The aim of the present study was to assess the prevalence of the Mediterranean dietary pattern (MDP) in the population of the Balearic Islands and socio-demographic and lifestyle factors that might determine adherence to the MDP. A cross-sectional nutritional survey was carried out in the Balearic Islands between 1999 and 2000. A random sample (n 1200) of the adult population (16–65 years) was interviewed. Dietary questionnaires incorporating questions related to socio-economic status, education level, lifestyle factors and health status were utilised. Dietary habits were assessed by means of two 24 h recalls, and a quantitative food-frequency questionnaire. Adherence to the MDP was defined according to a score constructed considering the consumption of nine MDP characteristic components: high MUFA:saturated fatty acids ratio, moderate ethanol consumption, high legumes, cereals and roots, fruits, vegetables, and fish consumption, and low consumption of meat and milk. Then, socio-demographic, lifestyle and health status variables that could determine a higher or lower adherence were assessed. Adherence to the MDP among the population of the Balearic Islands was found to be 43·1 (sd 5·8) %, and was similar in all socio-demographic and lifestyle groups, with some differences according to age, sex and physical status. There was an increase in the percentage of adherence with age, which was greater in males than in females. A more physically active lifestyle was associated with a higher adherence to the MDP. The promotion of the Mediterranean lifestyle, including the MDP and greater physical activity, should be reinforced in the population of the Balearic Islands and especially in the younger generations.

White adipose tissue is now recognised to be a multifunctional organ; in addition to the central role of lipid storage, it has a major endocrine function secreting several hormones, notably leptin and adiponectin, and a diverse range of other protein factors. These various protein signals have been given the collective name ‘adipocytokines’ or ‘adipokines’. However, since most are neither ‘cytokines’ nor ‘cytokine-like’, it is recommended that the term ‘adipokine’ be universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It is suggested that the term is restricted to proteins secreted from adipocytes, excluding signals released only by the other cell types (such as macrophages) in adipose tissue. The adipokinome (which together with lipid moieties released, such as fatty acids and prostaglandins, constitute the secretome of fat cells) includes proteins involved in lipid metabolism, insulin sensitivity, the alternative complement system, vascular haemostasis, blood pressure regulation and angiogenesis, as well as the regulation of energy balance. In addition, there is a growing list of adipokines involved in inflammation (TNFα, IL-1β, IL-6, IL-8, IL-10, transforming growth factor-β, nerve growth factor) and the acute-phase response (plasminogen activator inhibitor-1, haptoglobin, serum amyloid A). Production of these proteins by adipose tissue is increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines has led to the view that the obese are characterised by a state of chronic low-grade inflammation, and that this links causally to insulin resistance and the metabolic syndrome. It is, however, unclear as to the extent to which adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and whether there is a generalised or local state of inflammation. The parsimonious view is that the increased production of inflammatory cytokines and acute-phase proteins by adipose tissue in obesity relates primarily to localised events within the expanding fat depots. It is suggested that these events reflect hypoxia in parts of the growing adipose tissue mass in advance of angiogenesis, and involve the key controller of the cellular response to hypoxia, the transcription factor hypoxia inducible factor-1.

Hypertension or high blood pressure is a significant health problem worldwide. Bioactive peptides that inhibit angiotensin I converting enzyme (ACE) in the cardiovascular system can contribute to the prevention and treatment of hypertension. These ACE inhibitory peptides are derived from many food proteins, especially milk proteins. An ACE inhibitory activity in vitro does not always imply an antihypertensive effect in vivo. Even if it does, it is very difficult to establish a direct relationship between in vitro and in vivo activity. This is mainly due to the bioavailability of the ACE inhibitory peptides after oral administration and the fact that peptides may influence blood pressure by mechanisms other than ACE inhibition. To exert an antihypertensive effect after oral ingestion, ACE inhibitory peptides have to reach the cardiovascular system in an active form. Therefore, they need to remain active during digestion by human proteases and be transported through the intestinal wall into the blood. The bioavailability of some ACE inhibitory peptides has been studied. It is also known that (hydroxy)proline-containing peptides are generally resistant to degradation by digestive enzymes. Peptides can be absorbed intact through the intestine by paracellular and transcellular routes, but the potency of the bioactivity after absorption is inversely correlated to chain length. In addition, some strategies are proposed to increase the bioavailability of ACE inhibitory peptides. Further research into the bioavailability of ACE inhibitory peptides will lead to the development of more effective ACE inhibitory peptides and foods.

