Knowledge of the cannabinoid system and its components has expanded greatly over the past decade. There is increasing evidence for its role in the regulation of food intake and appetite. Cannabinoid system activity in the hypothalamus is thought to contribute to the homeostatic regulation of energy balance, under the control of the hormone leptin. A second component of cannabinoid-mediated food intake appears to involve reward pathways and the hedonic aspect of eating. With the cannabinoid system contributing to both regulatory pathways, it presents an attractive therapeutic target for the treatment of both obesity and eating disorders.

The discovery of the production of leptin by the stomach, in addition to its production by adipose tissue, has initiated new investigation into the possible role of this protein in the digestive physiology, in particular in the short-term control of energy balance. Leptin has been identified in the lower half of the stomach glands both in the pepsinogen granules of chief cells and in the granules of a specific endocrine cell type, suggesting that leptin action is exerted by both exocrine and endocrine pathways. Gastric leptin is sensitive to the nutritional state, being rapidly mobilized in response to food intake following fasting, or after the administration of satiety factors; this suggests a role for this protein in the short-term regulation of feeding, acting in collaboration with satiety peptides such as cholecystokinin. Leptin, produced by gastric cells and by adipocytes, could act on both acute and chronic regulation of feeding behaviour respectively, giving information to the brain on the availability of external (food) and internal (fat depots) energy resources, thus participating in short- and long-term satiation.

The effect of polyunsaturated fatty acids (PUFA), in particular conjugated linoleic acid (CLA), on Ca and bone metabolism is unclear. In a 2 × 2 factorial design study, forty male 4-week-old rats were fed a control diet containing 70 g added fat (soyabean oil (SBO; n–6 PUFA-rich diet) or menhaden oil–safflower oil (MSO; n−3 PUFA-rich diet))/kg diet with 0 or 10 g CLA/kg for 8 weeks. Ex vivo prostaglandin E2biosynthesis by bone organ culture was significantly higher (P<0·001) in rats consuming SBO compared with MSO, irrespective of CLA. Addition of the CLA treatment to either diet further lowered (P<0·05) ex vivo prostaglandin E2 production. Neither PUFA type nor CLA altered circulating or femoral mRNA levels of osteocalcin (a marker of bone formation) or insulin-like growth factor-I (a mediator of bone metabolism). While urinary pyridinium crosslinks levels (markers of bone resorption) were unaffected by CLA irrespective of PUFA type, they were significantly higher (P<0·05) in rats consuming SBO compared with MSO irrespective of CLA. Net fractional (%) and absolute (mg) Ca absorption were significantly (P<0·01 and P<0·05 respectively) higher in CLA-supplemented than unsupplemented animals fed on the n−3 PUFA-rich diet, whereas CLA had no effect in animals fed the n–6 PUFA-rich diet. There was no effect of CLA supplementation on bone mineral mass. In conclusion, CLA supplementation over 8 weeks appeared to enhance Ca absorption in young growing rats fed an n−3 PUFA-rich diet, but had no measurable effect on bone metabolism or bone mass over this time frame.

The cellular uptake of ammonia affects the intracellular pH (pHi) of polar and non-polar cells. A predominant uptake of NH3 and its intra-cellular protonation tend to alkalinise the cytoplasm, whereas a predominant uptake of NH4+ acidifies the cytoplasm by reversing this reaction. Hence, the well-known absorption of ammonia across the rumen epithelium probably causes a change in the pHi. The magnitude and direction of this change in pHi (acid or alkaline) depends on the relative transport rates of NH3 and NH4+. Consequently, the intra-cellular availability of protons will influence the activity of the Na+-H+ exchanger, which could affect transepithelial Na+ transport. The aim of the present study has been to test this possible interaction between ruminal ammonia concentrations and Na+ transport. The term ammonia is used to designate the sum of the protonated (NH4+) and unprotonated (NH3) forms. Isolated ruminal epithelium of sheep was investigated by using the Ussing-chamber technique in vitro. The present results indicate that ammonia inhibits Na+ transport across the rumen epithelium of hay-fed sheep, probably by binding intracellular protons and thus inhibiting Na+-H+ exchange. By contrast, ammonia stimulates Na+ transport in concentrate-fed and urea-fed sheep, which develop an adaptation mechanism in the form of an increased metabolism of ammonia in the rumen mucosa and/or an increased permeability of rumen epithelium to the charged ammonium ion (NH4+). Intracellular dissociation of NH4+ increases the availability of protons, which stimulate Na+ –H+ exchange. This positive effect of ruminal ammonia on Na+ absorption may significantly contribute to the regulation of osmotic pressure of the ruminal fluid, because intraruminal ammonia concentrations up to 40 mmol/l have been reported.

