The popularity of high-protein diets for weight reduction is immense. However, the potential benefits from altering the source of dietary protein rather than the amount is scarcely investigated. In the present study, we examined the effects of fish protein supplement on glucose and lipid metabolism in overweight adults. A total of thirty-four overweight adults were randomised to 8 weeks' supplementation with fish protein or placebo tablets (controls). The intake of fish protein supplement was 3 g/d for the first 4 weeks and 6 g/d for the last 4 weeks. In this study, 8 weeks of fish protein supplementation resulted in lower values of fasting glucose (P< 0·05), 2 h postprandial glucose (P< 0·05) and glucose-area under the curve (AUC) (five measurements over 2 h, P< 0·05) after fish protein supplementation compared to controls. Glucose-AUC was decreased after 8 weeks with fish protein supplement compared to baseline (P< 0·05), concomitant with increased 30 min and decreased 90 min and 2 h insulin C-peptide level (P< 0·05), and reduced LDL-cholesterol (P< 0·05). Body muscle % was increased (P< 0·05) and body fat % was reduced (P< 0·05) after 4 weeks' supplementation. Physical activity and energy and macronutrients intake did not change during the course of the study. In conclusion, short-term daily supplementation with a low dose of fish protein may have beneficial effects on blood levels of glucose and LDL-cholesterol as well as glucose tolerance and body composition in overweight adults. The long-term effects of fish protein supplementation is of interest in the context of using more fish as a protein source in the diet, and the effects of inclusion of fish in the diet of individuals with low glucose tolerance should be evaluated.

Low-carbohydrate diets have become increasingly popular for weight loss. Although they may improve some metabolic markers, particularly in type 2 diabetes mellitus (T2D) or the metabolic syndrome (MS), their net effect on arterial wall function remains unclear. The objective was to evaluate the relation between dietary macronutrient composition and the small artery reactive hyperaemia index (saRHI), a marker of small artery endothelial function, in a cohort of patients at increased cardiovascular (CV) risk. The present cross-sectional study included 247 patients. Diet was evaluated by a 3-d food-intake register and reduced to a novel low-carbohydrate diet score (LCDS). Physical examination, demographic, biochemical and anthropometry parameters were recorded, and the saRHI was measured in each patient. Individuals in the lowest LCDS quartile (Q1, 45 % carbohydrate; 20 % protein; 32 % fat) had higher saRHI values than those in the top quartile (Q4, 29 % carbohydrate, 24 % protein, 40 % fat; 1·66 (sd 0·41) v. 1·52 (sd 0·22), P= 0·037). These results were particularly strong in patients with the MS (Q1 = 1·82 (sd 0·32) v. Q4 = 1·61 (sd 027); P= 0·021) and T2D (Q1 = 1·78 (sd 0·31) v. Q4 = 1·62 (sd 0·35); P= 0·011). Multivariate analysis demonstrated that individuals in the highest LCDS quartile had a significantly negative coefficient of saRHI, which was independent of confounders (OR − 0·85; 95 % CI 0·19, 0·92; P= 0·031). These findings suggest that a dietary pattern characterised by a low amount of carbohydrate, but high amounts of protein and fat, is associated with a poorer small artery vascular reactivity in patients with increased CV risk.

Dietary oils containing large amounts of conjugated linolenic acids (CLnA) may be regarded as a source of conjugated linoleic acids (CLA), which have been suspected to bear health-promoting properties. Indeed, CLnA can be converted into CLA in mammals. The objective of the present study was to investigate the uptake of CLnA and their metabolism into CLA in Caco-2 cells, as a validated in vitro model of the intestinal barrier. Caco-2 cells were incubated for 24 h in the presence of either α-eleostearic, β-eleostearic, catalpic or punicic acid. We first observed that Caco-2 cells take these CLnA up at different rates and then convert them but with varying efficiency depending on the structure of the Δ13 double bond. Finally, the distribution of CLnA between neutral lipids (NL) and phospholipids appeared to be linked to their number of trans double bonds: the higher the number, the higher the accumulation in the NL fraction.