Diabetes mellitus and CVD are some of the leading causes of mortality and morbidity. Accumulating data indicate that a diet characterised by low-glycaemic index (GI) foods may improve the management of diabetes or lipid profiles. The objective of the present meta-analysis was to critically analyse the scientific evidence that low-GI diets have beneficial effects on carbohydrate and lipid metabolism compared with high-GI diets. We searched for randomised controlled trials with a crossover or parallel design published in English between 1981 and 2003, investigating the effect of low-GI v. high-GI diets on markers for carbohydrate and lipid metabolism. Unstandardised differences in mean values were examined using the random effects model. The main outcomes were fructosamine, glycated Hb (HbA1c), HDL-cholesterol, LDL-cholesterol, total cholesterol and triacylglycerol. Literature searches identified sixteen studies that met the strict inclusion criteria. Low-GI diets significantly reduced fructosamine by –0·1 (95 % CI –0·20, 0·00) mmol/l (P=0·05), HbA1c by 0·27 (95 % CI –0·5, –0·03) % (P=0·03), total cholesterol by –0·33 (95 % CI –0·47, –0·18) mmol/l (P>0·0001) and tended to reduce LDL-cholesterol in type 2 diabetic subjects by –0·15 (95 % CI –0·31, –0·00) mmol/l (P=0·06) compared with high-GI diets. No changes were observed in HDL-cholesterol and triacylglycerol concentrations. No substantial heterogeneity was detected, suggesting that the effects of low-GI diets in these studies were uniform. Results of the present meta-analysis support the use of the GI as a scientifically based tool to enable selection of carbohydrate-containing foods to reduce total cholesterol and to improve overall metabolic control of diabetes.

Conjugated linoleic acid (CLA) refers to the positional and geometric dienoic isomers of linoleic acid. The dietary intake of CLA has been associated with changes in lipid metabolism. The aim of the present work was to assess the effects of the two main isomers of CLA on sterol regulatory element binding protein (SREBP)-1a and SREBP-1c mRNA levels, as well as on mRNA levels and the activities of several lipogenic enzymes in liver. For this purpose hamsters were fed an atherogenic diet supplemented with 5 g linoleic acid, cis-9,trans-11 or trans-10,cis-12 CLA/kg diet for 6 weeks. The trans-10,cis-12 isomer intake produced significantly greater liver weight, but also significantly decreased liver fat accumulation. No changes in mRNA levels of SREBP-1a, SREBP-1c and lipogenic enzymes, or in the activities of these enzymes, were observed. There was no effect of feeding cis-9,trans-11 CLA. These results suggest that increased fat accumulation in liver does not occur on the basis of liver enlargement produced by feeding the trans-10,cis-12 isomer of CLA in hamsters. The reduction in hepatic triacylglycerol content induced by this isomer was not attributable to changes in lipogenesis.

We studied the effects of five high-fat semi-purified diets varying at a 4 % (w/w) level in either stearic, oleic, linoleic, α-linolenic, or γ-linolenic acid on body fat and energy metabolism in BALB/c mice. A diet containing caprylic, capric, lauric, and myristic acid was used as a reference diet and a diet with 4 % conjugated linoleic acid (CLA) was used as a positive control as it is known to effectively lower body fat in mice. The diets were fed for 35 d. Body fat was significantly lower in the CLA group than in the other groups but was not significantly different among the non-CLA groups. Among the non-CLA groups, the linoleic acid group tended to have the highest and the α-linolenic acid group the lowest proportion of body fat. In energy-balance studies, the percentage of energy intake that was stored in the body was significantly lower in the CLA group compared with the other dietary groups. The percentage of energy intake eliminated in excreta was highest in the stearic acid group followed by the γ-linolenic acid group. These results were reflected in apparent fat digestibility, which was lowest in the stearic acid group. The percentage of energy intake expended as heat was highest in the CLA-fed mice. The results of the present study suggest that body fat and energy accretion in mice fed diets containing different C18 fatty acids is by far the lowest with CLA and that linoleic acid produced the highest fat intake and energy accretion.