Lycopene, the main carotenoid found in tomatoes and tomato-based products, has been reported to be protective against several types of cancer. Assessment of changes in plasma concentration of carotenoids following ingestion of lycopene-rich food sources does not necessarily predict changes in lycopene concentration or distribution of its isomers in other body tissues. Our aim was to determine the relationship between concentrations of lycopene and other tomato carotenoids in human serum and body tissues after tomato-oleoresin supplementation. Tomato lycopene oleoresin (30 mg/d) or a placebo was administered for 1 to 7 weeks to seventy-five volunteers undergoing elective haemorrhoidectomy or peri-anal fistulotomy. Carotenoid concentration and isomer distribution in blood and in the surgically removed skin and adipose tissues was measured by HPLC. The serum concentration of lycopene increased after supplementation from 0·26 (sd 0·12) to 0·52 (sd 0·25) μmol/l (n 35; P<0·0001). In the placebo group (n 40), lycopene serum concentration did not change significantly. Serum lycopene concentration after treatment was 2·2-fold greater in the lycopene group than in the placebo group, a slightly higher ratio than that found in skin and adipose tissue (1·6- and 1·4-fold higher than the placebo, respectively). A significant correlation between serum and tissue concentrations was found for both β-carotene and lycopene in the placebo group, whereas in the lycopene-supplemented group the correlation between serum and tissues remained the same for β-carotene but for lycopene was weak. Lycopene supplementation did not significantly change the proportion of all-trans v. cis isomers in the serum and tissues, despite the fact that more than 90 % of the supplemented lycopene was in the all-trans form. These results show that tomato-oleoresin supplementation increases lycopene concentrations in serum and in adipose tissue and skin. The ability to increase lycopene levels in tissues is one of the prerequisites for using it as a food supplement with health benefits.

Phytosterols are plant sterols found in foods such as oils, nuts and vegetables. Phytosterols, in the same way as cholesterol, contain a double bond and are susceptible to oxidation. The objective of the present study was to assess the potential toxic effects of β-sitosterol oxides on U937 cells. The effects of increasing concentrations (0-120 μM) of β-sitosterol oxides on cellular cytotoxicity, apoptosis, anti-oxidant status and genotoxicity was assessed over 12, 24 and 48h exposure periods. Following 12h, the viability of cells treated with 120 μM-β-sitosterol oxides was reduced to 51·7% relative to control. At 24 and 48 h, both 60 and 120 μM-β-sitosterol oxides caused a significant decrease in cell viability. For comparison, a decrease in viability of cells treated with a cholesterol oxide, 7β-hydroxycholesterol (7β-OH, 30 μM), was evident at 24 h. An increase in apoptotic cells, assessed using Hoechst 33342, indicates that the mode of cell death in U937 cells following exposure to 7β-OH (30 μM) and β-sitosterol oxides (60 and 120 μM) was by apoptosis. The increase in apoptotic cells after 12h following treatment with 120 μM-β-sitosterol oxides was accompanied by a decrease in cellular glutathione. Similarly, 7β-OH (30 μM) treatment resulted in decreased glutathione at 12 h. Catalase activity was not affected by any of the treatments. β-Sitosterol oxides had no genotoxic effects on U937 and V79 cells as assessed by the comet and sister chromatid exchange assays respectively. In general, the results indicate that thermally oxidised derivatives of β-sitosterol demonstrate similar biological effects as 7β-OH in U937 cells, but at higher concentrations.

