Human beings are susceptible to sustained weight gain in the modern environment. Although both men and women can get fat, they get fat in different ways, and suffer different consequences. We review differences between men and women in the incidence of obesity, fat deposition patterns, fat metabolism, and the health consequences of obesity, and examine potential evolutionary explanations for these differences. Women generally have a larger proportion of body mass as fat, and are more likely to deposit fat subcutaneously and on their lower extremities; men are more likely to deposit fat in the abdominal region. Excess adipose tissue in the abdominal region, especially visceral fat, is associated with more health risks. Women have higher rates of reuptake of NEFA into adipose tissue; however, they also have higher rates of fat oxidation during prolonged exercise. Oestrogen appears to underlie many of these differences. Women bear higher nutrient costs during reproduction. Fat and fertility are linked in women, through leptin. Low leptin levels reduce fertility. Ovarian function of adult women is associated with their fatness at birth. In our evolutionary past food insecurity was a frequent occurrence. Women would have benefited from an increased ability to store fat in easily metabolisable depots. We suggest that the pattern of central obesity, more commonly seen in men, is not adaptive, but rather reflects the genetic drift hypothesis of human susceptibility to obesity. Female obesity, with excess adiposity in the lower extremities, reflects an exaggeration of an adaptation for female reproductive success.

Vitamin D deficiency is common in non-Western immigrant groups living in Western countries. A comparison of vitamin D status in individuals who have emigrated and individuals who remain in their country of origin is needed in order to provide information about the effect of moving to northern latitudes. A total of 196 participants aged 30–60 years in a cross-sectional population-based study in Kandy, Sri Lanka (latitude 7° north) and 242 Sri Lankans aged 31–60 years participating in a cross-sectional population-based study in Oslo, Norway (latitude 60° north) were included in the analysis. All serum samples were analysed for serum 25-hydroxyvitamin D (s-25(OH)D) in the same laboratory. Sri Lankans living in Norway had substantially lower s-25(OH)D (mean 31·5 nmol/l) compared with those living in Sri Lanka (mean 54·2 nmol/l), and the prevalence of s-25(OH)D <  25 nmol/l was 9·3 times higher (95 % CI 4·4, 19·6) in Norway compared with Sri Lanka. In Sri Lanka there was a clear seasonal variation with the lowest s-25(OH)D levels in August–September and the highest levels in November–December. We conclude that vitamin D status among Sri Lankans living in Kandy, Sri Lanka was considerably higher than that among Sri Lankans living in Oslo, Norway. The low vitamin D status commonly observed in non-Western immigrant groups living at northern latitudes should not be regarded as normal levels for these groups. However, also in Sri Lanka we found a profound seasonal variation with the lowest levels in August and September after the Monsoon.

The aim of the present study was to confirm that olive oil phenols reduce human platelet aggregability and to verify the hypothesis that cAMP- and cGMP- phosphodiesterases (PDE) could be one of the targets of the biological effect. Four extracts from oils characterized by a high phenol content (HPE), and low phenol levels (LPE) were prepared and analyzed quali- and quantitatively by HPLC-UV and electrospray ionization–MS/MS. Human washed platelets stimulated with thrombin were used for the aggregation assay. Human platelet cAMP-PDE and recombinant PDE5A1 were used as enzyme source. Platelet aggregation and enzyme activity were assayed in the presence of HPE, LPE and individual phenols. The phenol content of HPE ranged between 250 and 500 mg/kg, whereas the LPE content was 46 mg/kg. The compounds identified were hydroxytyrosol (HT), tyrosol (TY), oleuropein aglycone (OleA) and the flavonoids quercetin (QU), luteolin (LU) and apigenin (AP). OleA was the most abundant phenol (range 23·3 to 37·7 %) and LU was the most abundant flavonoid in the extracts. Oil extracts inhibited platelet aggregation with an 50% inhibitory concentration interval of 1·23–11·2 μg/ml. The inhibitory effect of individual compounds (10 μm) including homovanillyl alcohol (HVA) followed this order: OleA>LU>HT = TY = QU = HVA, while AP was inactive. All the extracts inhibited cAMP-PDE, while no significant inhibition of PDE5A1 (50μg/ml) was observed. All the flavonoids and OleA inhibited cAMP-PDE, whereas HT, TY, HVA (100 μm) were inactive. Olive oil extracts and part of its phenolic constituents inhibit platelet aggregation; cAMP-PDE inhibition is one mechanism through which olive oil phenols inhibit platelet aggregation.