Premature infants constitute a risk group for thiamin deficiency but only little is known about their thiamin status. The aim of the present study was to investigate the thiamin status of premature infants by determination of thiamin diphosphate (TDP) and to identify risk factors for low TDP concentrations. In a prospective, longitudinal study TDP was determined by HPLC in whole blood in the first days of life and approximately every 2 weeks. Demographical data, weight gain, type of nutrition and thiamin intake were recorded. A total of 111 premature infants were included at the Children's Hospital of the University of Cologne, Germany from May 2009 until December 2010 and 222 blood samples were analysed. TDP concentrations showed an age-dependent decline (age 0–10 d, mean TDP = 110·6 ng/ml; age 11–20 d, mean TDP = 95·4 ng/ml; age 21–103 d, mean TDP = 33·6 ng/ml). There was no significant difference between males and females. Young gestational age and low birth weight were associated with low TDP concentrations. No infant was diagnosed with thiamin deficiency. The current nutritional regimen in our hospital did not lead to thiamin deficiency in the study cohort. Further research is required to evaluate how TDP concentrations are regulated in premature infants.

DHA deficiency has been related to skeletal malformations in fish, but high DHA levels have produced controversial results that could relate to the oxidative status of fish tissues in the different reports. In the present study, gilthead seabream (Sparus aurata) larvae were fed deficient, adequate or high DHA levels, or high DHA levels supplemented with the antioxidant α-tocopherol. Larvae fed deficient DHA levels tended to be smaller, and showed the highest incidence of urinary bladder calculi, lordosis and kyphosis and the lowest number of mineralised vertebrae for any given size class. Elevation of dietary DHA increased larval growth and significantly enhanced the expression of the insulin-like growth factor 1 (IGF-1) gene. However, a DHA level increase up to 5 % raised the degree of lipid oxidation in larval tissues and deformities in cranial endochondral bones and in axial skeletal haemal and neural arches. The increase in dietary α-tocopherol supplementation in high-DHA feeds reduced again the occurrence of skeletal deformities. Moreover, the expression of genes coding for specific antioxidants such as catalase, superoxide dismutase or glutathione peroxidase, which neutralised reactive oxygen substances formed by increased dietary DHA, was significantly decreased in larvae fed high α-tocopherol levels. These results denoted the importance of DHA for early bone formation and mineralisation. Low dietary DHA levels delay early mineralisation and increase the risk of cranial and axial skeletal deformities. Excessive DHA levels, without an adequate balance of antioxidant nutrients, increase the production of free radicals damaging cartilaginous structures before bone formation.

The effects of maternal moderate–low physical training on postnatal development, glucose homeostasis and leptin concentration in adult offspring subjected to a low-protein diet during the perinatal period were investigated. Male Wistar rats (aged 150 d old) were divided into four groups according to maternal group: untrained (NTp, n 8); trained (Tp, n 8); untrained with a low-protein diet (NT+LPp, n 8); trained with a low-protein diet (T+LPp, n 8). The trained mothers were subjected to a protocol of moderate physical training over a period of 4 weeks (treadmill, 5 d/week, 60 min/d, at 65 % VO2max) before mating. At pregnancy, the intensity and duration of exercise was progressively reduced (50–20 min/d, at 65–30 % VO2max). The low-protein diet groups received an 8 % casein diet, and their peers received a 17 % casein diet during gestation and lactation. The pups' birth weight and somatic growth were recorded weekly up to the 150th day. Fasting blood glucose, cholesterol, serum leptin concentration, glucose and insulin tolerance tests were evaluated. The Tp animals showed no changes in somatic and biochemical parameters, while the NT+LPp group showed a greater abdominal circumference, hyperglycaemia, hypercholesterolaemia, glucose intolerance and lower plasma leptin. In the T+LPp animals, all of those alterations were reversed except for plasma leptin concentration. In conclusion, the effects of a perinatal low-protein diet on growth and development, glucose homeostasis and serum leptin concentration in the offspring were attenuated in pups from trained mothers.