The present study examined the effects of a 3-week fish-oil supplementation (6 g/d) on the rate of plasma glucose disappearance (Rd glucose), hepatic glucose production (HGP), carbohydrate oxidation and lipid oxidation during exercise. Six untrained males (23±1 years; 67·6±2·7kg) performed two 90min cycling exercise sessions at 60% of maximal O2 output separated by 20 d. During the 20 d before the first test, they ingested 6g olive oil/d, then 6g fish oil/d during the 20 d before the second test. Plasma glucose fluxes and lipolysis were traced using 6,6-[2H2]glucose and 1,1,2,3,3-[2H5]glycerol respectively. Substrates oxidation was obtained from indirect calorimetry. At rest HGP and the Rd glucose were similar after olive oil and fish oil (1.83 (se 0·05) v. 1·67 (se 0·11) mg/kg per min). During exercise, fish oil reduced the stimulation of both the Rd glucose (5·06 (se 0·23) v. 6·37 (se 0·12) mg/kg per min; P<0·05) and HGP (4·88 (se 0·24) v. 5·91 (se 0·21) mg/kg per min; P<0·05). Fish oil also reduced glucose metabolic clearance rate (6·93 (se 0·29) v. 8·30 (se 0·57) ml/min). Carbohydrate oxidation tended to be less stimulated by exercise after fish oil than after olive oil (12·09 (se 0·60) v. 13·86 (se 1·11) mg/kg per min; NS). Lipid oxidation tended to be more stimulated by exercise after fish oil (7·34 (se 0·45) v. 6·85 (se 0·17) mg/kg per min; NS). Glycaemia, lactataemia, insulinaemia and glucagonaemia were similarly affected by exercise after fish oil and olive oil. Lipolysis at rest was similar after fish oil and olive oil (2·92 (se 0·42) v. 2·94 (se 0·28) μmol/kg per min) and similarly stimulated by exercise (6·42 (se 0·75) v. 6·77 (se 0·72) μmol/kg per min). It is concluded that fish oil reduced the Rd glucose by 26% by reducing glucose metabolic clearance rate, possibly by facilitating fat oxidation, and reduced HGP by 21%, possibly by a feedback mechanism.

Alkylresorcinols (AR) are amphiphilic 1,3-dihydroxy-5-alkyl phenolic lipids. AR in food are only found in the outer layers of wheat and rye grains, and in whole grains are present at concentrations of 500–1000 μg/g. In wheat and rye, there are five main homologues, differing in the length of the odd-numbered alkyl chain (from seventeen to twenty-five C atoms long). Because AR may be bioactive, and might serve as biomarkers for these cereals, their absorption was investigated in model experiments with pigs and rats. Pigs with a cannula in the terminal ileum were fed four diets containing rye fractions with different levels of AR and the ileal effluents were analysed. The ileal recovery of AR was found to vary between 21 and 40 %, with no major difference between different chain-length homologues. The absorption of AR by rats was investigated by feeding 14C-labelled heneicosylresorcinol (C21:0). Of the total activity, about 34% was recovered in the urine, showing that the labelled AR was absorbed and metabolised by rats. AR were mostly cleared from rats by 60h. It is concluded that AR are absorbed in the small intestine of single-stomached animals and excreted in metabolised form in the urine, and might contribute to the nutritional qualities of wholegrain wheat and rye diets.

Many orange-coloured fruits contain β-cryptoxanthin in its non-esterified as well as its esterified form. Information concerning the absorption of β-cryptoxanthin, especially with regard to the metabolism of its fatty acid esters, is rather scarce. The present study assessed the plasma concentration reached after consumption of a single dose of native β-cryptoxanthin esters from papaya (Carica papaya L.) or non-esterified β-cryptoxanthin in equal total amounts. In a randomized, single-blind crossover study, twelve subjects were served a portion of yoghurt containing esterified or non-esterified β-cryptoxanthin (1.3 mg absolute) together with a balanced breakfast. Between the two intervention days, there was a 2-week depletion period. After a fasting blood sample had been taken, futher samples were taken from the subjects at 3, 6, 9, 12 and 24 h. The concentration of non-esterified β-cryptoxanthin in the whole plasma was determined by HPLC; β-cryptoxanthin identification was confirmed by liquid chromatography–atmospheric pressure chemical ionization–MS analyses. Irrespective of the consumed diet, the plasma β-cryptoxanthin concentrations increased significantly (P=0·05) and peaked after 6–12 h. The concentration curves, as well as the areas under the curves, were not distinguishable according to two-sided F and t tests (P=0·05). Standardization of β-cryptoxanthin concentrations to plasma triacylglycerol and cholesterol had no impact on the results. Thus, the present study indicates comparable bioavailability of both non-esterified β-cryptoxanthin and mixtures of β-cryptoxanthin esters. The results support the existence of an effective enzymatic cleavage system accepting various β-cryptoxanthin esters.

