1. We have investigated the relations between changes in plasma insulin and 3,5,3'-triiodothyronine (T3), and muscle growth and protein turnover in the rat in response to diets of varying protein concentrations.

2. Young rats were fed ad lib. on a control (180 g casein/kg) diet or low-protein diets containing 80, 45 and 0 g casein/kg in four separate experiments. Measurements were made of food intakes, muscle and body-weight growth rates, muscle protein turnover in vivo, plasma insulin, and plasma free and total T3.

3. The food intakes of the 80 and 45 g casein/kg diet groups were variable, with the 80 g casein/kg diet group consuming either the same or more than the controls, and the 45 g casein/kg diet group consuming less or more than the controls. Body-weight and skeletal-muscle growth rates varied with the protein but not energy intakes, which in turn reflected both dietary composition and the food intake, with the hyperphagic 80 g casein/kg diet group of rats growing almost normally and the 0 g casein/kg diet group losing body-weight and muscle mass.

4. Changes in rates of muscle growth were accompanied by parallel changes in rates of protein synthesis and degradation, as well as parallel changes in concentrations of plasma insulin and free T3, to the extent that all these variables were highly correlated with each other.

5. Partial correlation analysis was used to separate interactions between variables. This indicated that dietary energy had no identifiable influence on muscle growth. In contrast dietary protein appeared to stimulate muscle growth directly by increasing muscle RNA content and inhibiting proteolysis, as well as increasing insulin and free T3 levels. Insulin and free T3 stimulated each other as well as muscle protein turnover; insulin stimulating the RNA activity particularly at low insulin levels, free T3 stimulating the RNA content and both hormones stimulating proteolysis.

6. These apparent relations are shown to be consistent in the main part with previous studies of the mechanism of action of insulin and T3 but the possibility cannot be discounted that other anabolic hormones not measured in these studies are involved, particularly in the apparent direct influence of dietary protein on muscle.

1. Twelve young adult male volunteers were given a low-fibre white bread diet (9 g neutral-detergent fibre (NDF)/d) and a medium-fibre coarse-bran bread diet (22 g NDF/d), each lasting 20 d. In a third period of 20 d the volunteers were subdivided in groups of four, consuming a high-fibre coarse-bran bread diet (35 g NDF/d), a medium-fibre fine-bran diet (22 g NDF/d, bran particle size > 0.35 mm) or a wholemeal bread diet (22 g NDF/d). Digestion of dietary fibre and its components hemicellulose, cellulose and lignin were determined as well as colonic function.

2. An increase of the amount of dietary fibre (through bran in bread) from 9 to 22 g NDF/d resulted in the following significant changes (P < 0.01): increase in faecal wet weight of 63 g/d, decrease in the percentage of faecal dry weight from 27 to 24, increase in defaecation frequency of 0.2 stools/d and reduction of the intestinal transit time of 36 h.

3. Further significant changes with regard to all factors mentioned were observed during the high-fibre diet. Faecal wet weight was significantly (P < 0.05) lower with the fine-bran bread diet than with the coarse-bran bread on a similar fibre intake of 22 g NDF/d. Results obtained in the wholemeal-bread period did not show significant differences compared with those from the coarse-bran bread period of 22 g NDF/d.

4. Mean digestibilities for the fibre from bread were: for NDF 0.34, for hemicellulose 0.46, for cellulose 0.20 and for lignin 0.04.

5. The results obtained suggest that the theory of sponge activity of the fibre matrix structure is the predominant factor accounting for the water binding capacity of fibre in the colon.

Lignans, derived from flaxseed, are phyto-oestrogens being increasingly studied for their health benefits. An 8-week, randomised, double-blind, placebo-controlled study was conducted in fifty-five hypercholesterolaemic subjects, using treatments of 0 (placebo), 300 or 600 mg/d of dietary secoisolariciresinol diglucoside (SDG) from flaxseed extract to determine the effect on plasma lipids and fasting glucose levels. Significant treatment effects were achieved (P < 0·05 to < 0·001) for the decrease of total cholesterol (TC), LDL-cholesterol (LDL-C) and glucose concentrations, as well as their percentage decrease from baseline. At weeks 6 and 8 in the 600 mg SDG group, the decreases of TC and LDL-C concentrations were in the range from 22·0 to 24·38 % respectively (all P < 0·005 compared with placebo). For the 300 mg SDG group, only significant differences from baseline were observed for decreases of TC and LDL-C. A substantial effect on lowering concentrations of fasting plasma glucose was also noted in the 600 mg SDG group at weeks 6 and 8, especially in the subjects with baseline glucose concentrations ≥ 5·83 mmol/l (lowered 25·56 and 24·96 %; P = 0·015 and P = 0·012 compared with placebo, respectively). Plasma concentrations of secoisolariciresinol (SECO), enterodiol (ED) and enterolactone were all significantly raised in the groups supplemented with flaxseed lignan. The observed cholesterol-lowering values were correlated with the concentrations of plasma SECO and ED (r 0·128–0·302; P < 0·05 to < 0·001). In conclusion, dietary flaxseed lignan extract decreased plasma cholesterol and glucose concentrations in a dose-dependent manner.

