Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition (fat amount and type, carbohydrate, protein, fibre, alcohol) and several lifestyle conditions (physical activity, tobacco use), physiological factors (age, gender, menopausal status) and pathological conditions (obesity, insulin resistance, diabetes mellitus). The roles of many genes have been explored in order to establish the possible implications of their variability in lipid metabolism and CHD risk. The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, A-V, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. Overall, the variability in postprandial response is important and complex, and the interactions between nutrients or dietary or meal compositions and gene variants need further investigation. The extent of present knowledge and needs for future studies are discussed in light of ongoing developments in nutrigenetics.

Provided that they are scientifically substantiated, nutrition and health (NH) claims linked to food products can help consumers make well-informed food choices. The new European legislation on NH claims made on foods entered into force on 19 January 2007. The law sets out conditions for their use, establishes a system for their scientific evaluation, and will create European lists of authorised claims. An important aspect of this proposed legislation is that it states, in article 5.2, ‘the use of nutrition and health claims shall only be permitted if the average consumer can be expected to understand the beneficial effects expressed in the claim’. The present review examines consumer understanding of NH claims from a consumer science perspective. It focuses on the type of data and information that could be needed to provide evidence that the average consumer adequately understands a particular NH claim. After exploring several different methodologies, it proposes a case-specific approach using a stepwise procedure for assessing consumer understanding of a NH claim.

Zn deficiency reduces food intake and growth rate in rodents. To determine the relationship between Zn deficiency and the regulation of food intake, we evaluated leptin gene expression in epididymal white adipose tissue (eWAT), and hypothalamic corticotropin-releasing hormone (hCRH) and hypothalamic neuropeptide Y (hNPY) of rats Zn-deficient only to show reduced food intake and growth rate but not food intake cycling. Growing male Sprague-Dawley rats (240 g) were randomly assigned to one of four dietary groups: Zn-adequate (ZA; 30 mg/kg diet), Zn-deficient (ZD; 3 mg/kg diet), pair-fed with ZD (PF; 30 mg/kg diet) and Zn-sufficient (ZS; 50 mg/kg diet) (n 8), and were fed for 3 weeks. Food intake and body weight were measured, as were blood mononuclear cells and pancreas Zn levels. eWAT leptin, hCRH and hNPY mRNA levels were determined. Food intake was decreased by about 10 % in ZD and PF rats compared to ZA and ZS rats. Growth and eWAT leptin mRNA levels were unaffected in PF rats but were significantly (P < 0·05) decreased in ZD rats. However, hNPY showed a tendency to increase, and hCRH significantly (P < 0·05) decreased, in both ZD and PF rats. These results suggest that while leptin gene expression may be directly affected by Zn, hNPY and hCRH are likely responding to reduced food intake caused by Zn deficiency.

There are nationwide folic acid (FA) fortification programmes of staple foods established or under consideration in order to prevent neural tube defects. Universal FA fortification still remains controversial because of the concern that additional FA in the diets of population groups (e.g. children and elderly) not initially targeted for fortification may suffer adverse effects. However, dietary surveys regarding folate generally deal with adults and little is known about the consumption and long-term effects of fortified food and supplements in growing individuals. Recent reports from our laboratory show several effects of high-dose folate supplementation in rats. In the present work, we studied the effect of FA on the methionine cycle in weanling (3-week-old) male rats after 4 weeks of supplementation with 40 mg FA/kg diet v. control (1 mg FA/kg diet). FA supplementation resulted in a reduction of homocysteine and creatinine concentrations v. control group. FA supplementation did not alter S-adenosylmethionine/S-adenosylhomocysteine ratio, DNA methylation, enzymatic activities or concentrations of vitamins involved in the nutritional regulation of the methionine cycle, except for folate. FA supplementation of 40 mg/kg did not lead to hepatic or renal damage. In conclusion, there were no apparent adverse effects on one-carbon metabolism after FA supplementation in the studied conditions.