To assess the effect of lupin protein on concentrations of lipids in plasma lipoproteins and liver and hepatic mRNA concentrations of genes involved in lipid metabolism, adult rats were fed egg albumin-based diets containing either lupin protein from Lupinus albus or casein (50 g/kg) supplemented (hypercholesterolaemic) or not (normolipaemic) with a cholesterol–cholate mixture for 20 d. Lupin protein compared with casein lowered the concentrations of TAG in liver (P < 0·01) and circulating VLDL + chylomicrons (P < 0·05) of hypercholesterolaemic rats, but not of normolipaemic rats. Hepatic mRNA concentrations of genes involved in fatty acid synthesis such as sterol regulatory element-binding protein-1c, glucose-6-phosphate dehydrogenase, fatty acid synthase, stearoyl-CoA desaturase-1 and acyl-CoA:glycerol-3-phosphate acyltransferase were lower and mRNA concentrations of lipoprotein lipase, hepatic lipase and apoA5 involved in TAG hydrolysis were higher in rats fed lupin protein than in rats fed casein. These effects were stronger in hypercholesterolaemic rats than in normolipaemic rats. Hypercholesterolaemic rats fed the lupin protein had higher liver cholesterol concentrations (P < 0·01) and lower levels of LDL-cholesterol (P < 0·05) than rats fed casein. No effect of lupin protein was observed on cholesterol concentration in VLDL + chylomicrons and HDL and hepatic mRNA concentrations of genes involved in cholesterol and bile acid metabolism. In conclusion, the present study shows that lupin protein has hypotriacylglycerolaemic action possibly via down regulation of fatty acid synthesis genes and up regulation of genes involved in TAG hydrolysis. Alterations in cholesterol metabolism could not be explained on the basis of mRNA data.

The mechanism that drives the growth of some colonic adenomas towards malignancy, while permitting others to remain for decades in quiescence, remains unknown. Diets can alter the growth rate of intestinal tumours but it is still unknown whether diets are able to alter the molecular biology of these adenomas in a way that predicts further outcome. To address this issue we fed Min/+ mice with two diets known to lead to different adenoma outcomes: a high-fat control diet (n 15) or a high-fat inulin-enriched (10 % w/w) diet (n 13). To study the effect of diet on cell signalling during adenoma growth, the adenomas of each Min/+ mouse were divided into three size-categories, and the levels of β-catenin, E-cadherin, cyclin D1 and matrix metalloproteinase-9, which are known to be involved in colon tumorigenesis, were determined. The growth-promoting inulin diet resulted in more large adenomas than the control feeding (P = 0·003) and doubled the total area of the adenomas (P = 0·008). The inulin diet increased the expression of nuclear β-catenin (P = 0·004) and its target cyclin D1 (P = 0·017) as the adenomas increased in size from small to large, indicating the presence of an accelerated cancerous process. Neither phenomenon was seen in the control group during adenoma growth. Our results suggest that in addition to the number, size, and growth rate of adenomatous polyps, the signalling pattern of the adenomas should also be considered when evaluating preventive dietary strategies.

