The present study was conducted to investigate the effect of digestion rate of dietary starch on postprandial systemic circulating glucose, insulin and lipid profiles, and the activity and gene expression of lipid metabolism-related enzymes in weaned pigs. A total of twenty-four weaned pigs, surgically fitted with a catheter in the jugular vein, were randomly assigned to three dietary treatment groups, representing the high digestion rate starch (HDRS) group, the moderate-digestion rate starch (MDRS) group and the low-digestion rate starch (LDRS) group. The amylopectin:amylose ratios in the diets of each group were 27·6:1, 27·6:8·5 and 1:27·6, respectively. The serum concentrations of glucose, TAG, total cholesterol, LDL-cholesterol and HDL-cholesterol in the HDRS group were increased to the peak point at postprandial 1·5, 2·5, 2·5, 1·5 and 1·5 h, those in the MDRS group were at postprandial 2·5, 3·5, 3·5, 3·5 and 3·5 h and those in the LDRS group were at postprandial 2·5, 3·5, 3·5, 1·5 and 3·5 h, respectively. The serum concentration of insulin in the HDRS group was higher (P < 0·05) than those in the MDRS group, and those in the MDRS group was also higher (P < 0·05) than those in the LDRS group at postprandial 0·5, 1·5 and 2·5 h, respectively. The serum concentrations of acetate, propionate and butyrate in the HDRS group were higher (P < 0·05) than those in the MDRS group, and those in the MDRS group were higher (P < 0·05) than in the LDRS group in each feeding cycle, in turn, respectively. The activity of fatty acid synthase (FAS) in the liver and abdominal adipose tissues, that of acetyl CoA carboxylase (ACC) in the myocardium and interscapular brown adipose tissues and that of the ATP-citrate lyase (ATP-CL) in the liver and interscapular brown adipose tissues in pigs of the HDRS group were higher (P < 0·05) than that of the MDRS group. The mRNA levels of FAS in the myocardium, liver and interscapular brown adipose tissues of pigs in the HDRS group were higher (P < 0·05) than those of the MDRS group. The activities and mRNA levels of FAS, ACC and ATP-CL in the myocardium, liver, abdominal and interscapular brown adipose tissues of the HDRS group were higher than those of the LDRS group. We conclude that the digestion rate of dietary starch affected not only the postprandial systemic circulating levels of glucose and insulin but also the lipid metabolism in weaned pigs. Dietary starch with higher digestion rate produces higher blood glucose and insulin response, ameliorates the blood lipid profiles and up-regulates the activity and gene expression profile of lipid metabolism-related genes in weaned pigs.

Epidemiological data indicate that low serum vitamin D concentrations are associated with an increased risk of a variety of human tumours. Cutaneous mast cell tumours (MCT) occur more frequently in dogs than in any other species. Canine MCT express the vitamin D receptor, and vitamin D derivatives have in vitro and in vivo anti-tumour activity. We sought to examine the association between vitamin D serum level and MCT in Labrador retrievers, a dog breed predisposed to MCT development. To examine this association, serum 25-hydroxyvitamin D3 (25(OH)D3) concentrations were examined in eighty-seven Labrador retrievers, including thirty-three with MCT and fifty-four unaffected controls. The relationship between cases and controls and 25(OH)D3 level, age and body condition score were evaluated using univariate and multivariate analyses. Potential differences in vitamin D oral intake, calculated on the basis of a dietary questionnaire, were also evaluated between groups. Mean 25(OH)D3 concentration (104 (sd 30) nmol/l) in dogs with MCT was significantly lower than that of unaffected dogs (120 (sd 35) nmol/l; P = 0·027). The mean calculated vitamin D intake per kg body weight in Labrador retrievers with MCT was not statistically different from that of unaffected Labrador retrievers (0·38 (sd 0·25) and 0·31 (sd 0·22) μg/kg body weight, respectively; P = 0·13). These findings suggest that low levels of 25(OH)D3 might be a risk factor for MCT in Labrador retrievers. Prospective cohort studies are warranted.

