l-Citrulline (l-Cit) is a non-essential amino acid that stimulates nitric oxide (NO) production and improves exercise performance by reducing muscle damage indices; however, the direct benefits of l-Cit on antioxidant markers are unclear. The aim of this study was to examine antioxidant responses to high-intensity interval exercise following acute l-Cit supplementation. Nine young men (21 (sd 1) years) participated in a double-blind crossover study in which they received 12 g of l-Cit and placebo (PL) an hour prior to high-intensity interval exercise on two occasions, separated by a 7-d washout period. Blood samples were obtained before (PRE), immediately after (IP), 10 (10P) and 30 min after exercise (30P) from the cubital vein using standard procedures. Serum concentrations of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and NO metabolites (NOx) were measured. The exercise protocol significantly elevated SOD (P = 0·01) and GPx (P = 0·048) from PRE to 10P in the l-Cit group with greater changes than the PL group. CAT concentrations increased IP (P = 0·014) and remained elevated at 10P (P = 0·03) and 30P (P = 0·015) in both the l-Cit and PL conditions. NOx concentrations increased IP (P = 0·05) in the l-Cit group with greater changes than PL group in PRE to IP, PRE to 10P and PRE to 30P (P < 0·05). Our data indicate that l-Cit supplementation (single 12 g dose pre-exercise) induces improvements in antioxidant markers following a session of high-intensity interval exercise in young men.

The absorption, transport and distribution of α-[3H]tocopherol were greatly decreased in protein deficiency. This was reflected in the subcellular distribution of α-[3H]tocopherol in livers of protein-deficient rats. The ratio, bound: free for α-[3H]tocopherol, also decreased in both serum and liver cytosol. After protein refeeding, absorption, transport and distribution patterns of α-[3H]tocopherol for the protein-deficient rats were restored to patterns similar to those of control animals.

The aim of the present study was to examine whether the level of dietary cis fatty acid (c FA), or the isomers (trans or cis) and/or the saturation of the fatty acids at high dietary fat levels altered the intracellular glucose metabolites and certain regulatory enzyme activities in the skeletal muscle and liver of rats. The animals were fed for 30 d on either a recommended control diet (7% c FA, w/w) or a high-fat diet (20% fatty acids, w/w). The high-fat diet was enriched with either c FA, trans fatty acid (t FA), a moderate proportion of saturated fatty acid (MSFA), or a high proportion of saturated fatty acid (HSFA). The most striking findings were observed in the gastrocnemius muscle with a HSFA diet. There was a significant increase in glucose-6-phosphate (306 %), glucose-1-phosphate (245 %), fructose-6-phosphate (400 %), fructose-1,6-bisphosphate (86 %), glyceraldehyde- 3-phosphate (38 %), pyruvate (341 %), lactate (325 %), citrate (79 %) and the bisphosphorylated sugars as compared with the cFA diet. These changes were paralleled by an increase in muscle triacylglycerol content (49 %) and a decrease in glucose (39 %). In addition, the amount of cFA and the other types of fatty acid (i.e. t FA and MSFA) led to no great differences in glucose metabolism as compared with the respective control group. These data support the hypothesis that glucose changes induced by a HSFA diet are a multifaceted abnormality. Glucose and lactate transport and intracellular glucose metabolism could be the key biochemical defects involved in this detrimental effect on glucose metabolism.

The aim of this study was to identify the dietary intake correlates of food insecurity (FI) in UK adults. We recruited groups of low-income participants who were classified as food insecure (n 196) or food secure (n 198). Participants completed up to five 24 h dietary recalls. There was no difference in total energy intake by FI status (β FI = −0·06, 95 % CI − 0·25, 0·13). Food insecure participants consumed a less diverse diet, as evidenced by fewer distinct foods per meal (β FI = −0·27, 95 % CI − 0·47, −0·07), and had more variable time gaps between meals (β FI = 0·21, 95 % CI 0·01, 0·41). These associations corresponded closely to those found in a recent US study using similar measures, suggesting that the dietary intake signature of FI generalises across populations. The findings suggest that the consequences of FI for weight gain and health are not due to increased energy intake. We suggest that there may be important health and metabolic effects of temporal irregularity in dietary intake, which appears to be an important component of FI.