Based on the potential benefits of cis-9, trans-11-conjugated linoleic acid (CLA) for human health there is interest in developing sustainable nutritional strategies for enhancing the concentration of this fatty acid in ruminant-derived foods. Most evidence to date suggests that endogenous synthesis is the major source of cis-9, trans-11 in milk fat and ruminal outflow is limited and largely independent of dietary 18 : 2n-6 supply. Four lactating cows fitted with a rumen cannula were used in a 4 × 4 Latin square with 14 d experimental periods to examine the effects of sunflower-seed oil (SFO) as a source of 18 : 2n-6 on ruminal lipid metabolism. Cows were offered grass silage-based diets supplemented with 0, 250, 500 or 750 g SFO/d. Supplements of SFO had no effect on DM intake, milk fat or protein secretion, but increased linearly (P < 0·01) milk yield and milk lactose output and shifted (P < 0·001) rumen fermentation towards propionate at the expense of acetate. SFO supplements increased linearly (P < 0·05) the flow of 18 : 0, 18 : 1, 18 : 2n-6 and total CLA at the omasum and enhanced ruminal cis-9-18 : 1, 18 : 2n-6 and 18 : 3n-3 metabolism. Flows of all-trans- (Δ4–16) and cis- (Δ9–16) 18 : 1 isomers were elevated, while increases in ruminal CLA outflow were confined to trans-8, trans-10 and geometric 9,11 and 10,12 isomers. It is concluded that supplementing grass silage-based diets with plant oils rich in 18 : 2n-6 enhances ruminal outflow of trans-11-18 : 1 and cis-9, trans-11-CLA in lactating cows.

This study examined the influence of different resistant starch (RS) varieties and conventional fibres on the efficiency of nutrient utilisation and intestinal fermentation in pigs. Thirty-six pigs (30 kg) were fed poultry meal-based diets supplemented with 10 % granular resistant corn starch (GCS), granular resistant potato starch (GPS), retrograded resistant corn starch (RCS), guar gum (GG) or cellulose for 36 d according to a completely randomised block design. Distal ileal and total tract recoveries were similar (P>0·05) among the RS varieties. Distal ileal starch recovery was higher (P < 0·05) in pigs consuming the RS diets (27–42 %) as compared with the control group (0·64 %). Consumption of GCS reduced (P < 0·05) apparent total tract digestibility and whole-body retention of crude protein in comparison with the control group. Consumption of GPS reduced (P < 0·05) total tract Ca digestibility and whole-body retention of Ca and P compared with the control group. However, consumption of RCS increased (P < 0·05) total tract Ca digestibility compared with the control group. Caecal butyrate concentration was increased (P < 0·05) following consumption of RCS and GG in comparison with the control group. Consumption of all the RS varieties reduced (P < 0·05) caecal indole concentrations compared with the control. Caecal butyrate concentrations were positively correlated (P < 0·05; r 0·63–0·83) with thermal properties among the RS varieties. We conclude that nutrient utilisation and intestinal fermentation are differentially affected by the consumption of different RS varieties and types of fibres. Thermal properties associated with different RS varieties may be useful markers for developing RS varieties with specific functionality.

Methionine is an essential amino acid and methyl donor for most transmethylation reactions in mammals. The product of transmethylation reactions is homocysteine, which is associated with enhanced risk for CVD. The aim of this study was to analyse metabolic and vascular functional consequences of a methionine-enriched diet in rats. The dose of methionine was chosen to reflect the range of over-nutrition in man. We quantified plasma levels of homocysteine, asymmetrical dimethylarginine and adenosine, determined methionine and its metabolites in tissues and blood plasma and assessed relaxation of mesenteric arteries toward acetylcholine and sodium nitroprusside. A methionine-enriched diet for 4 weeks elevated homocysteine levels in plasma 2-fold and in spleen by 70 %. The level of S-adenosylhomocysteine was increased in liver only, while methionine and S-adenosylmethionine were unchanged in all organs studied. Plasma adenosine and asymmetrical dimethylarginine levels were unchanged, as were vessel relaxations. A 2-fold elevation of plasma homocysteine, which is assigned a risk indicator for cardiovascular events, did not impair mesenteric artery vasodilatation during 4 weeks of a methionine-rich diet. Furthermore, asymmetrical dimethylarginine and adenosine, which have been shown to be changed in more severe degrees of hyperhomocysteinaemia, remained unaltered.