The increase in fractional rate of protein synthesis (Ks) in the skeletal muscle of growing rats during the transition from fasted to fed state has been explained by the synergistic action of a rise in plasma insulin and branched-chain amino acids (BCAA). Since growing lambs also exhibit an increase in Ks with level of feed intake, the objective of the present study was to determine if this synergistic relationship between insulin and BCAA also occurs in ruminant animals. Six 30 kg fasted (72 h) lambs (8 months of age) received each of four treatments, which were based on continuous infusion into the jugular vein for 6 h of: (1) saline (155 mmol NaCl/l); (2) a mixture of BCAA (0·778 μmol leucine, 0·640 μmol isoleucine and 0·693 μmol valine/min·kg); (3) 18·7 μmol glucose/min·kg (to induce endogenous insulin secretion); (4) co-infusion of BCAA and glucose. Within each period all animals received the same isotope of phenylalanine (Phe) as follows: (1) l-[1-13C]Phe; (2) l-phenyl-[ring 2H5]-alanine; (3) l-[15N]Phe; (4) l-[ring 2,6-3H]Phe. Blood was sampled serially during infusions to measure plasma concentrations of insulin, glucose and amino acids, and plasma free Phe isotopic activity; biopsies were taken 6 h after the beginning of infusions to determine Ks in m. longissimus dorsi and vastus muscle. Compared with control (saline-infused) lambs, Ks was increased by an average of 40 % at the end of glucose infusion, but this effect was not statistically significant in either of the muscles sampled. BCAA infusion, alone or in combination with glucose, also had no significant effect on Ks compared with control sheep. Ks was approximately 60 % greater for vastus muscle than for m. longissimus dorsi (P>0·01), regardless of treatment. It is concluded that there are signals other than insulin and BCAA that are responsible for the feed-induced increase in Ks in muscle of growing ruminant animals.

We investigated the blood-pressure-lowering effects of γ-aminobutyric acid (GABA) and a GABA-enriched fermented milk product (FMG) by low-dose oral administration to spontaneously hypertensive (SHR/Izm) and normotensive Wistar–Kyoto (WKY/Izm) rats. FMG was a non-fat fermented milk product produced by lactic acid bacteria, and the GABA contained in FMG was made from the protein of the milk during fermentation. A single oral dose of GABA or FMG (5 ml/kg; 0·5 mg GABA/kg) significantly (P>0·05) decreased the blood pressure of SHR/Izm from 4 to 8 h after administration, but did not increase that of WKY/Izm rats. The hypotensive activity of GABA was dose-dependent from 0·05 to 5·00 mg/kg in SHR/Izm. During the chronic administration of experimental diets to SHR/Izm, a significantly slower increase in blood pressure with respect to the control group was observed at 1 or 2 weeks after the start of feeding with the GABA or FMG diet respectively (P>0·05) and this difference was maintained throughout the period of feeding. The time profile of blood-pressure change due to administration of FMG was similar to that of GABA. FMG did not inhibit angiotensin 1-converting enzyme. Furthermore, an FMG peptide-containing fraction from reverse-phase chromatography lacked a hypotensive effect in SHR/Izm rats. The present results suggest that low-dose oral GABA has a hypotensive effect in SHR/Izm and that the hypotensive effect of FMG is due to GABA.