The amino acid arginine is a well-known growth hormone (GH) stimulator and GH is an important modulator of linear growth. The aim of the present study was to investigate the effect of dietary arginine on growth velocity in children between 7 and 13 years of age. Data from the Copenhagen School Child Intervention Study during 2001–2 (baseline), and at 3-year and 7-year follow-up, were used. Arginine intake was estimated via a 7 d precoded food diary at baseline and 3-year follow-up. Data were analysed in a multilevel structure in which children were embedded within schools. Random intercept and slopes were defined to estimate the association between arginine intake and growth velocity, including the following covariates: sex; age; baseline height; energy intake; puberty stage at 7-year follow-up and intervention/control group. The association between arginine intake and growth velocity was significant for the third and fourth quintile of arginine intake (2·5–2·8 and 2·8–3·2 g/d, respectively) compared with the first quintile ( < 2·2 g/d) (P for trend = 0·04). Protein intake (excluding arginine) was significantly associated with growth velocity; however, the association was weaker than the association between arginine intake and growth velocity (P for trend = 0·14). The results of the present study suggest a dose-dependent physiological role of habitual protein intake, and specifically arginine intake, on linear growth in normally growing children. However, since the study was designed in healthy children, we cannot firmly conclude whether arginine supplementation represents a relevant clinical strategy. Further research is needed to investigate whether dietary arginine may represent a nutritional strategy potentially advantageous for the prevention and treatment of short stature.

The sensitisation of insulin action in response to a meal (i.e. meal-induced insulin sensitisation, MIS) represents one of the major means of increased glucose disposal in peripheral tissues during the postprandial state. MIS occurs when the release of hepatic insulin-sensitising substance (HISS) stimulates skeletal muscle glucose uptake. Our previous study had demonstrated that the HISS pathway is impaired in age-associated insulin resistance, and in the rats which were part of that study, voluntary exercise improved the response to insulin by restoring HISS action. The present study tests the hypothesis that voluntary exercise would reverse insulin resistance in diet-induced models of insulin resistance, and that the benefits are attributed through the improvement in HISS action. In this study, two experimental diets, a high-fat diet (for 4 weeks) and 35 % sucrose solution (for 9 and 16 weeks), were used to induce insulin resistance in rats. These rats were assigned to the exercise/no-exercise intervention. The effect of 7 d voluntary running-wheel exercise was determined by measuring insulin- and HISS action in the exercised rats and comparing them with the non-exercised controls. Voluntary exercise reversed insulin resistance, caused by dietary manipulation, through restoration of the HISS action. The direct insulin action was not changed by either diet or exercise. The metabolic improvements and reduced adiposity correlated with the extent of reversal of HISS action induced by exercise. Exercise improves insulin sensitivity in diet-induced insulin resistance primarily by restoration of HISS-mediated glucose uptake.

The digestive function of low birth weight (LBW) pigs post-weaning has been poorly studied. Therefore, newborns from eleven hyperprolific sows were weighed, weaned at 27·2 d and fed a starter diet until sampling. Sampling was done between 18 and 28 d post-weaning. An LBW piglet (n 19) was defined as a piglet having a birth weight less than 1 kg and less than the lower quartile of litter birth weights. Normal birth weight (NBW) piglets (n 13) were having a birth weight close to the mean litter birth weight. For each piglet, eighty-eight variables were determined. Data were analysed with linear models with type of piglet and litter as predictors. A principal component analysis was performed to determine the most important discriminating variables. In the LBW pig, the development of the digestive tract post-weaning was delayed: lower small-intestinal weight:length ratio due to a thinner tela submucosa and tunica muscularis and a higher secretory capacity, both in the distal jejunum. These observations might be a consequence of lower circulating insulin-like growth factor-1 (IGF-1) concentrations (126 (se 10·0) v. 158 (se 12·0) ng/ml for LBW and NBW, respectively) and a lower density of IGF-1 receptors in the proximal small intestine. Additionally, the plasma antioxidant capacity was lower for the LBW pig. Taken together, in the LBW piglet, the normal gut maturation post-weaning was retarded and this did not seem to be related to the weaning transition as such.