Metabolic diseases in China have been on the rise during recent decades. To investigate dietary glycaemic load (GL) and its correlation with the prevalence of metabolic diseases in hospitalised Chinese adults, we analysed the total energy and macronutrient intakes in 1040 patients. Dietary GL was calculated based upon glycaemic index (GI), carbohydrate content and daily intake of individual foods. Dietary patterns at different dietary GL levels and the distribution of dietary GL were analysed in patients from the internal medical departments v. those from surgical departments. Height and weight were measured using a standardised protocol. The present study results demonstrated that in hospitalised adults, 95·5 % of dietary GL came from cereals. Average GL was higher in male patients than in female patients, and was higher in patients from surgical departments than in patients from medical departments. Patients with lower dietary GL consumed inadequate carbohydrates and excessive fats, and therefore had a higher prevalence of overweight and obesity. Dietary GL analysis may be helpful to nutrition assessment and rational diet intervention in hospitalised Chinese patients.

Phenolic compounds are one of the main reasons behind the healthy properties of virgin olive oil (VOO). However, their daily intake from VOO is low compared with that obtained from other phenolic sources. Therefore, the intake of VOO enriched with its own phenolic compounds could be of interest to increase the daily dose of these beneficial compounds. To evaluate the effectiveness of enrichment on their bioavailability, the concentration of phenolic compounds and their metabolites in human plasma (0, 60, 120, 240 and 300 min) from thirteen healthy volunteers (seven men and six women, aged 25 and 69 years) was determined after the ingestion of a single dose (30 ml) of either enriched virgin olive oil (EVOO) (961·17 mg/kg oil) or control VOO (288·89 mg/kg oil) in a cross-over study. Compared with VOO, EVOO increased plasma concentration of the phenol metabolites, particularly hydroxytyrosol sulphate and vanillin sulphate (P < 0·05). After the consumption of VOO, the maximum concentration of these peaks was reached at 60 min, while EVOO shifted this maximum to 120 min. Despite these differences, the wide variability of results indicates that the absorption and metabolism of olive oil phenols are highly dependent on the individual.

Se plays many important roles in humans. Marginal Se status has been associated with adverse health effects including an increased risk of chronic disease such as cancer. There are few Australian data, but the population of Tasmania, Australia, is potentially at risk of marginal Se status. A cross-sectional study of 498 men and women aged 25–84 years was undertaken to assess the Se status of the northern Tasmanian population. Se status was assessed using dietary estimates and measures of serum Se and glutathione peroxidase (GPx). Mean Se intakes were 77·4 (sd 31·3) and 65·1 (sd 23·7) μg/d for men and women, respectively; 27 % of the subjects consumed less than the Australian/New Zealand estimated average requirement. Mean serum Se concentration was 89·1 (sd 15·1) μg/l; 83 % of the study subjects had serum Se concentrations below 100 μg/l and 60 % had serum Se concentration below 90 μg/l, suggesting that Se status in many subjects was inadequate for maximal GPx activity. This was supported by the positive association between serum Se and serum GPx (P < 0·001), indicating that enzyme activity was limited by Se concentrations. The lowest mean serum Se concentrations were observed in the oldest age ranges; however, the prevalence of marginal Se status was similar across age ranges and did not appear to be influenced by sex or socio-economic status. The prevalence of marginal Se status was high in all sex and age subgroups, suggesting that the northern Tasmanian population could benefit from increasing Se intakes.