The purposes of the present study were to investigate the effects of feeding a cereal grain containing NSP on body growth and the intestinal microenvironment of recently weaned pigs, and to examine resultant associations with pathogenic Escherichia coli in the intestinal tract. In Expt 1, pearl barley, a grain rich in soluble NSP, was incorporated (250, 500 or 750 g/kg diet) into a low-fibre control diet based on cooked white rice and fed for 7–10 d following weaning. Consumption of pearl barley did not significantly alter piglet live-weight gain compared with the control cooked rice diet, but it accelerated large intestinal growth and fermentation, decreased ileal starch digestibility and increased intestinal viscosity. Expt 2 was conducted to determine whether these differences would favour proliferation of enterotoxigenic E. coli, the bacterium causing post-weaning colibacillosis (PWC). Three groups of pigs were weaned onto diets based on cooked white rice, rice with 500 g pearl barley/kg, or rice with 500 g pearl barley/kg supplemented with exogenous enzymes (Porzyme(tm) 8100; Danisco, Marlborough, Wilts., UK). Pigs were inoculated orally with haemolytic E. coli serovar O8;K87;K88 after weaning. Animals eating the pearl barley had increased viscosity of the intestinal contents, greater intestinal colonisation with the E. coli strain and more diarrhoea than pigs fed the rice-only diet. The enzymes did not reduce viscosity or protect from PWC. The results suggest that pearl barley alters the intestinal microenvironment and predisposes to PWC, whilst a low-viscosity, highly digestible diet based on cooked white rice is protective.

The objective of the present study was to evaluate the consequence of Camembert consumption on the composition and metabolism of human intestinal microbiota. Camembert cheese was compared with milk fermented by yoghurt starters and Lactobacillus casei as a probiotic reference. The experimental model was the human microbiota-associated (HM) rat. HM rats were fed a basal diet (HMB group), a diet containing Camembert made from pasteurised milk (HMCp group) or a diet containing fermented milk (HMfm group). The level of micro-organisms from dairy products was measured in faeces using cultures on a specific medium and PCR–temporal temperature gradient gel electrophoresis. The metabolic characteristics of the caecal microbiota were also studied: SCFA, NH3, glycosidase and reductase activities, and bile acid degradations. The results showed that micro-organisms from cheese comprised 105–108 bacteria/g faecal sample in the HMCp group. Lactobacillus species from fermented milk were detected in HMfm rats. Consumption of cheese and fermented milk led to similar changes in bacterial metabolism: a decrease in azoreductase activity and NH3 concentration and an increase in mucolytic activities. However, specific changes were observed: in HMCp rats, the proportion of ursodeoxycholic resulting from chenodeoxycholic epimerisation was higher; in HMfm rats, α and β-galactosidases were higher than in other groups and both azoreductases and nitrate reductases were lower. The results show that, as for fermented milk, Camembert consumption did not greatly modify the microbiota profile or its major metabolic activities. Ingested micro-organisms were able to survive in part during intestinal transit. These dairy products exert a potentially beneficial influence on intestinal metabolism.

Amongst the various claimed beneficial effects of pro- and prebiotics for the human host, it has been hypothesised that functional foods are able to suppress the generation and accumulation of toxic fermentation metabolites (NH3, p-cresol). Direct evidence supporting this hypothesis is lacking mainly because of the unavailability of reliable biomarkers. Preliminary data indicate that lactose-[15N]ureide and [2H4]tyrosine may be potential biomarker candidates. The aim of the present study was to evaluate the effect of pro- and prebiotics on the colonic fate of these biomarkers in a randomised, placebo-controlled, cross-over study with nineteen healthy volunteers. At the start of the study and at the end of each 2-week study period, during which they were administered either a probiotic (n 10; 6·5×109Lactobacillus casei Shirota cells twice daily) or a prebiotic (n 9; lactulose 10 g twice daily), the volunteers consumed a test meal containing the two biomarkers. Urine was collected during 48 h. Results were expressed as percentage of the administered dose. As compared with the placebo, the decrease in the percentage dose of p-[2H4]cresol in the 24–48 h urine fraction was significantly higher after probiotic intake (P=0·042). Similar changes were observed for the 15N tracer (P=0·016). After prebiotic intake, a significantly higher decrease in the percentage dose of p-[2H4]cresol (P=0·005) and 15N tracer (P=0·029) was found in the 0–24 h urine collection. The present results demonstrate that suppression of the generation and accumulation of potentially toxic fermentation metabolites by pro- and prebiotics can reliably be monitored in vivo by the use of stable isotope-labelled biomarkers.