Probiotics are live micro-organisms that when administered in adequate amounts confer a health benefit on the host. Cell surface molecules of these micro-organisms are being studied in relation to their ability to interact with the host. The cell wall of lactobacilli possesses lipoteichoic acids (LTA) which are molecules with immunomodulatory properties. UV radiation (UVR) has been proposed as the main cause of skin cancer because of its mutagenic and immunosuppressive effects. Photoprotection with some nutrition interventions including probiotics has recently been shown. The aim of the present study was to investigate whether the oral administration of purified LTA from Lactobacillus rhamnosus GG can modulate the immune-suppressive effect of UVR and skin tumour development in female Crl:SKH-1-hrBR mice. For this purpose, two irradiation models were studied: (1) a chronic irradiation scheme consisting of daily irradiations during twenty consecutive days and (2) a long-term irradiation schedule, irradiating the animals three times per week, during 34 weeks for tumour development. The results showed that T-cells in the inguinal lymph node of LTA-treated mice produced higher levels of (1) interferon-γ and (2) a number of total, helper and cytotoxic T-cells compared with non-treated mice. Moreover, a significant delay in tumour appearance was found in LTA-treated mice. An increased IgA+ cell number was found in the small intestine together with a higher number of activated dendritic cells in the mesenteric lymph nodes. The latter results might be indicative of a direct effect of LTA in the gut, affecting the cutaneous immune system and restoring homeostasis through the gut–skin axis.

College students are susceptible to upper respiratory infections (URI) due to inadequate sleep, stress and close living quarters. Certain probiotic strains modulate immune function and may improve health-related quality of life (HRQL) during URI. The present study recruited apparently healthy college students and assessed the effect of probiotics on HRQL outcomes (i.e. self-reported duration, symptom severity and functional impairment of URI) in those who developed URI. Missed school and work days due to URI were also considered. Subjects (n 231) were apparently healthy college students living on campus in residence halls at the Framingham State University (Framingham, MA, USA), and were randomised to receive placebo (n 117) or probiotic-containing powder (daily dose of minimum 1 billion colony-forming units of each Lactobacillus rhamnosus LGG® (LGG®) and Bifidobacterium animalis ssp. lactis BB-12® (BB-12®); n 114) for 12 weeks. Subjects completed The Wisconsin Upper Respiratory Symptom Survey-21 to assess HRQL during URI. The final analyses included 198 subjects (placebo, n 97 and probiotics, n 101). The median duration of URI was significantly shorter by 2 d and median severity score was significantly lower by 34 % with probiotics v. placebo (P< 0·001), indicating a higher HRQL during URI. Number of missed work days was not different between groups (P= 0·429); however, the probiotics group missed significantly fewer school days (mean difference = 0·2 d) compared to the placebo group (P= 0·002). LGG® and BB-12® may be beneficial among college students with URI for mitigating decrements in HRQL. More research is warranted regarding mechanisms of action associated with these findings and the cost–benefit of prophylactic supplementation.

Secondary metabolites of herbs and spices are widely used as an alternative strategy in the therapy of various diseases. The polyphenols naringenin, quercetin and curcumin have been characterised as anti-diabetic agents. Conversely, in vitro, naringenin and quercetin are described to inhibit phosphoinositide-3-kinase (PI3K), an enzyme that is essential for the neuronal control of whole body glucose homoeostasis. Using both in vitro and in vivo experiments, we tested whether the inhibitory effect on PI3K occurs in neurons and if it might affect whole body glucose homoeostasis. Quercetin was found to inhibit basal and insulin-induced phosphorylation of Akt (Ser473), a downstream target of PI3K, in HT-22 cells, whereas naringenin and curcumin had no effect. In Djungarian hamsters (Phodopus sungorus) naringenin and quercetin (10 mg/kg administered orally) diminished insulin-induced phosphorylation of Akt (Ser473) in the arcuate nucleus, indicating a reduction in hypothalamic PI3K activity. In agreement with this finding, glucose tolerance in naringenin-treated hamsters (oral) and mice (oral and intracerebroventricular) was reduced compared with controls. Dietary quercetin also impaired glucose tolerance, whereas curcumin was ineffective. Circulating levels of insulin and insulin-like growth factor-binding protein were not affected by the polyphenols. Oral quercetin reduced the respiratory quotient, suggesting that glucose utilisation was impaired after treatment. These data demonstrate that low doses of naringenin and quercetin acutely and potently impair glucose homoeostasis. This effect may be mediated by inhibition of hypothalamic PI3K signalling. Whether chronic impairments in glucose homoeostasis occur after long-term application remains to be identified.