The effects of macronutrient intake on obesity are controversial. This research aims to investigate the associations between macronutrient intake and new-onset overweight/obesity. The relationship between the consumption of carbohydrate and total fat and obesity was assessed by the multivariable Cox model in this 11-year cohort, which included 6612 adults (3291 men and 3321 women) who were free of overweight and obesity at baseline. The dietary intake was recorded using a 24-h recall method for three consecutive days. Moreover, substitution models were developed to distinguish the effects of macronutrient composition alteration from energy intake modification. During 7·5 person years (interquartile range 4·3, 10·8) of follow-up, 1807 participants became overweight or obese. After adjusting for risk factors, the hazard ratio (HR) of overweight/obesity in extreme quintiles of fat was 1·48 (quintile 5 v. quintile 1, 95 % CI 1·16, 1·89; Ptrend = 0·02) in women. Additionally, replacing 5 % of energy from carbohydrate with equivalent energy from fat was associated with an estimated 4·3 % (HR 1·043, 95 % CI 1·007, 1·081) increase in overweight/obesity in women. Moreover, dietary carbohydrate was inversely associated with overweight/obesity (quintile 5 v. quintile 1, HR 0·70, 95 % CI 0·55, 0·89; Ptrend = 0·02) in women. Total fat was related to a higher risk of overweight/obesity, whereas high carbohydrate intake was related to a lower risk of overweight/obesity in women, which was not observed in men.

Se, an essential biological trace element, is required for fish growth. However, the underlying mechanisms remain unclear. Protein deposition in muscle is an important determinant for fish growth. This study was conducted on juvenile rainbow trout (Oncorhynchus mykiss) to explore the nutritional effects of Se on protein deposition in fish muscle by analysing the postprandial dynamics of both protein synthesis and protein degradation. Trout were fed a basal diet supplemented with or without 4 mg/kg Se (as Se yeast), which has been previously demonstrated as the optimal supplemental level for rainbow trout growth. After 6 weeks of feeding, dietary Se supplementation exerted no influence on fish feed intake, whereas it increased fish growth rate, feed efficiency, protein retention rate and muscle protein content. Results of postprandial dynamics (within 24 h after feeding) of protein synthesis and degradation in trout muscle showed that dietary Se supplementation led to a persistently hyperactivated target of rapamycin complex 1 pathway and the suppressive expression of numerous genes related to the ubiquitin–proteasome system and the autophagy–lysosome system after the feeding. However, the ubiquitinated proteins and microtubule-associated light chain 3B (LC3)-II:LC3-I ratio, biomarkers for ubiquitination and autophagy activities, respectively, exhibited no significant differences among the fish fed different experimental diets throughout the whole postprandial period. Overall, this study demonstrated a promoting effect of nutritional level of dietary Se on protein deposition in fish muscle by accelerating postprandial protein synthesis. These results provide important insights about the regulatory role of dietary Se in fish growth.

We investigated the effects of high-Ca fat-free milk phase (MD) (prescription of approximately 1500 mg of Ca/d) v. low-Ca phase (CD) (prescription of approximately 800 mg of Ca/d) in an energy-restricted diet on the metabolic syndrome (MetS) and cardiometabolic measures in individuals with type 2 diabetes mellitus (T2DM) and low habitual Ca consumption (<600 mg/d). In this randomised cross-over design, fourteen adults with T2DM (49·5 (sd 8·6) years, BMI 29·4 (sd 4·5) kg/m2) consumed either MD or CD for 12 weeks, with a washout of 18 weeks between phases. A breakfast shake containing 700 mg (MD) or 6·4 mg (CD) of Ca was consumed in the laboratory. In addition, energy-restricted diets were prescribed (800 mg of dietary Ca/d). Waist circumference (WC), fasting glucose, fasting TAG, systolic (SBP) and diastolic blood pressure (DBP), fasting total cholesterol, fasting LDL-cholesterol, fasting HDL-cholesterol, HDL:LDL ratio, HDL:TAG ratio and lipid accumulation product (LAP) index were assessed at baseline and after each phase. Ca consumption during the study was equivalent to 1200 mg/d during MD and 525 mg/d during CD. There was a greater reduction in WC, SBP, DBP and LAP index after MD compared with CD. HDL:LDL ratio increased and total cholesterol, LDL-cholesterol, SBP, DBP and LAP index decreased only in MD. The consumption of approximately 1200 mg of Ca/d (700 mg from fat-free milk+500mg from other dietary sources) associated with an energy-restricted diet decreased some of the MetS components and cardiometabolic measures in adults with T2DM.