Sun-dried raisins are a source of dietary fibre and tartaric acid. The effects of tartaric acid on colon function have not been the focus of extensive research. The purpose of the present study was to evaluate the effects of dietary fibre and tartaric acid from sun-dried raisins on colon function and on faecal bile acid and short-chain fatty acid (SCFA) excretion in healthy adults. Thirteen healthy subjects were fed 120 g sun-dried raisins/d or 5 g cream of tartar (equivalent to the tartaric acid in 120 g sun-dried raisins)/d for 9 weeks, divided into 3-week cycles. The experimental diets were fed in a crossover design after an initial control period. Faeces were collected for the last 4 d of each cycle for analysis of SCFA and bile acids. Intestinal transit time decreased from 42h on the baseline diet to 31h on cream of tartar (P<0·1) and to 28h on sun-dried raisins (P<0·05). Faeces were softer on both sun-dried raisins and cream of tartar, but sun-dried raisins increased faecal wet weight (P<0·05), while cream of tartar did not. Sun-dried raisins caused significant reductions from baseline values in total bile acid concentration (from 1·42 (sd 1·03) to 1·09 (sd 0·76) mg/g, P<0·05), whereas cream of tartar did not (1·40 (sd 1·06) mg/g). Sun-dried raisins also significantly reduced the lithocholic (LC):deoxylithocholic acid (DC) ratio (from 1·63 (sd 0·85) to 1·09 (sd 0·50), P<0·02), whereas cream of tartar reduced the ratio, but to a lesser extent (1·29 (sd 0·79), NS). Both faecal bile acids and the LC:DC ratio are indicators of reduced risk for colon cancer. Sun-dried raisins increased total SCFA excretion (from 5·6 (sd 3·4) to 7·6 (sd 3·0) g/4d, P<0·05), which remained unchanged with cream of tartar (5·6 (sd 3·0) g/4d). Both sun-dried raisins and cream of tartar appear to be good stool softeners and to shorten intestinal transit time, although the fibre in sun-dried raisins has the added benefit of increasing faecal weight. Both sun-dried raisins and cream of tartar modulate the composition of faecal bile acids and SCFA in a way that has potential health benefits.

The nutritional basis of breakdown of immunity to parasites may be addressed in a rodent model. We hypothesized that lactating rats would show a breakdown of immunity to Nippostrongylus brasiliensis, and that this breakdown of immunity would be sensitive to protein supply. Rats were immunized with 1600 infective N. brasiliensis larvae and subsequently mated. During lactation, these rats were offered foods with 90 (low protein; LP) or 210 (high protein, HP) g crude protein (N X 6.25)/kg and re-infected with 400, 800 or 1600 larvae on day 2 post-parturition. Immunized non-reproducing rats were offered a food containing 60 g crude protein/kg and re-infected with 1600 larvae. Seven days after secondary infection, lactating rats had more adult nematodes in their small intestine and nematode eggs in their colon contents than the non-reproducing rats. Protein supply did not affect worm or egg counts, although LP rats carried relatively more female nematodes than the HP rats. All lactating rats had lower intakes than expected from previous studies using similar nutritional protocols. This may have resulted in insufficient protein supply, even for the HP rats, and this could explain the absence of effects of protein supply on egg and worm counts. We conclude that a breakdown of immunity to N. brasiliensis can occur in lactating rats; this strongly suggests that the lactating rat is a suitable model for elucidating a possible nutritional basis of breakdown of immunity to parasites. However, sufficient protein intake must be achieved to address the hypothesis that breakdown of immunity to N. brasiliensis is sensitive to protein supply.

Many adult diseases, including type 2 diabetes, hypertension and cardiovascular disease, are related to low birth weight. The mechanistic basis of this relationship is not known. To investigate the role of fetal undernutrition, we used a rat model of maternal protein restriction in which dams were fed a diet containing 80 g protein/kg (v. 200 g/kg in the control group) throughout gestation and lactation. Offspring were born smaller than controls and in adulthood developed diabetes, hyperinsulinaemia and tissue insulin resistance. To determine possible mechanisms of fetal programming, circulating levels of several hormones were measured in maternal plasma at gestational days 14, 17 and 21 and fetal plasma at gestational day 21. Several differences were noted at day 14, when glucose concentrations in maternal and feto–placental blood were raised significantly (P=0·04 and P=0·0001 respectively); insulin levels in the low-protein (LP) dams were raised (P=0·04), prolactin levels were raised (P=0·047) and progesterone levels were reduced (P=0·02). Circulating 17β-oestradiol in the LP dams was raised by 35% over those of the controls from day 17 to day 21 (P=0·008). A significant decrease in maternal leptin levels (P=0·004) was observed at gestation on day 21. Neither oestradiol nor leptin levels were altered in the fetal circulation at day 21. Maternal and fetal corticosterone levels were comparable with control levels, suggesting that they do not initiate the programming effects in this model. Our present results suggest that maternal protein restriction imposes changes in maternal levels of glucose, insulin, prolactin, progesterone, oestradiol and leptin; these changes could influence the programming of eventual adult disease in the developing fetus.