The weaning period is associated with an increased prevalence of gastrointestinal infection in many species. Glutamine (Gln) has been shown to improve intestinal barrier function and immune function in both in vivo and in vitro models. The objective of the present study was to determine the effect of dietary Gln supplementation on intestinal barrier function and intestinal cytokines in a model of Escherichia coli infection. We randomised 21-d-old piglets (n 20) to nutritionally complete isonitrogenous diets with or without Gln (4·4 %, w/w) for 2 weeks. Intestinal loops were isolated from anaesthetised pigs and inoculated with either saline or one of the two E. coli (K88AC or K88 wild-type)-containing solutions. Intestinal tissue was studied for permeability, cytokine expression, fluid secretion and tight-junction protein expression. Animals receiving Gln supplementation had decreased potential difference (PD) and short-circuit current (Isc) in E. coli-inoculated intestinal loops (PD 0·628 (sem 0·151) mV; Isc 13·0 (sem 3·07) μA/cm2) compared with control-fed animals (PD 1·36 (sem 0·227) mV; Isc 22·4 (sem 2·24) μA/cm2). Intestinal tissue from control, but not from Gln-supplemented, animals responded to E. coli with a significant increase in mucosal cytokine mRNA (IL-1β, IL-6, transforming growth factor-β and IL-10). Tight-junction protein expression (claudin-1 and occludin) was reduced with exposure to E. coli in control-fed animals and was not influenced in Gln-supplemented piglets. Gln supplementation may be useful in reducing the severity of weaning-related gastrointestinal infections, by reducing the mucosal cytokine response and altering intestinal barrier function.

A 6-month experiment with nine dietary treatments was conducted to determine amounts of S plus Mo supplements required to maintain normal hepatic concentrations of Cu and Mo and to prevent chronic Cu toxicity in lambs fed palm kernel cake (PKC) diets. All diets consisted of PKC supplemented with minerals and vitamins, and with appropriate amounts per kg DM of S (level 0 or level 1 = 1 g) as sodium sulfate and/or Mo (level 0; level 1 = 4 mg; level 2 = 8 mg; level 3 = 16 mg; level 4 = 32 mg) as ammonium molybdate to form treatments S0Mo1, S0Mo2, S0Mo3, S0Mo4, S1Mo0, S1Mo1, S1Mo2, S1Mo3 and S1Mo4.There was no effect (P>0·05) of dietary treatments on the growth performance of the lambs. The dietary supplement of 1 g S plus 8 mg Mo per kg dietary DM (treatment S1Mo2) prevented accumulation of Cu in the liver without elevation of the concentration of Mo (P>0·05). The treatments S0Mo1, S0Mo2 and S0Mo3 increased (P < 0·05) hepatic Cu concentrations from 376 μg/g DM to between 1090 and 1294 μg/g DM. Also, the treatments S1Mo3 and S1Mo4 resulted in higher (P < 0·05) hepatic Mo concentrations compared with the treatment S1Mo0. It was concluded that the dietary supplement of 1 g S plus 8 mg Mo/kg PKC DM added to the PKC used is sufficient to maintain normal hepatic concentrations of Cu and Mo and to prevent chronic Cu toxicity in sheep fed diets containing any amount of PKC.

Excessive iodine intake can cause thyroid function disorders as can be caused by iodine deficiency. There are many people residing in areas with high iodine levels in drinking-water in China. The main aim of the present study was to map the geographical distribution of drinking-water with high iodine level in China and to determine the relationship between high iodine level in drinking-water and goitre prevalence. Iodine in drinking-water was measured in 1978 towns of eleven provinces in China, with a total of 28 857 water samples. We randomly selected children of 8–10 years old, examined the presence of goitre and measured their urinary iodine in 299 towns of nine provinces. Of the 1978 towns studied, 488 had iodine levels between 150 and 300 μg/l in drinking-water, and in 246 towns, the iodine level was >300 μg/l. These towns are mainly distributed along the original Yellow River flood areas, the second largest river in China. Of the 56 751 children examined, goitre prevalence was 6·3 % in the areas with drinking-water iodine levels of 150–300 μg/l and 11·0 % in the areas with drinking-water iodine >300 μg/l. Goitre prevalence increased with water and urinary iodine levels. For children with urinary iodine >1500 μg/l, goitre prevalence was 3·69 times higher than that for those with urinary iodine levels of 100–199 μg/l. The present study suggests that drinking-water with high iodine levels is distributed in eleven provinces of China. Goitre becomes more prevalent with the increase in iodine level in drinking-water. Therefore, it becomes important to prevent goitre through stopping the provision of iodised salt and providing normal drinking-water iodine through pipelines in these areas in China.