Red meat consumption is associated with increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions: aberrant crypt foci (ACF) and mucin-depleted foci (MDF) in rats. We have also shown that dietary Ca, antioxidant mix and olive oil inhibit haemin-induced ACF promotion, and normalize faecal lipoperoxides and cytotoxicity. Here we tested if these strategies are effective also against red meat promotion in dimethylhydrazine-induced rats. Three diets with 60 % beef meat were supplemented with calcium phosphate (31 g/kg), antioxidant agents (rutin and butylated hydroxyanisole, 0·05 % each) and olive oil (5 %). ACF, MDF, faecal water cytotoxicity, thiobarbituric acid reactive substances (TBARS) and urinary 1,4-dihydroxynonane mercapturic acid (DHN-MA) were measured. Beef meat diet increased the number of ACF (+30 %) and MDF (+100 %) (P < 0·001), which confirms our previous findings. Promotion was associated with increased faecal water TBARs ( × 4) and cytotoxicity ( × 2), and urinary DHN-MA excretion ( × 15). Ca fully inhibited beef meat-induced ACF and MDF promotion, and normalized faecal TBARS and cytotoxicity, but did not reduce urinary DHN-MA. Unexpectedly, high-calcium control diet-fed rats had more MDF and ACF in the colon than low-Ca control diet-fed rats. Antioxidant mix and olive oil did not normalize beef meat promotion nor biochemical factors. The results confirm that haem causes promotion of colon carcinogenesis by red meat. They suggest that Ca can reduce colorectal cancer risk in meat-eaters. The results support the concept that toxicity associated with the excess of a useful nutrient may be prevented by another nutrient.

Studies have shown that soya consumption has been associated with low incidence of CVD. Because the chemical structures of soya isoflavones are similar to oestrogen, the beneficial outcome may be attributed to the oestrogenicity of these compounds. In this study, effect of the soya isoflavone genistein on the mRNA expression of apoA-1 in the human hepatoma HepG2 cell was investigated. Without oestrogen receptor (ER) α transfection, soya isoflavones in the physiological range had no effect on the apoA-1 transcription. Once ERα was ectopically expressed in these cells, soya isoflavone dramatically increased the apoA-1 mRNA abundance quantified by real-time PCR. ApoA-1-reporter assays with plasmid constructed from the 5′-flanking segment upstream to the coding region revealed that the transactivation of the apoA-1 promoter was induced by the soya isoflavone in HepG2 cells expressing ERα. This induction was reduced by the anti-oestrogen ICI 182780, but not the inhibitors of protein kinase (PK) C, PKA, or mitogen-activated PK. Based on the previously identified response elements on the promoter, a series of truncated promoter reporter plasmids were then constructed. An induction profile of genistein was built and insulin response core element at − 411 to − 404 appeared to be a potential site of interaction. This study illustrated that soya isoflavones at physiological concentrations could up regulate apoA-1 mRNA expression in ERα-transfected HepG2 cells.

Despite adequate scientific evidence of the potential benefits of probiotics to human health or disease prevention, their contribution to the growth of adipose tissue remains to be established. Four-week-old male Sprague-Dawley rats were fed a diet containing skim milk (control diet) or skim milk fermented by Lactobacillus gasseri SBT2055 (LGSP diet) for 4 weeks. Their body weight gain, adipose tissue weight, adipocyte size distribution profile, blood and hepatic lipids, and serum leptin, glucose and adiponectin levels were determined. There was a significant reduction in average adipocyte size in mesenteric white adipose tissue (P = 0·004). Moreover, the rats fed the LGSP diet displayed greater numbers of small adipocytes from mesenteric and retroperitoneal adipose tissues than did those on the control diet. Whereas adiponectin concentrations did not differ between the groups, serum leptin concentrations were decreased to 32 % in the LGSP diet group compared with the control group. Concentrations of serum glucose and lipids, and liver lipids, except for the liver TAG level, were similar in the two groups. These results indicate a possible role for a fermented milk product in the regulation of adipose tissue growth.