The digestion of polysaccharides from the wheat cultivars Caphorn and Isengrain was investigated, and the efficiency of an enzyme preparation was tested using the TNO gastrointestinal model (TIM-1). The apparent digestibility (AD) of carbohydrates was determined based on the measurement of organic matter (OM), total monosaccharides, reducing ends (RE) and end products (EP: glucose, maltose and xylobiose). The AD of the OM from Caphorn and Isengrain measured using caecectomised cockerels did not differ from that measured using TIM-1: 72·0 (sd 2·6) v. 70·6 (sd 0·6) % for Caphorn (P = 0·580) and 73·0 (sd 2·3) v. 71·1 (sd 1·9) % for Isengrain (P = 0·252). After the 6 h TIM-1 digestion, 41·4–58·9 % of the OM, RE and EP were recovered from the jejunal compartment and 18·3–27·1 % from the ileal compartment, while ileal deliveries and digestive residues constituted the remainder. A commercial enzyme cocktail tested at 0·2 μl/g of wheat improved TIM-1 digestibility of Caphorn and Isengrain polysaccharides: 3·9 % (P = 0·0203) and 3·4 % (P = 0·0058) based on the OM; 9·7 % (P < 0·0001) and 3·1 % (P = 0·031) based on the total glucose; 47·2 % (P < 0·0001) and 14·2 % (P = 0·0004) based on the RE, respectively. The enzyme cocktail improved the release of the EP for Caphorn (3·8 %, P = 0·008) but not for Isengrain ( − 0·8 %, P = 0·561). The higher efficiency of the enzyme supplementation on the digestion of Caphorn polysaccharides compared with Isengrain seems to be linked to the higher soluble carbohydrate contents and/or less ramified arabinoxylan of Caphorn.

In our previous studies, veratric acid (VA) shows beneficial effect on hypertension and its associated dyslipidaemia. In continuation, this study was designed to investigate the effect of VA, one of the major benzoic acid derivatives from vegetables and fruits, on cardiovascular remodelling in hypertensive rats, primarily assessed by functional studies using Langendorff isolated heart system and organ bath system. Hypertension was induced in male albino Wistar rats by oral administration of Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) (40 mg/kg body weight (b.w.)) in drinking water for 4 weeks. VA was orally administered at a dose of 40 mg/kg b.w. l-NAME-treated rats showed impaired cardiac ventricular and vascular function, evaluated by Langendorff isolated heart system and organ bath studies, respectively; a significant increase in the lipid peroxidation products such as thiobarbituric acid-reactive substances and lipid hydroperoxides in aorta; and a significant decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase and levels of GSH, vitamin C and vitamin E in aorta. Fibrotic remodelling of the aorta and heart were assessed by Masson’s Trichrome staining and Van Gieson’s staining, respectively. In addition, l-NAME rats showed increased heart fibronectin expression assessed by immunohistochemical analysis. VA supplementation throughout the experimental period significantly normalised cardiovascular function, oxidative stress, antioxidant status and fibrotic remodelling of tissues. These results of the present study conclude that VA acts as a protective agent against hypertension-associated cardiovascular remodelling.

