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.

To explore whether differences in vitamin K nutrition might, at least in part, underlie differences in fracture incidence between Asian and European populations, the vitamin K status of older individuals in Shenyang, China (eighty-six men, ninety-two women) and in Cambridge, UK (sixty-seven men, sixty-seven women) was compared. Dietary information was collected by food questionnaire in Shenyang and food diary in Cambridge and used to estimate the intake and sources of phylloquinone. Fasting blood was analysed for phylloquinone, triacylglycerol, total osteocalcin (tOC) and undercarboxylated osteocalcin (expressed as percentage of tOC; %ucOC). The mean intakes of green leafy vegetables were 127 (SD 90) g/d in Shenyang and 39 (SD 48) g/d in Cambridge. The estimated phylloquinone intakes (geometric means) were 247 (95% CI 226, 270) μg/d in Shenyang and 103 (95% CI 94, 112) μg/d in Cambridge. Plasma phylloquinone concentrations (geometric means) were significantly higher in the Shenyang subjects (2·17 (95% CI 1·95, 2·42) nmol/l) than in the Cambridge subjects (0·69 (95% CI 0·63, 0·76) nmol/l; P<0·001). Plasma phylloquinone concentration was positively related to phylloquinone intake in both the Shenyang (coefficient 0·17 (SE 0·08); P=0·03) and Cambridge subjects (coefficient 0·29 (SE 0·10); P=0·005). tOC concentration and %ucOC (after adjusting for tOC) were significantly lower in the Shenyang than in the Cambridge subjects (tOC 25·2 (SE 4·2) % and %ucOC 68·5 (SE 10·0) % lower respectively; P<0·001). After adjusting for tOC and triacylglycerol, %ucOC was negatively related to plasma phylloquinone concentration in both the Shenyang (coefficient −0·41 (SE 0·11); P=0·0003) and Cambridge subjects (coefficient −0·17 (SE 0·07); P=0·02). The present study demonstrates that older individuals in northern China have a better vitamin K status compared with their British counterparts in Cambridge, UK.

The ability of laying hens to adjust their intake of available P (AP) was investigated with a maize–soyabean diet fed to forty-eight individually caged birds in a 2×4 factorial experiment. From 19 to 25 weeks of age (phase 1) twenty-four birds were fed a normal-P (NP) diet (2·2 g AP/kg DM) and twenty-four were fed a low-P (LP) diet (1·1 g AP/kg). LP eggs were lighter (51 v. 54 (sem 1·0) g; P>0·05), providing evidence that the LP diet was deficient in AP. From 25 to 28 weeks of age six hens from each phase 1 treatment were fed either the NP or LP diet alone or a choice of the LP and NP feeds or a choice of the LP feed and a phytase-supplemented (PP) feed (LP diet with 400 microbial phytase units/kg). With a choice of the NP and LP feeds, the hens fed the LP diet in phase 1 ate a smaller proportion of the LP feed (34 (sem 12·0)%) than the hens fed the NP diet in phase 1 (72 (sem 12·0)%; P>0·05), showing that P deficiency influenced subsequent selection for AP, i.e. an appetite for P was demonstrated. In those birds offered the LP and PP feeds, the presence of phytase in one of the two feeds significantly alleviated the effect of P deficiency on egg and body weights. The proportion of the LP diet chosen was not significantly affected by phase 1 treatment; it was not necessary for the hens to eat more than 50% of PP feed.

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.

Dietary microparticles are non-biological, bacterial-sized particles. Endogenous sources are derived from intestinal Ca and phosphate secretion. Exogenous sources are mainly titanium dioxide (TiO2) and mixed silicates (Psil); they are resistant to degradation and accumulate in human Peyer's patch macrophages and there is some evidence that they exacerbate inflammation in Crohn's disease (CD). However, whether their intake differs between those with and without CD has not been studied. We aimed to identify dietary microparticle sources and intakes in subjects with and without CD. Patients with inactive CD and matched general practice-based controls (ninety-one per group) completed 7d food diaries. Intake data for dietary fibre and sucrose were compared as positive controls. All foods, pharmaceuticals and toothpastes were examined for microparticle content, and intakes of Ca and exogenous microparticles were compared between the two groups. Dietary intakes were significantly different between cases and controls for dietary fibre (12 (SD 5) v. 14 (sd 5) g/d; P=0.001) and sucrose (52 (sd 27) v. 45 (sd 18) g/d; P=0·04) but not for Ca. Estimated median TiO2 and Psil intakes (2·5 and 35mg/individual per d respectively, totalling 1012–1013 microparticles/individual per d) were broadly similar to per capita estimates and while there was wide variation in intakes between individuals there was no significant difference between subjects with CD and controls. Hence, if exposure to microparticles is associated with the inflammation of CD, then the present study rules out excess intake as the problem. Nonetheless, microparticle-containing foods have now been identified which allows a low-microparticle diet to be further assessed in CD.