Phytochemicals may protect cellular DNA by direct antioxidant effect or modulation of the DNA repair activity. We investigated the repair activity towards oxidised DNA in human mononuclear blood cells (MNBC) in two placebo-controlled antioxidant intervention studies as follows: (1) well-nourished subjects who ingested 600 g fruits and vegetables, or tablets containing the equivalent amount of vitamins and minerals, for 24 d; (2) poorly nourished male smokers who ingested 500 mg vitamin C/d as slow- or plain-release formulations together with 182 mg vitamin E/d for 4 weeks. The mean baseline levels of DNA repair incisions were 65·2 (95 % CI 60·4, 70·0) and 86·1 (95 % CI 76·2, 99·9) among the male smokers and well-nourished subjects, respectively. The male smokers also had high baseline levels of oxidised guanines in MNBC. After supplementation, only the male smokers supplemented with slow-release vitamin C tablets had increased DNA repair activity (27 (95 % CI 12, 41) % higher incision activity). These subjects also benefited from the supplementation by reduced levels of oxidised guanines in MNBC. In conclusion, nutritional status, DNA repair activity and DNA damage are linked, and beneficial effects of antioxidants might only be observed among poorly nourished subjects with high levels of oxidised DNA damage and low repair activity.

Obesity and type 2 diabetes are inextricably linked. It is therefore unfortunate that insulin, the ultimate treatment to improve glycaemic control in type 2 diabetes, is associated with significant weight gain. The aim of the present investigation was to ascertain whether a dietitian-led intensive lifestyle intervention could attenuate weight gain associated with commencing insulin therapy. Subjects (n 50) with type 2 diabetes, within 4 weeks of starting insulin therapy, were randomly allocated to a control or intervention group. The control group continued with standard care whilst the intervention group followed a dietitian-led intensive lifestyle intervention. Over 6 months the control group gained 4·9 (sd 3·6) kg (P < 0·001), whilst the intervention group maintained their weight ( − 0·6 (sd 5·1) kg (NS). The difference in weight change between the groups was 5·5 kg (P < 0·001). The control group had significant increases whilst the intervention group had slight decreases in: BMI (+1·7 (sd 1·3) kg/m2 (P < 0·001) v. − 0·3 (sd 2·0) kg/m2 (NS)), waist circumference (+5·3 (sd 5·0) cm (P < 0·001) v. − 0·4 (sd 5·2) cm (NS)) and percentage body fat (+1·5 (sd 2·0) % (P < 0·001) v. − 0·4 (sd 2·8) % (NS)). Differences between the groups for these parameters were significant (P < 0·01). Throughout the study, both groups experienced significant reductions in HbA1c, but only minor changes in blood lipids. The present study demonstrates that weight gain is not an inevitable consequence of starting insulin therapy, but attenuation of the weight gain requires a high level of intervention. The first 6 months to 1 year after initiating insulin therapy provides the ideal ‘window of opportunity’.

Himalaya 292 (Hordeum vulgare var. Himalaya 292) is a novel hull-less barley variety lacking activity of a key enzyme of starch synthesis giving a grain containing less total starch, more amylose and higher total dietary fibre. Animal trials have shown that Himalaya 292 contains more resistant starch and has greater positive impact on biomarkers of large-bowel health than comparable wholegrain cereal products. The present study compared the effects of foods made from wholegrain Himalaya 292 with those made from wholegrain wheat on faecal biomarkers of bowel health in human subjects. Seventeen male and female volunteers aged 31–66 years consumed similar quantities of Himalaya 292, whole-wheat or refined cereal foods daily for 4 weeks in a randomised cross-over design. Total dietary fibre intakes from weighed food records were 45, 32 and 21 g/d for the Himalaya 292, whole-wheat and refined cereal periods, respectively. Compared with the refined cereal foods, consumption of Himalaya 292 foods resulted in 33 % higher faecal weight, a lowering of faecal pH from 7·24 to 6·98, a 42 % higher faecal concentration and a 91 % higher excretion of butyrate, a 57 % higher faecal total SCFA excretion and a 33 % lower faecal p-cresol concentration. pH and butyrate concentration and excretion were also significantly different compared with wholemeal wheat. It is concluded that consumption of a diet that included foods made from Himalaya 292 supplied more fibre and improved indices of bowel health compared with refined cereal foods and, for some indices, similar wholemeal wheat foods at equivalent levels of intake.