Visceral adipose tissue and skeletal muscle have central roles in determining whole-body insulin sensitivity. The peroxisome proliferator-activated receptor-γ (PPARγ) is a potential mediator of insulin sensitivity. It can directly modulate the expression of genes that are involved in glucose and lipid metabolism, including GLUT4, lipoprotein lipase (LPL) and adipocytokines (leptin and adiponectin). In this study, we aimed to determine the effects of obesity-associated insulin resistance on mRNA expression of PPARγ and its target genes. Dogs were studied when they were lean and at the end of an overfeeding period when they had reached a steady obese state. The use of a sensitive, real-time PCR assay allowed a relative quantification of mRNA expression for PPARγ, LPL, GLUT4, leptin and adiponectin, in adipose tissue and skeletal muscle. In visceral adipose tissue and/or skeletal muscle, mRNA expression of PPARγ, LPL and GLUT4 were at least 2-fold less in obese and insulin-resistant dogs compared with the same animals when they were lean and insulin-sensitive. The mRNA expression and plasma concentration of leptin was increased, whereas the plasma level and mRNA expression of adiponectin was decreased, by obesity. In adipose tissue, PPARγ expression was correlated with leptin and adiponectin. These findings, in an original model of obesity induced by a prolonged period of overfeeding, showed that insulin resistance is associated with a decrease in PPARγ mRNA expression that could dysregulate expression of several genes involved in glucose and lipid metabolism.

Three groups of five wethers with ruminal and duodenal cannulas and maintained as either fauna-free (FF) or inoculated with total mixed fauna (TF) or Entodinium caudatum as a single-species monofauna (EN) were used in an experiment with two 28 d periods. In the first period, the sheep were fed a control barley-based diet (40:60 concentrate to silage DM) and in the second period the diet was supplemented with 187 g DM of Enterolobium cyclocarpum for the last 12 d of the period. The diets of period 1 and 2 were isonitrogenous. There was no effect of fauna on apparent ruminal and total tract organic matter and fibre digestion, but bacterial and microbial N flow and efficiency were improved in FF sheep compared to TF sheep. In period 2, protozoal numbers were reduced between 31 and 88 % 2 h after feeding E. cyclocarpum for the third to twelfth day of supplementation and by an average of 25 % in samples collected over the 24 h feeding cycle. Supplementation of the diet with E. cyclocarpum and the consequent protozoal reduction in TF and EN sheep improved the flow of non-ammonia N and bacterial N to the small intestine and the efficiency of microbial synthesis. However, E. cyclocarpum reduced ruminal organic matter digestion, especially in faunated sheep, and total tract organic matter, N and fibre digestion. Thus, a reduction in the protozoal cell numbers of 25 % was sufficient to achieve the beneficial effects of reduced fauna on the bacterial protein supply, but diet digestibility was reduced.

Fetal undernutrition programmes risk of later metabolic disorders. Postnatal factors modify the programmed phenotype. This study aimed to assess the effects of a postnatal high-fat (HF) challenge on body weight gain, adiposity and gene expression following prenatal undernutrition. Pregnant rats were fed either a control diet or a low-protein (LP) diet, targeted at days 0–7 (LPE), days 8–14 (LPM), or days 15–22 (LPL) gestation. At 12 weeks of age offspring were either fed standard laboratory chow diet (4·13 % fat), or a 39·5 % fat diet, for 10 weeks. LP exposure had no effect on weight gain or abdominal fat in males. Females exposed to LP diet in utero exhibited a similar weight gain on HF diet as on the chow diet. Programming of fat deposition was noted in LPE females and males of the LPM and LPL groups (P = 0·019). Hypothalamic expression of galanin mRNA was similar in all groups, but expression of the galanin-2 receptor was modified by LP exposure in female offspring. Hepatic expression of sterol response element binding protein (SREBP-1c) was decreased by LP at both the mRNA (P = 0·008) and protein (P < 0·001) level. HF feeding increased expression of SREBP-1c mRNA three-fold in controls, with little response noted in the LP groups. Interactions of factors such as postnatal diet, age and sex act together with prenatal factors to determine metabolic function and responsiveness at any stage of postnatal life. This study further establishes a role for prenatal nutrition in programming the genes involved in lipid metabolism and appetite regulation.