The effect of yoghurt and soya yoghurt containing Bifidobacterium lactis Bb-12 or B. longum Bb-46 on Ehrlich ascites tumour cell proliferation was investigated in vitro and in vivo. Tumour cells were incubated with B. lactis Bb-12 or B. longum Bb-46 cultivated in de Mann Rogosa Sharpe (MRS) broth medium, or with their centrifuged supernatant fractions or sediments, for 2 h at 37°C. Treatment resulted in the inhibition of tumour cell proliferation by 85·42 (sd 0·78) and 85·10 (sd 1·28) % by intact micro-organisms, 77·61 (sd 0·29) and 71·43 (sd 1·75) % by their supernatant fractions, but only 4·00 (sd 0·19) and 9·09 (sd 1·24) % by the two sedimented bacteria, respectively. The incubation of tumour cells with yoghurt and soya yoghurt containing Bb-12 for 2 h resulted in 83·01 (sd 0·11) and 88·23 (sd 0·06) % inhibition, respectively, while it was 83·82 (sd 0·24) and 86·36 (sd 0·06) %, respectively for the same products containing Bb-46. Corresponding values for plain yoghurt and soya milk (without bifidobacteria) were 32·81 (sd 0·14) and 5·55 (sd 0·12) %, respectively. The differences between yoghurt or soya yoghurt containing Bb-12 or Bb-46 and plain yoghurt, soya milk or control treatments were statistically significant (n 3; P>0·05). Female Swiss albino mice were injected intraperitoneally with the same tumour cells. The lifespan of mice fed diets supplemented with yoghurt or soya yoghurt containing Bb-12 or Bb-46 was prolonged by 16, 23, 34 and 39%, respectively compared with that of the positive control group (n 6; P>0·05). The lifespan of groups fed plain yoghurt or soya milk was prolonged by 15 and 8%, respectively. Prolongation of lifespan was positively correlated with faeces bifidobacterial count in the groups fed yoghurt or soya yoghurt containing bifidobacteria (r 0·917; P>0·05).

There are two key methods in which fat intake may be manipulated; the ‘substitution model’ and the ‘reduction model’. However insufficient information is known about the mechanisms of dietary fat reduction in individuals who have successfully reduced their fat intake, to be clear as to which strategy offers the greatest chance of success. Our objective was to ascertain the most effective dietary intervention for improving cardiovascular risk profile. Eighty female volunteers (high fat consumers) were recruited. Each subject was randomly allocated into one of the following groups. Substitution of high-fat foods was made with reduced-fat products, by the reduction of high-fat foods, by a combination of substitution and reduction strategies, or no advice was given. Each intervention lasted 3 months. Anthropometric measures and fasting blood samples were taken at baseline and follow-up. The substitution intervention resulted in weight loss (mean −1.4 (95% CI −2.4, −0.2) kg) and reduced percentage body fat (mean −1.3 (95% CI −2.0, −0.5)%). There was no significant weight change with the other interventions. Fasting triacylglycerols (−0.2 (SEM 0.07) mM; P=0.04), cholesterol and C-reactive protein (CRP) levels (0.8 (SEM 0.2) mg/l; P=0.04) fell with the substitution intervention, but not with the other interventions. Insulin-like growth factor-1 increased with both substitution and reduction (P=0.02). There was no significant change in fasting insulin or glucose with any intervention. The substitution model of dietary intervention is effective even over a relatively short interval of time in reducing fasting total cholesterol, triacylglycerols and CRP. Although the group size for the present study was small and involved females only, it has significant implications for population intervention strategies.

The possibility of using exfoliated colonic epithelial cells for assessing the bioavailability of β-carotene was examined. Analysis of exfoliated colonic epithelial cells showed the presence of β-carotene and vitamin A. The β-carotene content was significantly lower in cells from stool samples of subjects on a β-carotene-poor diet than those receiving a single dose of a β-carotene supplement. Colonic epithelial cells isolated from stool samples collected daily during a wash-out period while the subjects were on a β-carotene-poor diet showed a steady decrease in β-carotene content, reaching the lowest value on day 7. Kinetic analysis showed that a single dose of a β-carotene supplement in the form of spirulina (Spirulina platensis) or agathi (Sesbania grandiflora) after the wash-out period caused an increase in the β-carotene content after a lag period of 5–7 d, but the vitamin A levels during these periods were not significantly affected. Analysis of plasma β-carotene concentration also showed similar changes, which correlated with those of exfoliated colonic cells. A relationship between the β-carotene content of the diet and that of the colonic epithelial cells suggests that analysis of the β-carotene content in exfoliated human colonic epithelial cells is a useful non-invasive method to assess the bioavailability of provitamin A β-carotene.