Cyanidin 3-glucoside (C3G) is one of the major dietary anthocyanins implicated in the prevention of chronic diseases. To evaluate the impact of human intestinal bacteria on the fate of C3G in the host, we studied the metabolism of C3G in human microbiota-associated (HMA) rats in comparison with germ-free (GF) rats. Urine and faeces of the rats were analysed for C3G and its metabolites within 48 h after the application of 92 μmol C3G/kg body weight. In addition, we tested the microbial C3G conversion in vitro by incubating C3G with human faecal slurries and selected human gut bacteria. The HMA rats excreted with faeces a three times higher percentage of unconjugated C3G products and a two times higher percentage of conjugated C3G products than the GF rats. These differences were mainly due to the increased excretion of 3,4-dihydroxybenzoic acid, 2,4,6-trihydroxybenzaldehyde and 2,4,6-trihydroxybenzoic acid. Only the urine of HMA rats contained peonidin and 3-hydroxycinnamic acid and the percentage of conjugated C3G products in the urine was decreased compared with the GF rats. Overall, the presence of intestinal microbiota resulted in a 3·7 % recovery of the C3G dose in HMA rats compared with 1·7 % in GF rats. Human intestinal bacteria rapidly degraded C3G in vitro. Most of the C3G products were also found in the absence of bacteria, but at considerably lower levels. The higher concentrations of phenolic acids observed in the presence of intestinal bacteria may contribute to the proposed beneficial health effects of C3G.

The study evaluates the effects of genistein on blood pressure (BP) and ultrastructural changes in kidney of fructose-fed hypertensive rats. Male Wistar rats were fed a diet containing 60 % starch or 60 % fructose as the source of carbohydrate. After 15 d, rats in each dietary group were divided into two groups and were treated with either genistein (1 mg/kg per d) in dimethylsulfoxide (DMSO) or 30 % DMSO alone. BP, pressor mechanisms, protein kinase C-βII (PKC-βII) expression, endothelial NO synthase (eNOS) expression and renal ultrastructural changes were evaluated after 60 d. Fructose-fed rats displayed significant elevation in BP and heart rate. Significant increase in plasma angiotensin-converting enzyme (ACE) activity, alterations in renal lipid profile, nitrite and kallikrein activity, enhanced expression of membrane-associated PKC-βII and decreased expression of eNOS were observed in them. Histology and electron microscopic studies showed structural changes in the kidney. Genistein administration lowered BP, restored ACE, PKC-βII and eNOS expression and preserved renal ultrastructural integrity. These findings demonstrate that genistein has effects on eNOS activity in renal cells, leading to eNOS activation and NO synthesis. These effects could have been mediated by activation of PKC-βII. The observed benefits of genistein make it a promising candidate for therapy of diabetic kidney disease.