A diet rich in fruit and vegetables can be effective in the reduction of oxidative stress, through the antioxidant effects of phytochemicals and other mechanisms. Protection against the carcinogenic effects of chemicals may also be exerted by an enhancement of detoxification and DNA damage repair mechanisms. To investigate a putative effect of flavonoids, a class of polyphenols, on the regulation of the gene expression of DNA repair and metabolic genes, a 1-month flavonoid-rich diet was administered to thirty healthy male smokers, nine of whom underwent gene expression analysis. We postulated that tobacco smoke is a powerful source of reactive oxygen species. The expression level of twelve genes (APEX, ERCC1, ERCC2, ERCC4, MGMT, OGG1, XPA, XPC, XRCC1, XRCC3, AHR, CYP1A1) was investigated. We found a significant increase (P < 0·001) in flavonoid intake. Urinary phenolic content and anti-mutagenicity did not significantly change after diet, nor was a correlation found between flavonoid intake and urinary phenolic levels or anti-mutagenicity. Phenolic levels showed a significant positive correlation with urinary anti-mutagenicity. AHR levels were significantly reduced after the diet (P = 0·038), whereas the other genes showed a generalized up regulation, significant for XRCC3 gene (P = 0·038). Also in the context of a generalized up regulation of DNA repair genes, we found a non-significant negative correlation between flavonoid intake and the expression of all the DNA repair genes. Larger studies are needed to clarify the possible effects of flavonoids in vivo; our preliminary results could help to better plan new studies on gene expression and diet.

Epidemiological studies have indicated that soya consumption may produce a better plasma lipid profile. The effect may be attributed to the phyto-oestrogens in soya. The red clover (Trifolium pratense) isoflavone biochanin A has a chemical structure similar to those phyto-oestrogens found in soya beans, and is marketed as a nutraceutical for alleviating postmenopausal symptoms. In the present study we investigated the effect of biochanin A on the mRNA expression of ApoA-1 in the hepatic cell line HepG2. Real-time PCR revealed that biochanin A increased ApoA-1 mRNA abundance in cells expressing oestrogen receptor (ER) α. Without ERα transfection, biochanin A had no effect on mRNA abundance. In order to study the transcriptional control, a fragment of the 5′-flanking region of the ApoA-1 gene was amplified and inserted in a firefly luciferase reporter plasmid. The reporter assay indicated that the transactivation of the ApoA-1 promoter was induced by biochanin A in HepG2 cells transfected with the ERα expression plasmid. This induction was reduced by the anti-oestrogen ICI 182,780, whereas the inhibitors of protein kinase (PK) C, PKA, or mitogen-activated kinase (ERK) had no suppressive effect. The present study illustrated that biochanin A might up regulate hepatic apoA-1 mRNA expression through an ER-dependent pathway.

A study was conducted to test the effects of Jerusalem artichoke inulin (JA) or chicory inulin (CH) in snack bars on composition of faecal microbiota, concentration of faecal SCFA, bowel habit and gastrointestinal symptoms. Forty-five volunteers participated in a double-blind, randomized, placebo-controlled, parallel-group study. At the end of a 7 d run-in period, subjects were randomly assigned to three groups of fifteen subjects each, consuming either snack bars with CH or JA, or snack bars without fructans (placebo); for 7 d (adaptation period), they ingested one snack bar per day (7·7 g fructan/d) and continued for 14 d with two snack bars per day. The composition of the microbiota was monitored weekly. The consumption of CH or JA increased counts of bifidobacteria (+1·2 log10 in 21 d) and reduced Bacteroides/Prevotella in number and the Clostridium histolyticum/C. lituseburense group in frequency at the end of intervention (P < 0·05). No changes in concentration of faecal SCFA were observed. Consumption of snack bars resulted in a slight increase in stool frequency. Stool consistency was slightly affected in subjects consuming two snack bars containing CH or JA per day (P < 0·05). Consumption of CH or JA resulted in mild and sometimes moderate flatulence in a few subjects compared to placebo (P < 0·05). No structural differences were detected between CH and JA before and after processing. In conclusion, adaptation on increased doses of CH or JA in bakery products stimulates the growth of bifidobacteria and may contribute to the suppression of potential pathogenic bacteria.