Studies have suggested that two major milk constituents, casein and Ca, favourably affect postprandial responses. However, effects of milk on postprandial metabolism are unknown. We therefore investigated effects of using milk with a fat-containing meal on lipid and glucose responses in overweight men. To identify the constituent responsible for possible effects, we also studied responses to Ca and protein. A total of sixteen men (BMI >27 kg/m2) participated in four postprandial tests. They consumed a breakfast (44 g of fat) plus a drink: a control drink, low-fat milk or a protein and Ca drink (500 ml). Blood samples were taken before the meals and at regular time points during 6 h thereafter. Compared with control, the incremental AUC (iAUC) for serum TAG was increased by 44 % after the protein meal (P= 0·015). Although the iAUC were not different (P= 0·051), peak glucose concentrations were reduced by 24 % after protein intake, as compared with control (P= 0·021). The decrease of 18 % after milk intake did not reach statistical significance. Compared with the milk meal, the iAUC for insulin was 52 % lower after the control meal (P= 0·035) and 51 % after the protein meal (P= 0·005). The present results indicate that the intake of milk with a fat-containing meal enhances postprandial TAG and insulin responses and may blunt glucose increases. The protein fraction of milk seems to be the main determinant for the effects on TAG and glucose. Ca did not change any of the postprandial responses.

A high-Na diet may lead to the development of hypertension in both humans and rats; however, the causes of Na intake in amounts greater than physiologically needed as well as the mechanisms whereby high-Na food elevates blood pressure are not clear. Therefore, we decided to test the hypothesis that a high-Na diet introduced after suckling affects Na intake, food preference, resting blood pressure and blood volume in adult rats. Male Wistar-Kyoto (WKY) rats, 4 weeks old, were divided into three groups and placed on either a high-Na (3·28%), a medium-Na (0·82%) or a regular diet (0·22%) with the same energy content for 8 weeks. Subsequently, food preference, resting arterial blood pressure, blood volume, plasma osmolality and Na blood level were evaluated. When offered a choice of diets, all the groups preferred the regular chow, and there was no significant difference in total Na intake between the groups. When the rats experienced the change from their initial chow to a new one with different Na content, they continued to eat the same amount of food. Body weight, resting arterial blood pressure, blood volume, plasma osmolality and Na blood level were comparable between the groups. In conclusion, the results show that a high-Na diet introduced immediately after suckling does not affect Na preference and Na intake in adult WKY rats. Furthermore, the findings provide evidence that both blood volume and arterial blood pressure are highly protected in normotensive rats on a high-Na diet.

A total of ten experimental diets with protein concentrations ranging from 154 to 400 g/kg and two lipid levels (46 and 85 g/kg) with identical energy densities were offered to 240 male Ross 308 broilers from 7 to 28 d post-hatch. Growth performance was monitored and nutrient utilisation (apparent metabolisable energy (AME), N-corrected AME (AMEn), AME daily intake, AME:gross energy ratios, N retention) was determined. The weight gain response of broiler chickens to dietary protein concentrations in diets containing high and low lipid levels was diverse, with the relevant quadratic regressions being significantly different (P<0·05). With low lipid levels, the predicted maximum weight gain of 1809 g/bird equated to 342 g/kg dietary protein, whereas, for high lipid levels the predicted maximum weight gain of 1694 g/bird equated to 281 g/kg dietary protein. AME was linearly correlated with dietary protein concentration but regressions in diets with different lipid content were not significantly different (P>0·05). AMEn was also linearly (P<0·0001) increased with dietary protein concentrations but regressions in diets with low and high lipid content were significantly different (P<0·03). Carcass protein content increased linearly with dietary protein content in diets containing high lipid concentrations (r 0·933, P<0·0001); by contrast, this relationship was quadratic (R2=0·93, P<0·0001) in diets with low lipid levels. In conclusion, predictably, the effects of dietary protein concentrations on broiler performance were profound; however, the impact of dietary protein on performance in broiler chickens was modified by dietary lipid concentrations.