The present study assessed the effects of mild dehydration on cognitive performance and mood of young males. A total of twenty-six men (age 20·0 (sd 0·3) years) participated in three randomised, single-blind, repeated-measures trials: exercise-induced dehydration plus a diuretic (DD; 40 mg furosemide); exercise-induced dehydration plus placebo containing no diuretic (DN); exercise while maintaining euhydration plus placebo (EU; control condition). Each trial included three 40 min treadmill walks at 5·6 km/h, 5 % grade in a 27·7°C environment. A comprehensive computerised six-task cognitive test battery, the profile of mood states questionnaire and the symptom questionnaire (headache, concentration and task difficulty) were administered during each trial. Paired t tests compared the DD and DN trials resulting in >1 % body mass loss (mean 1·59 (sd 0·42) %) with the volunteer's EU trial (0·01 (sd 0·03) %). Dehydration degraded specific aspects of cognitive performance: errors increased on visual vigilance (P = 0·048) and visual working memory response latency slowed (P = 0·021). Fatigue and tension/anxiety increased due to dehydration at rest (P = 0·040 and 0·029) and fatigue during exercise (P = 0·026). Plasma osmolality increased due to dehydration (P < 0·001) but resting gastrointestinal temperature was not altered (P = 0·238). In conclusion, mild dehydration without hyperthermia in men induced adverse changes in vigilance and working memory, and increased tension/anxiety and fatigue.

Vegetable oils containing α-linolenic acid (ALA; 18 : 3n-3) have been shown to modulate the functions of immunocompetent cells. The aim of the present study was to understand the modulatory effect of ALA-rich garden cress (Lepidium sativum L.) seed oil (GCO) on lipid composition, spleen lymphocyte (SL) proliferation and inflammatory mediator production by peritoneal macrophages (PMΦ) in rats. Female Wistar rats were fed diets containing either GCO (2·5, 5·0 and 10 %, w/w) or sunflower oil (SFO, 10 % w/w) for 8 weeks. Ex vivo proliferation of SL was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. IL-2 and TNF-α in SL and PMΦ were analysed by ELISA. Inflammatory mediators such as NO, leukotriene B4 (LTB4) and H2O2 were measured in mitogen-activated PMΦ. GCO significantly increased the levels of ALA, EPA and DHA, but reduced linoleic acid and arachidonic acid in SL and PMΦ lipids. GCO (10 %) significantly decreased the concanavalin A (Con-A)- and phytohaemagglutinin-mediated proliferation of SL by 54 and 38 %, respectively, in comparison with SFO. A marginal decrease in IL-2 and TNF-α was observed in Con-A-stimulated SL and lipopolysaccharide-stimulated PMΦ. LTB4 levels in Ca ionophore-stimulated PMΦ were reduced by 40 % in GCO-fed rats. NO release in response to various stimuli was significantly decreased in PMΦ of GCO-fed rats. The present study is the first report on the modulatory efficacy of GCO on immunomediators in rats. GCO modulated inflammatory mediators such as NO and LTB4, and thus may play a role in alleviating inflammatory conditions favourably.