Haemodialysis patients display an increased cardiac mortality, which may be partly related to increased sympathoadrenal activity and insulin resistance. Fish oil decreases adrenal activation induced by mental stress and has an insulin sensitizing effect in healthy subjects. Whole-body glucose metabolism after oral glucose was studied in eight haemodialysis patients before and after a 3-week oral fish oil supplementation (i.e. EPA + DHA at 1·8 g/d). Plasma glucose fluxes were traced by using [6,6-2H2]glucose infusion. Substrate oxidation was determined by using indirect calorimetry. Each patient was studied in the basal state and over the 6 h following absorption of a 1 g/kg glucose load. Energy expenditure in response to glucose re-increased over the last 2 h of the experiment (P < 0·05), which coincided with an increase in plasma catecholamines, especially epinephrine (P < 0·05), strongly suggesting a sympathoadrenal overactivity. Fish oil supplementation blunted both re-increase in thermogenic response and concomitant increase in plasma epinephrine, but not in plasma norepinephrine, over the last 2 h of the experiment. Fish oil did not alter either whole-body glucose metabolism or substrate oxidation. These data show that in haemodialysis patients, fish oil attenuates adrenal overactivity induced by oral glucose but does not modulate whole-body glucose metabolism and insulin sensitivity.

The objective of the present study was to investigate the bioavailability and the configurational isomer distribution of the carotenoid astaxanthin (AST) in human plasma after ingestion of wild (Oncorhynchus spp.) and aquacultured (Salmo salar) salmon. In a randomised and double-blind trial, twenty-eight healthy men consumed 250 g wild or aquacultured salmon daily for 4 weeks which provided 5 μg AST/g salmon flesh. The plasma AST concentrations as well as the isomer distribution were measured by HPLC using a reversed and a chiral stationary phase. After 6 d of intervention with salmon, plasma AST concentrations reached a plateau of 39 nmol/l after consumption of wild salmon and of 52 nmol/l after administration of aquacultured salmon. At days 3, 6, 10 and 14 – but not at day 28 – the AST concentrations in human plasma were significantly greater after ingestion of aquacultured salmon. After administration of wild salmon, the (3S,3′S) isomer predominated in plasma (80 %), whereas after intake of aquacultured salmon the meso form (3R,3′S) prevailed (48 %). Therefore, the AST isomer pattern in human plasma resembles that of the ingested salmon. However, after consumption of both wild and aquacultured salmon for 28 d the relative proportion of the (3S,3′S) isomer was slightly higher and the (3R,3′R) form lower in human plasma compared with the isomer distribution in salmon flesh. A selective process of isomer absorption could be responsible for the observed differences in the relative proportions of the (3S,3′S) and (3R,3′R) isomers in human plasma compared with salmon flesh.

Both cigarette smoking and high fat meals induce oxidative stress, which is associated with the pathogenesis of numerous diseases. We compared blood antioxidant status, oxidative stress biomarkers and TAG in twenty smokers and twenty non-smokers, matched for age and physical activity, in response to a high fat test meal standardized to body mass. Blood samples were collected before feeding (resting and fasted) and at 1, 2, 4 and 6 h post feeding and analysed for antioxidant capacity (trolox equivalent antioxidant capacity; TEAC), xanthine oxidase activity (XO), hydrogen peroxide (H2O2), malondialdehyde (MDA) and TAG. Smoking status (P < 0·001) and time (P ≤ 0·01) effects were noted for all variables, with smokers demonstrating higher values compared with non-smokers for all variables except for TEAC, for which values were lower for smokers. XO, H2O2, MDA and TAG increased following feeding with a peak response at the 4 h post feeding time point, with the opposite response occurring for TEAC. Although no interaction effects were noted (P>0·05), contrasts revealed greater values in smokers compared with non-smokers for XO, H2O2, MDA and TAG, and lower values for TEAC at times from 1–6 h post feeding (P ≤ 0·05). Our findings indicate that young cigarette smokers experience an exaggerated oxidative stress response to feeding, as well as hypertriacylglycerolaemia, as compared with non-smokers. These data provide insight into another possible mechanism associating cigarette smoking with ill health and disease.