Postprandial glycaemic control is important in the prevention and therapy of type 2 diabetes and related diseases. Agents that may reduce postprandial glycaemia and/or insulinaemia, such as consumption of high-amylose foods, are considered beneficial; however, little is known about the dose–response relationship and the effects of cooking. The aim of the present study was to define the dose–response curve for postprandial glycaemic and insulinaemic excursions following meals of different amylose content and to compare the dose–response curves for meals containing cooked and uncooked starches. Following an overnight fast, rats ingested a test meal and blood was sampled over 2 h. The meal was given at 1.0 g carbohydrate/kg body weight, with an amylose content of 0, 270, 600 or 850 g/kg total starch. The area under the glucose curve did not differ under any condition investigated. For the uncooked-starch diets, area under the insulin curve was higher for the 0 g amylose/kg total starch meal than all other meals (P = 0·0001). For the cooked-starch diets, area under the insulin curve was higher in the O than the 600 and 850 g amylose/kg total starch groups (P < 0·01), but did not differ from the 270 amylose/kg total starch group. These results suggest that even a relatively small proportion of uncooked amylose (270 g/kg total starch) is sufficient to achieve a maximal attenuating effect on postprandial insulin concentrations as compared with 0 g amylose/kg total starch. Following cooking, however, a much higher proportion of amylose (≥ 600 g/kg total starch) is needed to achieve a similar effect.

Upon admission to hospital, 30–50% of patients either are or become malnourished. There is no generally accepted definition of malnutrition or guidelines on the best way to establish nutritional status. We consider it self-evident that the nursing staff have an important role in screening patients at risk of malnutrition on admission and thereafter at regular times. This is why we developed the nursing nutritional screening form (NNSF). The NNSF was tested by nurses, dietitians and clinicians, in pairs, to establish the extent of agreement in two phases on sixty-nine and forty patients. Later, the form was used in practice by nursing staff on five wards (334 patients). Based on the results of the NNSF, patients were referred to a dietitian. The dietitian established whether the patient was indeed at risk, or was actually malnourished, using a complete nutritional history. The degree of concurrence within pairs was reasonable to good. The same applied to the concurrence between nursing staff and dietitians, but concurrence between clinicians and nursing staff was less. In total, 334 patients were screened and sixty-nine of them were referred to the dietitian. It was established that 86% of the referred patients were potentially at risk of malnutrition or were malnourished. Without the NNSF, 39% (n 27) of the patients referred to the dietitian would not have been referred, or would have been referred much later. The NNSF makes it possible for nurses to detect malnourished patients or patients at risk of malnutrition at an early stage of their hospitalization.

The objective of the present study was to examine the relationship between body composition and blood pressure (BP) in Bahraini adolescents. A sample of 504 Bahraini schoolchildren aged 12–17 years (249 boys and 255 girls) was selected using a multi-stage stratified sampling procedure. BP measurements were performed on the students. Anthropometric data including weight, height, waist circumference (WC), hip circumference, and triceps, subscapular and medial calf skinfold thicknesses were also collected. BMI, percentage body fat, waist:hip (WHR), and subscapular:triceps skinfold ratio were calculated. Mean systolic BP and mean diastolic BP were higher in males than in females. Weight and height in boys and weight only in girls were significantly associated with systolic BP independent of age or percentage fat. Nearly 14% of the adolescents were classified as having high BP. BMI and percentage body fat were significantly and positively associated with the risk of having high BP in the boys and girls. Adolescents with high WHR or WC, as indicators for central obesity, tended to have higher BP values. The results from the present study indicate that obesity influences the BP of Bahraini adolescents and that simple anthropometric measurements such as WHR and WC are useful in identifying children at risk of developing high BP. These findings together with the known tracking of BP from adolescence into adulthood underline the importance of establishing intervention programmes in order to prevent the development of childhood and adolescent obesity.