The nutritional and physiological modifications that occur during the weaning period induce adaptations of tissue metabolism in all mammal species. Among the adaptations due to weaning in ruminants, the regulation of lipoprotein lipase (LPL) activity, one of the rate-limiting steps of fatty acid utilization by tissues, was still unknown. The present study aimed at comparing LPL activity and gene expression in the heart, seven skeletal muscles and three adipose tissue sites between two groups of seven preruminant (PR) or ruminant (R) calves having a similar age (170 d), similar empty body weight (194 kg) at slaughter, and similar net energy intake from birth onwards. Triacylglycerol content of adipose tissues was 16 % lower in R than in PR calves, (P<0·01). This could be partly the result from a lower LPL activity (-57 %, P<0·01). LPL mRNA levels were also lower in R calves (-48 % to -68 %, P<0·01) suggesting a pretranslational regulation of LPL activity. Activity and mRNA levels of LPL did not differ significantly in the heart and skeletal muscles except in the masseter in which LPL activity and mRNA levels were higher (+50 % and +120 % respectively, P<0·01) in the R calves. Regulation of LPL in masseter could be explained by the high contractile activity of this muscle after weaning due to solid food chewing. In conclusion, weaning in the calf affects LPL activity and expression in adipose tissues, but not in skeletal muscles except the masseter.

Given the current interest in the cardiovascular complications of Mg deficiency, the aim of the present experiment was to investigate the effect of Mg deficiency on the time-course of lipoprotein oxidation and to assess whether short-term Mg deficiency results in vitamin E depletion that predisposes lipoproteins and tissues to subsequent oxidation. Weanling rats were pair-fed for 8 d with control and Mg-deficient diets respectively. Plasma triacylglycerol and α-toeopherol levels were significantly greater in Mg-deficient rats compared with control animals. The increase in plasma apolipoprotein B concentration indicated that a corresponding increase in plasma triacylglycerol-rich lipoproteins (TGRLP) occurred in Mg-deficient animals. Hyperlipaemia was associated with modifications in the composition of TGRLP. The proportion of triacylglycerols was elevated whereas that of cholesterol and protein was reduced, and Mg deficiency resulted in a slight significant reduction in α-tocopherol content. When the TGRLP fractions were subjected to in vitro Cu-induced oxidation the lipoprotein fractions from Mg-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats. Mg deficiency did not modify the α-tocopherol content of liver, heart and skeletal muscle. However, after exposure of tissue homogenates to Fe-induced lipid peroxidation, thiobarbituric acid-reactive substances were significantly higher in tissues from Mg-deficient rats compared with those from control rats. These results complement previous findings, showing that Mg deficiency increases the susceptibility of TGRLP and tissues to peroxidation and suggest that oxidative damage is not the result of a decrease in vitamin E antioxidant status.

Gene polymorphisms provide a means to obtain unconfounded associations between carotenoids and various health outcomes. In the present study, we tested whether gene polymorphisms and gene scores linked to low serum carotenoid status are related to metabolic disturbance and depressive symptoms in African-American adults residing in Baltimore city, MD, using cross-sectional data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study (age range 30–64 years, n 873–994). We examined twenty-four SNP of various gene loci that were previously shown to be associated with low serum carotenoid status (SNPlcar). Gene risk scores were created: five low specific-carotenoid risk scores (LSCRS: α-carotene, β-carotene, lutein+zeaxanthin, β-cryptoxanthin and lycopene) and one low total-carotenoid risk score (LTCRS: total carotenoids). SNPlcar, LSCRS and LTCRS were entered as predictors for a number of health outcomes. These included obesity, National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome and its components, elevated homeostatic model assessment of insulin resistance, C-reactive protein, hyperuricaemia and elevated depressive symptoms (EDS, Center for Epidemiologic Studies-Depression score ≥ 16). Among the key findings, SNPlcar were not associated with the main outcomes after correction for multiple testing. However, an inverse association was found between the LTCRS and HDL-cholesterol (HDL-C) dyslipidaemia. Specifically, the α-carotene and β-cryptoxanthin LSCRS were associated with a lower odds of HDL-C dyslipidaemia. However, the β-cryptoxanthin LSCRS was linked to a higher odds of EDS, with a linear dose–response relationship. In summary, gene risk scores linked to low serum carotenoids had mixed effects on HDL-C dyslipidaemia and EDS. Further studies using larger African-American population samples are needed.