Longitudinal studies indicate that milk and fermented milk products lower basal plasma cholesterol concentrations, despite their high content of saturated fat, and therefore have favourable health effects. However, there have been few studies on the postprandial effects of milk products. The present study compared the effect of whole milk with a fermented milk, A-38, on postprandial carbohydrate and lipid metabolism, gastric emptying and appetite. Eight healthy young men participated. On the two test days, they arrived fasting for collection of baseline values before consuming the meals, which for a 75 kg subject consisted of 1·4 litre milk or fermented milk, plus 165 mg [13C]acetate (for later determination of gastric emptying by a [13C]acetate breath test). Lactose (15 g) was added to the A-38 meal to equalize the lactose content. Postprandially the A-38 meal resulted in a slower gastric emptying rate than milk (P>0·001). Furthermore, the A-38 meal resulted in a greater increase and a quicker decrease of the triacylglycerol content in all lipoprotein fractions (LDL-fraction, P>0·05; other fractions, P>0·001) and of the gastrointestinal hormones (cholecystokinin and peptide YY, P>0·05; gastric inhibitory polypeptide and glucagon-like polypeptide-1, P>0·001). There were no significant differences in appetite sensations (measured by visual analogue scale) or in the glucose and insulin response (P<0·10). The slower emptying rate of the liquid phase after the A-38 meal is probably due to the higher viscosity of A-38. The lower and more prolonged triacylglycerol response after the milk meal might be caused by coagulation of milk in the stomach.

We conducted a cross-sectional study in 118 well-trained athletes to investigate 'high exposure' to sub-deficient antioxidant status, and consequently to oxidative damage, in relation to estimated daily energy expenditure (EE) and dietary antioxidant intake. Subjects completed 7 d food and activity records. Blood samples were obtained on day 8. Of the athletes 81, 60 and 43 % had intakes of vitamins E, C and β-carotene below two-thirds of the French RDA respectively, which is adjusted for EE (FRDAa). The deficit in vitamin E intake was positively correlated with EE (r 0·51, P>0·0001). All the athletes had normal plasma vitamins E and C and 14 % had marginal plasma β-carotene. Plasma thiobarbituric acid-reactive substances (TBARS) did not increase with increased EE. As evidenced by ANOVA, EE-induced vitamin C intakes increased and consequently led to increased plasma ascorbic acid concentrations. In male athletes, plasma total carotenoids were negatively correlated with plasma TBARS concentrations (r –0·31, P>0·006). The relationship between vitamin C intakes and plasma concentrations was logarithmic (r 0·59, P> 0·0001). To summarize, it is not clear whether vitamin E requirements are overestimated with reference to EE in the FRDAa. Daily requirements for vitamin C do not exceed 200 mg. Our present results could be interpreted as meaning that carotenoids play a protective role as exogenous antioxidants. Carotenoid intakes in athletes must be considered carefully.

Fighting type 2 diabetes and its high risk of CVD, lifestyle intervention with diet and exercise is of uttermost importance. Epidemiological studies strongly suggest an inverse association between increased physical activity, moderate alcohol drinking and the incidence of both type 2 diabetes and CVD. However, alcohol is known to increase postprandial lipaemia, a risk marker of CVD, and exercise to reduce postprandial lipaemia in healthy individuals. The aim of the present study was to investigate how type 2 diabetic men respond, in the postprandial period, to a single exercise session feasible to perform on a daily basis for type 2 diabetic men. The twelve participants ingested a test meal containing 100 g butter, 50 g carbohydrate, together with 40 g alcohol, at each meal test, imitating a social meal situation. Two protocols included exercise sessions with 40 min at 40 % VO2max, one where they exercised 3·5 h after, and another the afternoon before the test meal. One protocol was without any exercise. No significant effect of low-intensity exercise on postprandial lipaemia following a fat-rich meal with alcohol was seen in the middle-aged type 2 diabetic men.

