Ling Yu, Shan Dong, Li-Fang Gao, Li Li, Yuan-Di Xi, Wei-Wei Ma, Lin-Hong Yuan, Rong Xiao
An epigenetic mechanism has been suggested to explain the effects of the maternal diet on the development of disease in offspring. The present study aimed to observe the effects of a maternal high-lipid, high-energy (HLE) diet on the DNA methylation pattern of male offspring in mice. Female C57BL/6J mice were fed an HLE diet during gestation and lactation. The genomic DNA methylations at promoter sites of genes in the liver, mRNA and protein levels of selected genes related to lipid and glucose metabolism were measured by microarray, real-time PCR and Western blot. The results indicated that the percentage of methylated DNA in offspring from dams that were fed an HLE diet was significantly higher than that from dams that were fed a chow diet, and most of these genes were hypermethylated in promoter regions. The nuclear protein content and mRNA levels of hypermethylated genes, such as PPARγ and liver X receptor α (LXRα), were decreased significantly in offspring in the HLE group. The results suggested that the DNA methylation profile in adult offspring livers was changed by the maternal HLE diet during gestation and lactation.
Metabolism and Metabolic Studies
Absorption and intermediary metabolism of purines and pyrimidines in lactating dairy cows
About 20 % of ruminal microbial N in dairy cows derives from purines and pyrimidines; however, their intermediary metabolism and contribution to the overall N metabolism has sparsely been described. In the present study, the postprandial patterns of net portal-drained viscera (PDV) and hepatic metabolism were assessed to evaluate purine and pyrimidine N in dairy cows. Blood was sampled simultaneously from four veins with eight hourly samples from four multi-catheterised Holstein cows. Quantification of twenty purines and pyrimidines was performed with HPLC–MS/MS, and net fluxes were estimated across the PDV, hepatic tissue and total splanchnic tissue (TSP). Concentration differences between veins of fifteen purine and pyrimidine nucleosides (NS), bases (BS) and degradation products (DP) were different from zero (P≤ 0·05), resulting in the net PDV releases of purine NS (0·33–1·3 mmol/h), purine BS (0·0023–0·018 mmol/h), purine DP (7·0–7·8 mmol/h), pyrimidine NS (0·30–2·8 mmol/h) and pyrimidine DP (0·047–0·77 mmol/h). The hepatic removal of purine and pyrimidine was almost equivalent to the net PDV release, resulting in no net TSP release. One exception was uric acid (7·9 mmol/h) from which a large net TSP release originated from the degradation of purine NS and BS. A small net TSP release of the pyrimidine DP β-alanine and β-aminoisobutyric acid ( − 0·032 to 0·37 mmol/h) demonstrated an outlet of N into the circulating N pool. No effect of time relative to feeding was observed (P>0·05). These data indicate that considerable amounts of N are lost in the dairy cow due to prominent intermediary degradation of purines, but that pyrimidine N is reusable to a larger extent.
Ping Deng, Kelly S. Swanson
Published online: 21 November 2014, pp. S6-S17
High-throughput DNA sequencing techniques allow for the identification and characterisation of microbes and their genes (microbiome). Using these new techniques, microbial populations in several niches of the human body, including the oral and nasal cavities, skin, urogenital tract and gastrointestinal tract, have been described recently. Very little data on the microbiome of companion animals exist, and most of the data have been derived from the analysis of the faeces of healthy laboratory animals. High-throughput assays provide opportunities to study the complex and dense populations of the gut microbiota, including bacteria, archaea, fungi, protozoa and viruses. Our laboratory and others have recently described the predominant microbial taxa and genes of healthy dogs and cats and how these respond to dietary interventions. In general, faecal microbial phylogeny (e.g. predominance of Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria) and functional capacity (e.g. major functional groups related to carbohydrate, protein, DNA and vitamin metabolism; virulence factors; and cell wall and capsule) of the canine and feline gut are similar to those of the human gut. Initial sequencing projects have provided a glimpse of the microbial super-organism that exists within the canine and feline gut, but leaves much to be explored and discovered. As DNA provides information only about potential functions, studies that focus on the microbial transcriptome, metabolite profiles, and how microbiome changes affect host physiology and health are clearly required. Future studies must determine how diet composition, antibiotics and other drug therapies, breed and disease affect or are affected by the gut microbiome and how this information may be used to improve diets, identify disease biomarkers and develop targeted disease therapies.