Probiotics are live micro-organisms that when given in adequate amounts can cause health benefits. The safety and efficacy of probiotics in the prevention and treatment of various clinical conditions have been evaluated in randomised controlled clinical trials, systematic reviews and meta-analyses. Generally, their safety has been documented. As a supplement to standard rehydration therapy, probiotics have been demonstrated to shorten the duration of diarrhoea resulting from acute viral gastroenteritis and in preventing antibiotic-associated diarrhoea in healthy children. Preliminary evidence suggests that probiotics might prevent necrotising enterocolitis in very-low-birth-weight infants, but further studies are needed before definite conclusions can be drawn. Probiotics have also been assessed in the treatment and prevention of allergic disease but the results, although promising, need further confirmation. Targeting a paediatric population, probiotics have been evaluated in the treatment of irritable bowel syndrome, ulcerative colitis, Helicobacter pylori gastritis and infantile colic, but at this stage, there is no evidence to support their routine use for these indications. There is a great need for studies aiming at disentangling the mechanisms by which probiotics mediate their clinical effects and for comparative studies between various probiotic bacteria. We still need to know which probiotic(s) to use and for which indications. A clearer message on dosages, optimal timing and duration of administration is needed. For this purpose, more carefully designed and sufficiently powered, randomised controlled trials with predefined outcomes are needed.

The present study analyses the effect of dietary chia seed rich in n-3 α-linolenic acid on the mechanisms underlying dyslipidaemia and liver steatosis developed in rats fed a sucrose-rich diet (SRD) for either 3 weeks or 5 months. The key hepatic enzyme activities such as fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), glucose-6-phosphate dehydrogenase (G-6-PDH), carnitine palmitoyltransferase-1 (CPT-1) and fatty acid oxidase (FAO) involved in lipid metabolism and the protein mass levels of sterol regulatory element-binding protein-1 (SREBP-1) and PPARα were studied. (1) For 3 weeks, Wistar rats were fed either a SRD with 11 % of maize oil (MO) as dietary fat or a SRD in which chia seed replaced MO (SRD+Chia). (2) A second group of rats were fed a SRD for 3 months. Afterwards, half the rats continued with the SRD while for the other half, MO was replaced by chia for 2 months (SRD+Chia). In a control group, maize starch replaced sucrose. Liver TAG and the aforementioned parameters were analysed in all groups. The replacement of MO by chia in the SRD prevented (3 weeks) or improved/normalised (5 months) increases in dyslipidaemia, liver TAG, FAS, ACC and G-6-PDH activities, and increased FAO and CPT-1 activities. Protein levels of PPARα increased, and the increased mature form of SREBP-1 protein levels in the SRD was normalised by chia in both protocols (1 and 2). The present study provides new data regarding some key mechanisms related to the fate of hepatic fatty acid metabolism that seem to be involved in the effect of dietary chia seed in preventing and normalising/improving dyslipidaemia and liver steatosis in an insulin-resistant rat model.

Previous national nutrition surveys in Irish adults did not include blood samples; thus, representative serum 25-hydroxyvitamin D (25(OH)D) data are lacking. In the present study, we characterised serum 25(OH)D concentrations in Irish adults from the recent National Adult Nutrition Survey, and determined the impact of vitamin D supplement use and season on serum 25(OH)D concentrations. Of the total representative sample (n 1500, aged 18+ years), blood samples were available for 1132 adults. Serum 25(OH)D was measured via immunoassay. Vitamin D-containing supplement use was assessed by questionnaire and food diary. Concentrations of serum 25(OH)D were compared by season and in supplement users and non-users. Year-round prevalence rates for serum 25(OH)D concentration < 30, < 40, < 50 and < 75 nmol/l were 6·7, 21·9, 40·1 and 75·6 %, respectively (11·1, 31·1, 55·0 and 84·0 % in winter, respectively). Supplement users had significantly higher serum 25(OH)D concentrations compared to non-users. However, 7·5 % of users had winter serum 25(OH)D < 30 nmol/l. Only 1·3 % had serum 25(OH)D concentrations >125 nmol/l. These first nationally representative serum 25(OH)D data for Irish adults show that while only 6·7 % had serum 25(OH)D < 30 nmol/l (vitamin D deficiency) throughout the year, 40·1 % had levels considered by the Institute of Medicine as being inadequate for bone health. These prevalence estimates were much higher during winter time. While vitamin D supplement use has benefits in terms of vitamin D status, at present rates of usage (17·5 % of Irish adults), it will have only very limited impact at a population level. Food-based strategies, including fortified foods, need to be explored.