It has been suggested that protein synthesis in peripheral tissues: (1) responds in a curvilinear manner to increasing feed intake over a wide range of feeding levels; and (2) has a greater sensitivity to intake than protein breakdown. The aim of the present experiment was to test these hypotheses across the ovine hindlimb. Six growing sheep (6–8 months, 30–35 kg), with catheters in the aorta (two), posterior vena cava and jugular vein, received each of four intakes of dried grass pellets (0·5, 1·0, 1·5 and 2·5×maintenance energy; M) for a minimum of 7 d. A U-13C-labelled algal hydrolysate was infused intravenously for 10 h and from 3–9 h para-aminohippuric acid was infused to measure plasma flow. Arterial and venous plasma were obtained over the last 4 h and the concentrations and enrichments of thirteen 13C-labelled amino acids (AA) were determined by GC–MS. As intake increased, a positive linear response was found for plasma flow, arterial concentrations of the aromatic and branched-chain AA, total flow of all AA into the hindquarters and net mass balance across the hindquarters (except glycine and alanine). Based on two separate statistical analyses, the data for protein synthesis showed a significant linear effect with intake (except for phenylalanine, glycine and alanine). No significant curvilinear effect was found, which tends not to support hypothesis 1. Nonetheless, protein synthesis was not significantly different between 0·5, 1·0 and 1·5×M and thus the 2·5×M intake level was largely responsible for the linear relationship found. There was no significant response in protein breakdown to intake, which supports hypothesis 2.

The Ca intake and food sources of Chinese postmenopausal women are quite different from those of their Western counterparts. But, little information on Ca metabolism is available in Chinese populations. We determined true fractional calcium absorption (TFCA), true Ca absorption ( = TFCA × Ca intake, Va), urinary Ca excretion (Vu) and the difference between Va and Vu (Va − u), in response to three dietary Ca intake levels. Twenty-one healthy postmenopausal Chinese women aged 49–64 years were recruited for this randomized crossover trial from a general community, Guangzhou, China. Subjects were randomly assigned to receive 0, 500 and 1000 mg Ca/d for 5 weeks separated by 2-week washout periods. TFCA using Ca stable isotopes, total urinary Ca excretion and Ca intake were determined after 4 weeks of adaptation. Mean values for total Ca intake (Vi) of the three phases were 391 (sd 197), 880 (sd 130) and 1382 (sd 160) mg/d. On usual diet, TFCA, Vu, Va and Va − u were 0·57 (sd 0·12), 175 (sd 59) mg/d, 216 (sd 98) mg/d and 41 (sd 99) mg/d, respectively. With the supplementations of 500 and 1000 mg Ca/d, TFCA significantly decreased to 0·52 (sd 0·12) and 0·43 (sd 0·13) (P < 0·001); whereas urinary Ca (P = 0·003), Va and Va − u increased significantly (P < 0·001). Using a mixed-effects nonlinear regression model, it was estimated that Va − u was approaching a plateau when mean Ca intake reached 1300 mg/d. In conclusion, the present findings suggest postmenopausal Chinese women have high Ca absorption efficiency and a mean Ca intake of about 1300 mg/d is required to maximize the Va − u.

Previous (mainly population-based) studies have suggested the health benefits of the elective, lifelong inclusion of whole-grain foods in the diet, forming the basis for public health recommendations to increase whole grain consumption. Currently, there is limited evidence to assess how public health recommendations can best result in longer-term improvements in dietary intake. The present study aimed to assess the impact of a previous 16-week whole-grain intervention on subsequent, elective whole grain consumption in free-living individuals. Participants completed a postal FFQ 1, 6 and 12 months after the end of the whole-grain intervention study period. This FFQ included inputs for whole-grain foods commonly consumed in the UK. Whole grain consumption was significantly higher (approximately doubled) in participants who had received whole-grain foods during the intervention (P< 0·001) compared with the control group who did not receive whole-grain foods during the intervention. This increased whole grain consumption was lower than whole grain intake levels required by participants during the intervention period between 60 and 120 g whole grains/d. Aside from a significant increase (P< 0·001) in NSP consumption compared with control participants (mean increase 2–3 g/d), there were no obvious improvements to the pattern of foods of the intervention group. The results of the present study suggest that a period of direct exposure to whole-grain foods in non-habitual whole-grain food consumers may benefit subsequent, elective dietary patterns of whole grain consumption. These findings may therefore aid the development of future strategies to increase whole grain consumption for public health and/or food industry professionals.