High doses of n–3 PUFA found in fish oils can reduce the circulating concentration of triacylglycerol (TG), which may contribute to the positive impact of these fatty acids on the risk of CVD. The present study aimed to establish the differential impact of EPA and docosahexaenoic (DHA) on plasma lipids and apo in adults. Forty-two normolipidaemic adult subjects completed a double-blind placebo controlled parallel study, receiving an EPA-rich oil (4·8 g EPA/d), DHA-rich oil (4·9 g DHA/d) or olive oil as control, for a period of 4 weeks. No effects of treatment on total cholesterol, LDL-cholesterol or HDL-cholesterol were evident. There was a significant 22 % reduction in TG level relative to the control value following the DHA treatment (P=0·032), with the 15 % decrease in the EPA group failing to reach significance (P=0·258). There were no significant inter-group differences in response to treatment for plasma apoA1, -C3 or -E levels, although a significant 15 % within-group increase in apoE was evident in the EPA (P=0·006) and DHA (P=0·003) groups. In addition, a within-group decrease in the apoA1:HDL-cholesterol ratio was observed in the DHA group, suggesting a positive impact of DHA on HDL particle size. The DHA intervention resulted in a significant increase in the proportion of EPA P=0·000 and DHA P=0·000 in plasma phospholipids, whilst significant increases in EPA P=0·000 and docosapentaenoic acid P=0·002, but not DHA P=0·193, were evident following EPA supplementation (P>0·05). Our present results indicate that DHA may be more efficacious than EPA in improving the plasma lipid profile.

The objectives of the present study were to study the correlation between the change in serum Fe and Fe absorption when administering 100 mg Fe (as FeSO4) orally, and to study the correlation between the absorption from a 3 mg and a 100 mg Fe (as FeSO4) dose. The study was conducted in a group of eleven male blood donors, without any evident infection, who had given blood 8 weeks before the study. On three consecutive mornings the subjects were served a wheat roll fortified with Fe. On the first 2 d the roll was fortified with 3 mg Fe labelled with 59Fe; on day 3 the roll was fortified with 100 mg Fe labelled with 55Fe. The serum Fe response to the 100 mg dose was followed for 6 h. Fe absorption was measured by whole-body counting. High correlations were seen between the absorption of Fe and the change in serum Fe after 100 mg Fe (r2 0·94, P>0·001), between the absorption from 3 mg and 100 mg Fe (r2 0·88, P>0·001), and between the absorption from 3 mg Fe and change in serum Fe after 100 mg Fe (r2 0·90, P>0·001). This strengthens the evidence that it is possible to use the change in serum Fe as a measure of Fe absorption, e.g. when establishing the relative bioavailability for Fe powders. The results also imply that the induced serum Fe increase following 100 mg Fe added to a food could predict the Fe absorption of a small dose of Fe added to the same meal.

Folate deficiency is often discussed as a potential risk factor for CVD and some cancers. Reliable assessment of folate status in large-scale epidemiological studies is therefore of major importance. The present study assessed the value of plasma folate (PF) compared with erythrocyte folate (EF) as a marker of folate status in 363 participants in the European Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort. EF and PF, total homocysteine (tHcy), pyridoxine, cobalamin, creatinine, total protein and packed cell volume were determined; glutamate carboxypeptidase (GCP) C1561T, reduced folate carrier (RFC) G80A and methylenetetrahydrofolate (MTHFR) C677T polymorphisms were analysed. Anthropometric measurements were taken and dietary intake was assessed with the EPIC-Potsdam food-frequency questionnaire. Comparison of EF and PF with factors that may modulate their concentrations was performed. Cross-classification of blood folates in quintile categories resulted in correct classification into the same or adjacent category of 75·5 % of all subjects. Age, BMI, pyridoxine and cobalamin, fruit and vegetable intake, and vitamin supplementation 24 h before blood draw were positively associated with EF and with PF. For tHcy an inverse association was found. Participants with the MTHFR 677TT genotype showed significantly elevated EF concentrations compared with those with 677CT genotype; EF and PF were more strongly correlated (r 0·78, P>0·0001) for participants with MTHFR 677TT genotype than for those with the 677CC or 677CT genotype. In summary, our present results indicate that plasma folate seems to be a suitable marker for assessment of folate status for use in large-scale epidemiological studies.