Bioavailability of free lysine and protein-bound lysine from casein and fishmeal in juvenile turbot (Psetta maxima)
In the present study, a linear regression analysis between lysine intake and lysine retention was conducted to investigate the efficiency of lysine utilisation (k Lys) at marginal lysine intake of either protein-bound or free lysine sources in juvenile turbot (Psetta maxima). For this purpose, nine isonitrogenous and isoenergetic diets were formulated to contain 2·25–4·12 g lysine/100 g crude protein (CP) to ensure that lysine was the first-limiting amino acid in all diets. The basal diet contained 2·25 g lysine/100 g CP. Graded levels of casein (Cas), fishmeal (FM) and l-lysine HCl (Lys) were added to the experimental diets to achieve stepwise lysine increments. A total of 240 fish (initial weight 50·1 g) were hand-fed all the experimental diets once daily until apparent satiation over a period of 56 d. Feed intake was significantly affected by dietary lysine concentration rather than by dietary lysine source. Specific growth rate increased significantly at higher lysine concentrations (P< 0·001). CP, crude lipid and crude ash contents in the whole body were affected by the dietary treatments. The linear regression slope between lysine retention and lysine intake (k Lys) was similar between all the dietary lysine sources. The k Lys values for the diets supplemented with Cas, Lys or FM were 0·833, 0·857 and 0·684, respectively. The bioavailability of lysine from the respective lysine sources was determined by a slope-ratio approach. The bioavailability of lysine (relative to the reference lysine source Cas) from FM and Lys was 82·1 and 103 %, respectively. Nutrient requirement for maintenance was in the range of 16·7–23·4 mg/kg0·8 per d, and did not differ between the treatments. There were no significant differences in lysine utilisation efficiency or bioavailability of protein-bound or crystalline lysine from the respective sources observed when lysine was confirmed to be the first-limiting nutrient.
Randomised controlled trials (RCT) testing the effects of antioxidant supplements on endothelial function (EF) have reported conflicting results. We aimed to investigate the effects of supplementation with antioxidant vitamins C and E on EF and to explore factors that may provide explanations for the inconsistent results. We searched four databases (MEDLINE, Embase, Cochrane Library and Scopus) from inception until May 2014 for RCT involving adult participants aged ≥ 18 years who were supplemented with vitamins C and E alone or in combination for more than 2 weeks and reporting changes in EF measured using flow mediated dilation or forearm blood flow. Data were pooled as standardised mean difference (SMD) and analysed using a random-effects model. Significant improvements in EF were observed in trials supplementing with vitamin C alone (500–2000 mg/d) (SMD: 0·25, 95 % CI 0·02, 0·49, P= 0·043) and vitamin E alone (300–1800 IU/d; 1 IU vitamin E = 0·67 mg natural vitamin E) (SMD: 0·48, 95 % CI 0·23, 0·72, P= 0·0001), whereas co-administration of both vitamins was ineffective (vitamin C: 500–2000 mg/d; vitamin E: 400–1200 IU/d) (SMD: 0·12, 95 % CI − 0·18, 0·42, P= 0·428). The effect of vitamin C supplementation on EF increased significantly with age (β 0·023, 95 % CI 0·001, 0·05, P= 0·042). There was a significant negative correlation between baseline plasma vitamin E concentration and the effect of vitamin E supplementation on EF (β − 0·03, 95 % CI − 0·06, − 0·001, P= 0·029). Supplementation with either vitamin C or vitamin E alone improves EF. However, subgroup analysis emphasises the importance of careful characterisation and selection of a population group which may benefit from such supplementation.