An increasing amount of fructose in the diet is suggested to play a causal role in the pathogenesis of the metabolic syndrome, type 2 diabetes and fatty liver. Our aim was to investigate and compare the effects of very high fructose and very high glucose in hyperenergetic diets on glucose and lipid metabolism and on fat depots in healthy humans. We conducted an exploratory, prospective, randomised, single-blinded, intervention trial. Participants in addition to a balanced weight-maintaining diet received 150 g of fructose or glucose/d for 4 weeks. Insulin sensitivity was estimated from oral glucose tolerance tests. Visceral and subcutaneous abdominal fat was determined with MRI. Liver fat and intramyocellular lipids of the tibialis anterior muscle were measured with 1H magnetic resonance spectroscopy. A total of twenty healthy subjects (fructose group n 10 and glucose group n 10; twelve males and eight females) completed the study. They had a mean age of 30·5 (sem 2·0) years and a mean BMI of 25·9 (sem 0·5) kg/m2. Insulin sensitivity appeared to decrease both in the fructose and glucose groups. TAG markedly increased in the fructose group. No strong alterations or treatment effects were found for liver fat, visceral fat, subcutaneous abdominal fat and intramyocellular lipids of the tibialis anterior muscle. In conclusion, the effects of very high fructose and very high glucose in hyperenergetic diets on glucose metabolism and body fat composition were not different in the healthy participants of the present study. However, elevation of plasma TAG seemed to be fructose-specific.

A low-carbohydrate, high-protein (LCHP) diet is often recommended for the prevention and management of diabetes in cats; however, the effect of macronutrient composition on insulin sensitivity and energetic efficiency for weight gain is not known. The present study compared the effect in adult cats (n 32) of feeding a LCHP (23 and 47 % metabolisable energy (ME)) and a high-carbohydrate, low-protein (HCLP) diet (51 and 21 % ME) on fasting and postprandial glucose and insulin concentrations, and on insulin sensitivity. Tests were done in the 4th week of maintenance feeding and after 8 weeks of ad libitum feeding, when weight gain and energetic efficiency of each diet were also measured. When fed at maintenance energy, the HCLP diet resulted in higher postprandial glucose and insulin concentrations. When fed ad libitum, the LCHP diet resulted in greater weight gain (P < 0·01), and was associated with higher energetic efficiency. Overweight cats eating the LCHP diet had similar postprandial glucose concentrations to lean cats eating the HCLP diet. Insulin sensitivity was not different between the diets when cats were lean or overweight, but glucose effectiveness was higher after weight gain in cats fed the HCLP diet. According to the present results, LCHP diets fed at maintenance requirements might benefit cats with multiple risk factors for developing diabetes. However, ad libitum feeding of LCHP diets is not recommended as they have higher energetic efficiency and result in greater weight gain.

Salmon provides long-chain (LC) n-3 PUFA and Se, which are well recognised for their health benefits. The n-3 and Se status of the New Zealand population is marginal. The objective of the present study was to compare the effects of consuming salmon v. supplementation with salmon oil on LC n-3 and Se status. Healthy volunteers (n 44) were randomly assigned to one of four groups consuming 2 × 120 g servings of salmon/week or 2, 4 or 6 salmon oil capsules/d for 8 weeks. Linear regression analysis predictive models were fitted to the capsule data to predict changes in erythrocyte LC n-3 levels with intakes of LC n-3 from capsules in amounts equivalent to that consumed from salmon. Changes in Se status (plasma Se and whole-blood glutathione peroxidase) were compared between the groups consuming salmon and capsules (three groups combined). Salmon, 2, 4 and 6 capsules provided 0·82, 0·24, 0·47 and 0·69 g/d of LC n-3 fatty acids. Salmon provided 7 μg/d and capsules < 0·02 μg/d of Se. The predictive model (r2 0·31, P = 0·001) showed that increases in erythrocyte LC n-3 levels were similar when intakes of 0·82 g/d LC n-3 from salmon or capsules (1·92 (95 % CI 1·35, 2·49) v. 2·32 (95 % 1·76, 2·88) %) were consumed. Plasma Se increased significantly more with salmon than with capsules (12·2 (95 % CI 6·18, 18·12) v. 1·57 (95 % CI − 2·32, 5·45) μg/l, P = 0·01). LC n-3 status was similarly improved with consumption of salmon and capsules, while consuming salmon had the added benefit of increasing Se status. This is of particular relevance to the New Zealand population that has marginal LC n-3 and Se status.

It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55–70 % carbohydrate, 9·5–16 % fat, 7–20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.