The prevalence of obesity among adults and children has increased steadily over the last few years worldwide, reaching epidemic proportions. Particularly alarming is the link between obesity and the development of chronic disorders such as heart disease, type 2 diabetes, hypertension and some cancers (Bjorntorp, 1997). Environmental causes of obesity are thought to include a sedentary lifestyle and an abundance of highly palatable energy-dense foods (Hill et al. 2003). Genetic factors also contribute to susceptibility to obesity, although the genetic basis of most human obesities is thought to be polygenic (Comuzzie & Allison, 1998; Barsh et al. 2000). The present paper considers some of the animal models used to infer aspects of human obesity, with an emphasis upon their usefulness.

The optimal dosage of ornithine α-ketoglutarate (OKG) for repleting tissue glutamine (Gln) concentrations and maintaining N homeostasis after injury is unknown. We set out to perform ‘dose-ranging’ of OKG supplementation after an endotoxaemic challenge. Sixty-one male Wistar rats were injected with 3 mg lipopolysaccharide (LPS) from Escherichia coli/kg (n 50) or saline vehicle (9 g NaCl/l; controls n 11). After a 24 h fast, survivors were fed by gavage for 48 h with a polymeric standard diet (879 kJ/kg per d and 1·18 g N/kg per d) supplemented with non-essential amino acids (control, n 11; LPS-OKG-0·0, n 9), or with 0·5 g OKG/kg per d (LPS-OKG-0·5, n 12), 1·5 OKG/kg per d (LPS-OKG-1.5, n 11) or 4·5 g OKG/kg per d (LPS-OKG-4·5, n 10). The diets for all groups were made isonitrogenous with the LPS-OKG-4·5 diet by adding an appropriate amount of non-essential amino acids. Rats were killed on day 3 for blood and tissue sampling (muscle, jejunum mucosa, liver). Urine was collected daily for 3-methylhistidine and total N assays. The OKG dose was correlated with Gln concentrations in every tissue and with cumulative N balance (Spearman test, P<0·01). 3-Methylhistidine excretion was increased in endotoxaemic groups compared with controls (ANOVA, P<0·05) except in the LPS-OKG-4·5 group. Only the LPS-OKG-4·5 group achieved a positive post-injury N balance (t test, P<0·05). In conclusion, OKG exerted a dose-dependent effect on tissue Gln concentration and N balance, but only the highest dosage counteracted myofibrillar hypercatabolism and caused a positive N balance.

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.

‘Orujo’ olive oil is obtained by chemical processes from the waste resulting from the mechanical extraction of virgin olive oil. The aim of the present study was to evaluate a new pharmacological property of two natural triterpenoids contained in olive oil, as vasodilatory agents, and to determine their mechanism of action. The two compounds studied were oleanolic acid and erythrodiol. The vasorelaxant effect induced by these pentacyclic triterpenoids was studied in isolated thoracic rat aorta. Oleanolic acid and erythrodiol, accumulatively added, showed vasorelaxant activities in aortic rings with endothelium pre-contracted by 10−6 M-phenylephrine (maximum percentage of relaxation 86·38 (SEM 2·89) and 73·53 (SEM 6·01), respectively). They had almost no relaxant effect on depolarised or endothelium-denuded aortic segments. The relaxation was significantly attenuated by pre-treatment with the NO synthase inhibitor Nω-nitro-L-arginine-methylester (L-NAME; 3×10−4 m). To characterise the involvement of endothelial factors, in addition to NO, arteries with endothelium were exposed to 10−5 M-indomethacin (INDO), a cyclo-oxygenase inhibitor, or INDO plus L-NAME. INDO did not have any significant effect on the relaxant response of both compounds. The combination of L-NAME plus INDO only abolished the oleanolic acid-induced relaxation. The present results suggest that the mechanism of relaxation seems to be mainly mediated by the endothelial production of NO; however, other mechanisms cannot be excluded. It can be concluded that oleanolic acid and erythrodiol may have interesting therapeutic potential as new vasodilator drugs, thus protecting the cardiovascular system. Therefore, the intake of ‘orujo’ olive oil, as a source of these compounds, might be beneficial in this regard.

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and α-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.