Despite recent concerns about the high prevalence of sub-clinical vitamin D deficiency in adolescents, relatively few studies have investigated the underlying reasons. The objective of the present study was to investigate the prevalence and predictors of vitamin D inadequacy among a large representative sample of adolescents living in Northern Ireland (54–55°N). Serum concentrations of 25-hydroxyvitamin D (25(OH)D) were analysed by enzyme-immunoassay in a subgroup of 1015 of the Northern Ireland Young Hearts 2000 cohort; a cross-sectional study of 12 and 15 year-old boys and girls. Overall mean 25(OH)D concentration throughout the year was 64·3 (range 5–174) nmol/l; 56·7 and 78·1 nmol/l during winter and summer, respectively. Reported intakes of vitamin D were very low (median 1·7 μg/d). Of those adolescents studied, 3 % and 36 % were vitamin D deficient and inadequate respectively, as defined by serum 25(OH)D concentrations < 25 and < 50 nmol/l. Of the subjects, 46 % and 17 % had vitamin D inadequacy during winter and summer respectively. Gender differences were also evident with 38 % and 55 % of boys and girls respectively classified as vitamin D inadequate during winter (P < 0·001). Predictors of vitamin D inadequacy during winter were vitamin D intake and gender. In conclusion, there is a high prevalence of vitamin D inadequacy in white-skinned adolescents in Northern Ireland, particularly during wintertime and most evident in girls. There is a clear need for dietary recommendations for vitamin D in this age group and for creative strategies to increase overall vitamin D status in the population.

Overweight and obesity is one of the risk factors for developing CVD. At present, very little is known about the acute effects of dietary fibre on lipids, glucose and insulin, resting energy expenditure and diet-induced thermogenesis in overweight and obese individuals. This study examined the postprandial metabolic effects of dietary fibre in overweight and obese men. Ten overweight and obese men consumed a mixed meal accompanied by either a high-fibre or low-fibre supplement on two separate visits, in a random order, 1 week apart. Two isoenergetic breakfast meals with similar composition were consumed by ten overweight/obese men. The meals contained either a low (3 g) or high (15 g) amount of fibre, low-fibre meal (LFM) and high-fibre meal (HFM) respectively. Analysis was carried out using paired t test and ANOVA. Serum TAG incremental area under the curve during 6 h of the postprandial period was significantly lower after the consumption of HFM compared with LFM. At the first hour of the postprandial period, plasma apo B48 concentration after consumption of HFM was significantly lower compared with LFM. The resting energy expenditure and diet-induced thermogenesis after both meals was similar during 6 h of the postprandial period. Collectively, these findings suggest that a single acute dose of dietary fibre in the form of psyllium supplement can decrease arterial exposure to TAG and modify chylomicron responses in the postprandial period.

Aerobic exercise has been shown to lower postprandial TAG concentrations after a meal(s) of high-fat content. This study examined the effects of moderate-intensity cycling on postprandial TAG concentrations and pre-heparin lipoprotein lipase concentrations after subjects consumed a meal of moderate-fat content (45 % of total energy). Twelve male subjects, aged 24 (sem 1) years, completed two 2 d trials (exercise and control) at least 1 week apart in a randomised, repeated measures design. On day 1, subjects either cycled for 30 min at 65 % of maximum heart rate in the afternoon or rested (no exercise). On day 2 of both trials, after an overnight stay with an 11 h fast, subjects consumed a test meal of moderate-fat content (0·61 g fat, 1·34 g carbohydrate, 0·37 g protein and 51 kJ energy/kg body mass) for breakfast. Blood samples were collected at baseline (before the exercise or at an equivalent time-point during the control trial on day 1), in the fasted state (0 h) and at 2, 4 and 6 h postprandially on day 2. The total and incremental areas under the serum TAG concentration v. time curve were 30 % (P = 0·039) and 33 % (P = 0·012) lower on the exercise trial compared with the control trial, respectively. Serum pre-heparin lipoprotein lipase concentrations did not differ between the exercise and control trials. These findings demonstrate that 30 min of moderate-intensity cycling performed the day before a meal of moderate-fat content is effective at lowering postprandial serum TAG concentrations but does not affect serum pre-heparin lipoprotein lipase concentrations in young men.