The hypolipidaemic effects of plant sterols are well established. However, mechanisms by which plant sterols lower plasma cholesterol levels, particularly at the molecular level, have not been clearly elucidated. The objective of the present study was to determine whether different plant sterol analogues reduce plasma cholesterol levels by up regulating the sterol transporters ABCG5 and ABCG8 in the liver and/or small intestine. Male Golden Syrian hamsters were divided into eight groups. Groups 1 and 2 were fed a maize starch–casein–sucrose-based diet that did not contain cholesterol (control; Con) or the Con diet with the addition of 0·25 % cholesterol (Ch-Con). Groups 3–8 were fed the Ch-Con diet supplemented with 1 % plant sterols, 1 % plant stanols, 1 % of a plant sterol and stanol mixture (50:50), 1·76 % plant sterol–fish oil esters, or 0·71 or 1·43 % stanol–ascorbic acid esters, respectively. After 5 weeks, the Ch-Con diet up regulated the ABCG5 mRNA expression and tended (P = 0·083) to increase ABCG8 mRNA expression in the liver, but did not affect both genes’ expression in the small intestine compared with the Con diet. Hamsters fed 0·7 % stanol esters showed lower plasma cholesterol levels (P < 0·001) and also lower liver ABCG5 mRNA expression (P < 0·05) compared with the Ch-Con diet. Plant stanols, stanol esters, and sterol esters did not affect the ABCG5 or ABCG8 mRNA expressions in the liver and intestine although they reduced plasma cholesterol levels. These results suggest that plant sterols and their derivatives reduce plasma cholesterol levels independently from the mRNA expression of ABCG5 and ABCG8 transporters.

Acute caffeine ingestion increases serum NEFA and plasma adrenaline and decreases insulin sensitivity. Although frequently suggested, it is not known if a tolerance to these alterations in glucose homeostasis is developed in habitual caffeine consumers. Our objective was to determine whether acute caffeine ingestion continued to alter insulin, glucose, NEFA and adrenaline during an oral glucose tolerance test (OGTT) following 14 d of caffeine consumption. Twelve caffeine-naive young males underwent four OGTTs over a 4-week period. Subjects ingested a gelatin-filled placebo (PLA) capsule on the first trial day and 5 mg caffeine/kg body weight on the remaining three trial days (day 0, day 7, day 14) before a 2 h OGTT. Following day 0 and day 7, subjects were given six dosages of 5 mg caffeine/kg to consume per d between trials. Serum insulin and blood glucose area under the curve (AUC) were significantly elevated (P < 0·05) v. PLA on day 0 (36 and 103 %, respectively) and were not different from PLA on day 7. On day 14, insulin AUC was 29 % greater than PLA (P < 0·05), and glucose was greater (P < 0·05) during the first hour, although the 50 % elevation in glucose AUC was not different from PLA. Before the OGTT, caffeine resulted in greater (P < 0·05) serum NEFA and plasma adrenaline concentrations in all three caffeine trials, but both NEFA and adrenaline concentrations were decreased (P < 0·05) on day 14 v. day 0. Although 14 d of caffeine consumption by previously caffeine-naive subjects reduced its impact on glucose homeostasis, carbohydrate metabolism remained disrupted.