Oral administration of raffinose, a naturally occurring indigestible oligosaccharide, has reportedly ameliorated atopic dermatitis in human subjects although the mechanism is unknown. The present study investigated the effect of dietary raffinose on allergen-induced airway eosinophilia in ovalbumin-sensitised Brown Norway rats as an atopic disease model. Brown Norway rats were immunised by subcutaneous injection with ovalbumin on day 0 and fed either a control diet or the diet supplemented with raffinose (50 g/kg diet). The rats were exposed to aerosolised ovalbumin on day 20, and broncho-alveolar lavage fluid was obtained on the next day. The number of eosinophils in the fluid was significantly lower in the rats fed the raffinose diet than in those fed the control diet. Dietary raffinose significantly reduced IL-4 and IL-5 mRNA levels in lung tissue and tended to lower ovalbumin-specific Ig E levels. Suppression of eosinophilia by dietary raffinose was still observed in caecectomised and neomycin-administered rats, suggesting little contribution by the colonic bacteria to the effect of raffinose. Intraperitoneal administration of raffinose also suppressed eosinophilia. Significant concentrations of raffinose were detected in portal venous and abdominal arterial plasma after the intragastric administration of raffinose. Overall, the findings suggest that dietary raffinose ameliorates allergic airway eosinophilia at least partly via post-absorptive mechanisms in Brown Norway rats.

Bioelectrical impedance analysis (BIA) is an easy-to-use, non-invasive and reproducible technique to evaluate changes in body composition and nutritional status. Phase angle, determined by BIA, has been found to be a prognostic indicator in several chronic conditions, such as HIV, liver cirrhosis, chronic obstructive pulmonary disease and lung cancer, and in patients undergoing dialysis. The present study investigated the prognostic role of phase angle in advanced pancreatic cancer. We evaluated a case series of fifty-eight stage IV pancreatic cancer patients treated at Cancer Treatment Centers of America® at Midwestern Regional Medical Center (Zion, IL, USA) between January 2000 and July 2003. BIA was conducted on all patients using a bioelectrical impedance analyser that operated at 50kHz. The phase angle was calculated as capacitance (Xc)/resistance (R) and expressed in degrees. The Kaplan–Meier method was used to calculate survival. Cox proportional hazard models were constructed to evaluate the prognostic effect of phase angle independent of other clinical and nutritional variables. The correlations between phase angle and traditional nutritional measures were evaluated using Pearson and Spearman coefficients. Patients with phase angle <5·0° had a median survival time of 6·3 (95% CI 3·5, 9·2) months (n 29), while those with phase angle >5·0° had a median survival time of 10·2 (95% CI 9·6, 10·8) months (n 29); this difference was statistically significant (P=0·02). The present study demonstrates that phase angle is a strong prognostic indicator in advanced pancreatic cancer. Similar studies in other cancer settings with larger sample sizes are needed to further validate the prognostic significance of the phase angle.

The aim of the present study was to analyse the changes in body composition of stunted children during a follow-up period and to test the hypothesis of a tendency to accumulate body fat as a consequence of undernutrition early in life. We selected fifty boys and girls aged 11 to 15, who were residents of slums in São Paulo, Brazil. Twenty were stunted (S) and thirty had normal stature (NS). The children's nutritional status and body composition were assessed through anthropometry and dual-energy X-ray absorptiometry, at the beginning of the present study and after 3 years, and changes in lean mass (LM and LM%) and fat mass (FM and FM%) were calculated. Stunted boys accumulated more body fat (FM%: S=1·62%, NS=−3·40%; P=0·003) and gained less lean mass (LM%: S=−1·46, NS=3·21%; P=0·004). Stunted girls gained less lean mass (S=7·87 kg, NS=11·96 kg; P=0·032) and had significantly higher values of FM% at follow-up when compared with their baseline values (P=0·008), whereas non-stunted girls had a non-significant difference in FM% over time (P=0·386). These findings are important to understand the factors involved in the increased prevalence of overweight and obesity among poor populations, which appear to be associated with hunger during infancy and/or childhood.