Energetic efficiency was evaluated in composite bred heifers born from dams receiving 1·8 or 1·2 kg/d winter supplementation for approximately 80 d before parturition. Heifers were then developed post-weaning and randomly assigned to heifer development treatments of either control (100 %; ad libitum; n 8/year) or restricted (80 %; fed 80 % of supplementation fed to controls adjusted to a common body weight: n 8/year) in a 2-year study. A glucose tolerance test (GTT) and acetate irreversible loss test (AILT) were administered to heifers at the termination of a 140 d development period when the heifers were approximately 403 d of age and consumed a silage-based diet, and again at 940 d of age when pregnant with their second calf and grazing dormant forage. No differences were measured (P>0·08) for dam winter nutrition or heifer development treatment for baseline serum metabolites or measures in either the GTT or the AILT. However, changes in baseline serum concentrations (P>0·05) were different between metabolic challenges, which occurred at different stages of development. No difference in acetate disappearance (P = 0·18) and half-life (P = 0·66) was measured between the two metabolic challenges. A trend for glucose half-life to be shorter in heifers born from dams receiving in utero winter treatments that supplied 1·2 kg/d of winter supplementation was observed (P = 0·083). Heifers developed with lower total DM intake during a 140 d development period had similar glucose and acetate incorporation rates as ad libitum-fed heifers when evaluated at two different production stages.

The goal of the present study was to elucidate the mechanisms of immunoregulation by which dietary punicic acid (PUA) prevents or ameliorates experimental inflammatory bowel disease (IBD). The expression of PPARγ and δ, their responsive genes and pro-inflammatory cytokines was assayed in the colonic mucosa. Immune cell-specific PPARγ null, PPARδ knockout and wild-type mice were treated with PUA and challenged with 2·5 % dextran sodium sulphate (DSS). The prophylactic efficacy of PUA was examined in an IL-10− / −  model of IBD. The effect of PUA on the regulatory T-cell (Treg) compartment was also examined in mice with experimental IBD. PUA ameliorated spontaneous pan-enteritis in IL-10− / −  mice and DSS colitis, up-regulated Foxp3 expression in Treg and suppressed TNF-α, but the loss of functional PPARγ or δ impaired these anti-inflammatory effects. At the cellular level, the macrophage-specific deletion of PPARγ caused a complete abrogation of the protective effect of PUA, whereas the deletion of PPARδ or intestinal epithelial cell-specific PPARγ decreased its anti-inflammatory efficacy. We provide in vivo molecular evidence demonstrating that PUA ameliorates experimental IBD by regulating macrophage and T-cell function through PPARγ- and δ-dependent mechanisms.

Maternal protein restriction causes metabolic alterations associated with hypothalamic dysfunction. Because the consequences of metabolic programming can be passed transgenerationally, the present study aimed to assess whether maternal protein restriction alters the expression of hypothalamic neuropeptides in offspring and to evaluate hormonal and metabolic changes in male offspring from the F1 and F2 generations. Female Swiss mice (F0) were mated and fed either a normal-protein (NP group; 19 % protein) or a low-protein (LP group; 5 % protein) diet throughout gestation of the F1 generation (NP1 and LP1). At 3 months of age, F1 females were mated to produce the F2 generation (NP2 and LP2). Animals from all groups were evaluated at 16 weeks of age. LP1 offspring had significantly lower weights and shorter lengths than NP1 offspring at birth, but they underwent a phase of rapid catch-up growth. Conversely, the LP2 offspring were not significantly different from the NP2 offspring in either weight or length. At 16 weeks, no differences were found in body mass among any of the groups, although LP1 and LP2 offspring showed hypercholesterolaemia, hypertriacylglycerolaemia, hyperglycaemia, glucose intolerance, insulin resistance, increased levels of insulin, leptin and resistin, decreased endogenous leptin sensitivity, increased adiposity with elevated leptin levels and leptin resistance characterised by altered expression of neuropeptide Y and pro-opiomelanocortin without any changes in the leptin receptor Ob-Rb. We conclude that severe maternal protein restriction promotes metabolic programming in F1 and F2 male offspring due to a dysregulation of the adipoinsular axis and a state of hypothalamic leptin resistance.