Plant sterols (PS) and MUFA are well-documented cholesterol lowering agents. We aimed to determine the effect of PS esterified to olive oil fatty acids (PS-OO) on blood lipid profile and lipid peroxidation in hypercholesterolaemic subjects. Twenty-one moderately overweight, hypercholesterolaemic subjects consumed three consecutive treatment diets, each lasting 28 d and separated by 4-week washout periods, using a randomized crossover design. Diets contained 30 % energy as fat, 70 % of which was provided by olive oil (OO), and differed only in the treatment oils: OO, PS esterified to sunflower oil fatty acids (PS-SO), and PS-OO. Both PS-SO and PS-OO treatments provided 1·7 g PS /d. PS-OO and PS-SO consumption resulted in a decrease (P = 0·0483) in LDL-cholesterol (LDL-C) concentrations compared with the OO diet. Although total cholesterol and apo B-100 levels were not significantly affected, PS-SO and, to some extent, PS-OO reduced the total:HDL-cholesterol (HDL-C) ratio (P = 0·0142) and the apo B-100:apo A-I ratio (P = 0·0168) compared with the OO diet. There were no differences across diets in lipoprotein(a) (Lp(a)) and lipid peroxidation levels. However, following consumption of OO and PS-SO, Lp(a) concentrations increased (P = 0·0050 and 0·0421, respectively), while PS-OO treatment did not affect Lp(a) levels. Furthermore, there was a decrease (P = 0·0097) in lipid peroxidation levels with PS-OO treatment during the supplementation phase. Our results suggest that supplementing an OO-rich diet with PS-OO favourably alters the plasma lipid profile and may decrease the susceptibility of LDL-C to lipid peroxidation in hypercholesterolaemic subjects.

Although, the safe limits of human daily boron (B) exposure are not absolutely clear, there is a growing interest in B and its effects on human health. The aim of the present study was to estimate daily B exposure in 66 males in Turkey living in a B-rich area using water containing at least 2 mg/l boron, with an average age of 38·55 (se 1·66) years and an average number of years of residence in the B-rich area of 35·89 (se 1·73). Another group of males (n 57), living in the city centres of Balıkesir and Ankara, were taken as controls; the average age and number of years of residence for this group were 29·44 (se 1·43) and 10·26 (se 1·83) years, respectively. As it is assumed that the B level in urine reflects daily B exposure, the amount of urinary B of both the study and control groups was analysed by using an inductively coupled plasma optical emission spectrometry (ICP-OES) technique. The average daily B exposure value was calculated as 6·77 (se 0·47) mg in the study group and 1·26 (se 0·1) mg in the controls. The results of this study are expected to contribute to creating a reference value for a safe daily B exposure.

Recent studies have shown a decreased risk of colon cancer with consumption of fish. However, most studies on fish consumption do not distinguish between lean and fatty fish, or between poached and fried fish. The aim of this study was to investigate any association between fish consumption and colon cancer in The Norwegian Women and Cancer (NOWAC) study. We focused mainly on lean fish, which was further divided into poached and fried fish. A total of 63 914 women were included in the analysis, 254 of whom were found to have colon cancer during follow-up. Since fish consumption was one of the main topics of interest in the NOWAC study, there is a predominance of women from northern Norway due to higher fish intake in this area; hence the study is not representative of the whole of Norway. The participants completed a semi-quantitative FFQ between 1996 and 1999, and were followed-up for incidence of colon cancer until 2004. No association between fish consumption and risk of colon cancer was seen, except for the third tertile of poached lean fish consumption (relative risk (RR) 1·46, 95 % CI 1·04, 2·06). This association disappeared when excluding women with less than 1 year of follow-up. In conclusion, the present study does not support the hypothesis of a protective effect of fish against colon cancer risk.

The identification of the target foods that most affect the fat content of a diet, independently whether or not they contain fat, can be a useful tool in the process of drawing up more effective dietary guidelines with nutritional education strategies more directed at the needs of each population. With this purpose, the contribution analysis designed by Block and colleagues and multiple linear regression models were applied to a representative sample of Catalonia. Olive oil was the food that provided the highest absolute and relative percentage of fat-derived energy intake and cheese the food that provided the highest percentage of saturated fat-derived energy intake. According to the results of the present work, during the last 10 years the consumption of fruits and vegetables in Catalonia has increased, more in women than men. The intake of white fish is significantly higher than the intake of blue fish, which should be increased in both men and women, and red meat is still the first meat source in this population. Special attention should be paid to the increasing sweet cereal consumption, which is a source of invisible fat to the diet.