Nutrient utilisation and growth performance responses of White Pekin ducks (Anas platyrinchos domesticus) offered diets containing low- or high-viscosity wheat supplemented with xylanase were investigated in two studies. In Expt 1, six diets consisting of low-viscosity wheat or high-viscosity wheat supplemented with 0·0, 1·5 or 3·0 g xylanase (2590 units/g)/kg diet were used in a true metabolisable energy (TME) bioassay with eight 8-week-old ducks per diet group. In Expt 2, eight pens of ten 3-d-old ducks per pen for each of six wheat-based diets arranged in a 2×3 factorial of low-viscosity or high-viscosity wheat and 0·0, 1·5 or 3·0 g xylanase/kg were used in a 42 d growth study. High-viscosity wheat depressed (P>0·001) TME and xylanase supplementation improved (P>0·001) TME, more so for high-viscosity than low-viscosity wheat. Xylanase supplementation of the high-viscosity wheat-based diet improved (P>0·05) weight gain and gain:feed ratio by 13 and 12% respectively. There was no weight gain or gain:feed ratio response to xylanase supplementation of the low-viscosity wheat-based diet. Xylanase supplementation reduced (P>0·001) the viscosity of duodenal and ileal digesta for high-viscosity but not low-viscosity wheat-based diets. Ileal digestibilities of nutrients and energy were higher (P>0·001) for low-viscosity than high-viscosity wheat-based diets; xylanase supplementation improved (P>0·05) energy, fat, N and starch digestibilities. Given that xylanase supplementation of high-viscosity wheat assuaged its anti-nutritional effect, it is surmised that digesta viscosity plays a role in anti-nutritional effects in wheat-based diets for ducks.

PUFA and their metabolites are important regulators of bone formation and resorption. The effect of PUFA on bone growth may be especially striking during the perinatal period. The aim of the present study was to investigate the effect of diets with different n-6:n-3 fatty acid (FA) ratios during the perinatal period on bone parameters in the adult offspring. During late gestation and throughout lactation, rat dams were fed an isoenergetic diet containing 70 g linseed oil (n-3 diet), soyabean oil (n-6+n-3 diet) or sunflower-seed oil (n-6 diet) per kg with n-6:n-3 FA ratios of 0·4, 9 and 216, respectively. The offspring were weaned onto an ordinary chow and followed until 30 weeks of age. Bone parameters were analysed using peripheral quantitative computerised tomography and dual-energy X-ray absorptiometry. Femur length and cortical cross-sectional bone area and bone mineral content were significantly higher in the n-6+n-3 group than in the other groups. Cortical bone thickness in the n-6+n-3 group was increased compared with the n-3 group, but most cortical bone parameters did not differ between the n-3 and n-6 groups. The results suggest that regulatory mechanisms were influenced by the n-6:n-3 FA ratio early in life and not compensated for by the introduction of an ordinary diet after weaning.

Peroxidation of LDL and other lipoproteins is thought to play a central role in atherogenesis. Dietary thermally oxidised oils may increase atherogenic risk in consumers by increasing their oxidative status. The present paper compares the effects of two diets containing unused sunflower-seed oil (US) or sunflower-seed oil repeatedly used in frying (FS) (both 15 g/100 g diet) on weight gain, food efficiency ratio, serum lipid levels and lipoprotein composition, and the content of thiobarbituric acid-reactive substances (TBARS) in the liver, serum, and lipoproteins in growing Wistar rats. After sixty potato fryings the FS contained 27·7 g polar material/100 g oil and 16·6 g oligomers/100 g oil. The FS-fed rats had a significantly lower weight gain and food efficiency ratio. Liver-TBARS increased due to the consumption of the highly altered oil and showed a significant linear relationship (all r<0·68; P>0·002) with the ingestion of thermally oxidised compounds. Serum-, VLDL-, LDL- and HDL-TBARS were significantly higher in the FS-fed rats (all P>0·001). Concentrations of serum total and non-esterified cholesterol and phospholipids were significantly higher in the FS-fed rats (P>0·05, P>0·05, and P>0·001, respectively). Serum triacylglycerol concentrations did not vary between the two dietary groups. Total and esterified cholesterol and phospholipid levels increased significantly in the HDL fraction (P>0·05, P>0·05, and P>0·001, respectively) of the FS-fed rats. HDL-cholesterol and HDL-phospholipids were significantly correlated with liver-TBARS (r<0·747; P>0·0001), VLDL-TBARS (r<0·642; P>0·003), LDL-TBARS (r<0·475; P>0·04), and HDL-TBARS (r<0·787; P>0·0001). The data suggest that the rat increases HDL as a protecting mechanism against the peroxidative stress induced by the consumption of a diet containing the thermally oxidised oil.

Genes are known to have independent influences on the height and weight of individuals, their overall levels of nutrient intakes and their meal sizes and frequencies. Recent evidence suggests that genes exert multiple and subtle influences on the controls of food intake. There are significant genetic influences on the level and responsiveness of the individual to physiological factors, such as the preprandial stomach contents of nutrients and subjective hunger, and also to environmental and psychological factors such as social facilitation of eating, diurnal rhythms of intake, palatability, cognitive restraint and dietary density. The general model of intake regulation provides an integrated and comprehensive account of how these physiological and environmental factors might fit together to produce the control of intake and body weight.