The unhealthy dietary patterns in the USA especially among low-income households demand complex strategies for health promotion. The present paper analysed the proximate determinants of 7 d food use by 919 participants in the National Food Stamp Program Survey conducted in 1996. The households' consumption of dietary energy, carbohydrate, protein, fibre, saturated, monounsaturated and polyunsaturated fats, Ca, Fe, β-carotene and vitamin C were explained by background, socio-economic and behavioural factors. Certain methodological issues arising in modelling food use data were addressed. The results showed that the subjects' knowledge of the US Department of Agriculture food pyramid, reading nutrition labels, adopting a low-fat diet, selecting fruits and vegetables, saving money at grocery stores and frequency of shopping trips were often significantly associated (P>0·05) with the densities of nutrient use. The results identified certain aspects of nutrition education programmes that deserve greater emphasis for improving diet quality. The model for energy intake indicated that disbursing half the food stamp benefits on a 2-week basis and better shopping practices can enhance food availability.

The aim of the present study was to investigate the anti-hypertensive and angiotensin-converting enzyme (ACE) inhibition effects of soyabean protein hydrolysate in spontaneously hypertensive rats (SHR). Soyabean protein hydrolysate was prepared by peptic hydrolysis and was added into the feed of SHR (0 % for the S0 group, 0·5 % for the S1 group, and 1 % for the S2 group) for 12 weeks. Systolic blood pressure and mean blood pressure of the S1 (164·3 (sem 4·7); 128·0 (sem 5·0) mmHg) and S2 (156·8 (sem 1·6); 120·8 (sem 3·4) mmHg) groups were significantly lower than those of the S0 group (199·4 (sem 5·2); 158·3 (sem 7·0) mmHg) at the end of the study. In the analysis of ACE activity, plasma and heart ACE activities of the S1 and S2 groups were significantly lower than those of the S0 group, and there were no significant differences in aorta, kidney, and lung ACE activities among all SHR. Soyabean protein hydrolysate had no significant effect on plasma lipids, electrolytes, or on left ventricular wall or aorta wall thickness. The results suggest that the long-term administration of soyabean protein hydrolysate might retard the development of hypertension in SHR by its inhibitory effect on ACE in vivo.

Nutrient restriction in pregnancy has been shown to programme adult obesity. Modulation of feeding behaviour may provide a mechanism through which obesity may be programmed. Pregnant Wistar rats were fed either a control diet or a low-protein (LP) diet throughout gestation. Their offspring were allocated to a self-selected-diet protocol to assess appetite and food preferences at 12 and at 30 weeks of age. Self-selection of high-fat, high-protein or high-carbohydrate foods by 12-week-old rats indicated that the prenatal environment influenced feeding behaviour. Both male and female offspring of LP-fed mothers consumed significantly more of the high-fat (P>0·001) and significantly less (P>0·02) of the high-carbohydrate food than the control animals. Female, but not male, offspring of LP-fed rats failed to adjust food intake to maintain a constant energy intake and had higher fat (P>0·005) and energy intakes (P>0·05) than control female rats. At 30 weeks of age there were no differences in the pattern of food selection between the two groups of animals. Male offspring of LP-fed rats had significantly more gonadal fat than control animals (P>0·05), but analysis of total body fat content indicated that there was no significant difference in overall adiposity. The present study suggests that in young adults at least, early life exposure to undernutrition determines a preference for fatty foods. Maternal nutrition may thus promote changes in systems that are involved in control of appetite or the perception of palatability.