The present study investigated dietary intake, glucose metabolism and sex hormones in women with polycystic ovary syndrome (PCOS). A total of forty-five women (aged 25–40 years) with PCOS and 161 control women (aged 25–43 years) with non-PCOS-related infertility were recruited. Anthropometry, glucose tolerance and sex hormones were determined and dietary intake was assessed. Women with PCOS had lower serum sex hormone-binding globulin and increased BMI, waist:hip ratio, luteinising hormone, ratio of luteinising hormone:follicle-stimulating hormone, testosterone and free androgen index (FAI). Postprandial glucose, fasting insulin and insulin resistance were elevated in women with PCOS. Women with PCOS had reduced energy and carbohydrate intake but higher fat intake. Serum sex hormone-binding globulin level was negatively associated with BMI in both groups and negatively correlated with macronutrient intake in the PCOS group with hyperandrogenism. However, FAI was positively correlated with BMI, waist circumference and glucose metabolic parameters in both groups. Therefore, women with PCOS consume lower energy and carbohydrate compared with those with non-PCOS-related infertility and macronutrient intake is only negatively associated with serum sex hormone-binding globulin level in the PCOS group with hyperandrogenism.

Lactating rats reinfected with Nippostrongylus brasiliensis fed low-crude protein (CP) foods show reduced lactational performance and less resistance to parasites compared with their high-CP counterparts. Here, we hypothesised that feeding high-CP foods deficient in specific essential amino acids (AA) would result in similar penalties. Second-parity lactating rats, immunised with 1600 N. brasiliensis infective larvae before mating, were fed foods with either 250 (high protein; HP) or 150 (low protein; LP) g CP/kg, or were HP deficient in either leucine (HP-Leu) or methionine (HP-Met). On day 1 of lactation, litter size was standardised at twelve pups. On day 2, dams were either reinfected with 1600 N. brasiliensis larvae or sham-infected with PBS. Dams and litters were weighed daily until either day 8 or 11, when worm burdens, and inflammatory cells and systemic levels of N. brasiliensis-specific Ig isotypes were assessed. Data from five out of sixteen HP-Met rats were omitted due to very high levels of food refusals from parturition onwards. Relative to feeding HP foods, feeding LP, HP-Met and HP-Leu foods reduced dam weight gain and, to a lesser extent, litter weight gain, and increased the number of worm eggs in the colon, indicative of a reduction in resistance to parasites. However, only feeding LP and HP-Leu foods resulted in increased worm numbers, while none of the feeding treatments affected systemic Ig, mast and goblet cells, and eosinophil numbers. The present results support the view that resistance to parasites during lactation may be sensitive to specific essential AA scarcity.

Physical functional ability and nutritional status are two major indicators for predicting the risk of mortality in older adults. The present study examined the complementarity of the Activities of Daily Living (ADL) and the Mini-Nutritional Assessment (MNA) for predicting follow-up 4-year all-cause mortality risk in elderly Taiwanese. We analysed data of the ‘Survey of Health and Living Status of the Elderly in Taiwan’, a population-based longitudinal cohort study which involved 2872 men and women of ≥ 65 years old at baseline (1999). We rated their functional dependency with the ADL scale and nutritional status with the MNA (both the long form, LF and the short form, SF) at baseline, and analysed the complementarity of the two scales in predicting follow-up 4-year all-cause mortality with Cox regression analysis and the net reclassification improvement (NRI) to quantify the improvement. The results showed that both ADL and MNA offered improvement in predicting follow-up mortality risk beyond that predicted by either one alone according to the Akaike information criterion and the NRI. The MNA-SF was nearly as effective as the MNA-LF in improving the predictive ability of the ADL. The present study suggests that the MNA (especially the SF because of its simplicity and time-saving feature) together with the ADL scale might be of value for predicting the mortality risk of frail elderly living in various settings.