The objective of the present study was to explore the consistency of dietary choices made by children as they grow up. The dietary habits of 342 healthy children were reported annually from 5 to 13 years on a forty-five-item FFQ and analysed by factor analysis. The same two principal dietary patterns – ‘Healthy’ and ‘Unhealthy’ – emerged each year, and their consistency was assessed using Tucker's congruence coefficient (φ). Individual dietary z-scores for both of these patterns were then calculated every year for each child, and their consistency was measured by Pearson's correlation coefficient (r). Linear mixed-effects modelling was used to investigate individual trends and to quantify reliability of the individual dietary z-scores. Dietary patterns were moderately consistent and systematic over time (0·65 ≤ φHealthy ≤ 0·76; 0·62 ≤ φUnhealthy ≤ 0·78). Individual choices were also consistent year-on-year (0·64 ≤ rHealthy ≤ 0·71; 0·57 ≤ rUnhealthy ≤ 0·68). Reliability rose from 70 % with a single measure to over 90 % with four consecutive measures. The quality of diet diminished over time in 29 % of the children and improved in only 14 %. Dietary habits appear to be set early and seldom improve spontaneously.

Menaquinone-7 (MK-7), a member of the vitamin K2 family, performs several functions, all related to its recognised effect on post-translational carboxylation of certain protein-bound glutamate residues. Due to its lipophilic structure MK-7 is soluble in olive oil, so the aim of the present study was to test whether extra-virgin (EV) olive oil enriched with MK-7 significantly increases MK-7 plasma levels and has an effect on osteocalcin and its carboxylation status. Healthy young volunteers (n 12) were administered 20 ml EV olive oil per d for 2 weeks, followed by 2 weeks of the same amount of olive oil enriched with 45 μg and then 90 μg MK-7, with an appropriate washout time in between. Blood was collected and plasma separated in each phase of the study. We found that integration of the diet with EV olive oil alone did not produce any significant variation of MK-7 plasma levels compared with baseline. Supplementation with MK-7-enriched olive oil resulted in a significant and dose-dependent increase in plasma levels. The high dose also significantly increased carboxylated osteocalcin (cOC) and decreased undercarboxylated osteocalcin (ucOC) plasma levels, resulting in a significant increase in the cOC:ucOC ratio. A significant correlation was also found between percentage variation of plasma cOCA:ucOC ratio and increase in plasma MK-7 levels. We conclude that regular consumption of MK-7-enriched olive oil may constitute a valid approach in order to preserve some key biochemical mechanisms controlling bone mineralisation.

Potatoes, especially mashed potatoes, are known to result in high glycaemic and insulinaemic responses. However, in most meals, potatoes are accompanied by other foods. The objective of the present study was to investigate how glycaemic and insulinaemic responses to a mashed potato meal changed when a high-fat food (rapeseed oil), a high-protein food (chicken breast) and/or salad were added to the meal. Healthy subjects (n 11) ingested the test meals once and the reference food (glucose solution) twice in a random order at 1-week intervals. Capillary blood samples were then drawn for 2 h, and glucose and insulin were analysed. The 2 h glycaemic responses to six mashed potato-containing meals varied more than twofold. The glycaemic index (GI) of pure mashed potato was 108, whereas combined with chicken breast, rapeseed oil and salad, it was only 54. The latter GI also differed considerably from its predicted value of 103, which was based on the individual GI of the components of the meal. The insulinaemic indices of the mashed potato-based meals varied between 94 and 148. Chicken breast in the meal increased the insulinaemic response, and rapeseed oil diminished it. However, the insulinaemic response to mashed potato with chicken breast and rapeseed oil was lower than that to mashed potato alone. In conclusion, the protein, fat and salad contents of a meal exert considerable influence on the glycaemic and insulinaemic responses to mashed potatoes. Furthermore, the estimation of the GI of a mixed meal by calculation is imprecise.