Faecal microbial changes associated with ageing include reduced bifidobacteria numbers. These changes coincide with an increased risk of disease development. Prebiotics have been observed to increase bifidobacteria numbers within humans. The present study aimed to determine if prebiotic galacto-oligosaccharides (GOS) could benefit a population of men and women of 50 years and above, through modulation of faecal microbiota, fermentation characteristics and faecal water genotoxicity. A total of thirty-seven volunteers completed this randomised, double-blind, placebo-controlled crossover trial. The treatments – juice containing 4 g GOS and placebo – were consumed twice daily for 3 weeks, preceded by 3-week washout periods. To study the effect of GOS on different large bowel regions, three-stage continuous culture systems were conducted in parallel using faecal inocula from three volunteers. Faecal samples were microbially enumerated by quantitative PCR. In vivo, following GOS intervention, bifidobacteria were significantly more compared to post-placebo (P = 0·02). Accordingly, GOS supplementation had a bifidogenic effect in all in vitro system vessels. Furthermore, in vessel 1 (similar to the proximal colon), GOS fermentation led to more lactobacilli and increased butyrate. No changes in faecal water genotoxicity were observed. To conclude, GOS supplementation significantly increased bifidobacteria numbers in vivo and in vitro. Increased butyrate production and elevated bifidobacteria numbers may constitute beneficial modulation of the gut microbiota in a maturing population.

There is increasing evidence that the postprandial state is an important contributing factor to chronic disease. The role of fruit phenolic compounds to protect health and lower disease risk through their actions in mitigating fed-state metabolic and oxidative stressors is of interest and the topic of the present paper. Two main questions are posed: first, what is the role of plant foods, specifically fruits rich in complex and simple phenolic compounds in postprandial metabolic management; and second, does the evidence support consuming these fruits with meals as a practical strategy to preserve health and lower risk for disease? This review provides an overview of the postprandial literature, specifically on the effect of fruits and their inherent phenolic compounds in human subjects on postprandial lipaemia, glycaemia/insulinaemia and associated events, such as oxidative stress and inflammation. Among the identified well-controlled human trials using a postprandial paradigm, >50 % of the trials used wine or wine components and the remaining used various berries. Notwithstanding the need for more research, the collected data suggest that consuming phenolic-rich fruits increases the antioxidant capacity of the blood, and when they are consumed with high fat and carbohydrate ‘pro-oxidant and pro-inflammatory’ meals, they may counterbalance their negative effects. Given the content and availability of fat and carbohydrate in the Western diet, regular consumption of phenolic-rich foods, particularly in conjunction with meals, appears to be a prudent strategy to maintain oxidative balance and health.

Coriandrum sativum (coriander) has been documented as a traditional treatment of diabetes. In the present study, coriander incorporated into the diet (62·5 g/kg) and drinking water (2·5 g/l, prepared by 15 min decoction) reduced hyperglycaemia of streptozotocin-diabetic mice. An aqueous extract of coriander (1 mg/ml) increased 2-deoxyglucose transport (1·6-fold), glucose oxidation (1·4-fold) and incorporation of glucose into glycogen (1·7-fold) of isolated murine abdominal muscle comparable with 10−8 m-insulin. In acute 20 min tests, 0·25–10 mg/ml aqueous extract of coriander evoked a stepwise 1·3–5·7-fold stimulation of insulin secretion from a clonal B-cell line. This effect was abolished by 0·5 mm-diazoxide and prior exposure to extract did not alter subsequent stimulation of insulin secretion by 10 mm-l-alanine, thereby negating an effect due to detrimental cell damage. The effect of extract was potentiated by 16·7 mm-glucose and 10 mm-l-alanine but not by 1 mm-3-isobutyl-1-methylxanthine. Insulin secretion by hyperpolarized B-cells (16·7 mm-glucose, 25 mm-KCl) was further enhanced by the presence of extract. Activity of the extract was found to be heat stable, acetone soluble and unaltered by overnight exposure to acid (0·1 m-HCl) or dialysis to remove components with molecular mass < 2000 Da. Activity was reduced by overnight exposure to alkali (0·1 m-NaOH). Sequential extraction with solvents revealed insulin-releasing activity in hexane and water fractions indicating a possible cumulative effect of more than one extract constituent. These results demonstrate the presence of antihyperglycaemic, insulin-releasing and insulin-like activity in Coriandrum sativum.

Fat is often included in common foods as an emulsion of dispersed oil droplets to enhance the organoleptic quality and stability. The intragastric acid stability of emulsified fat may impact on gastric emptying, satiety and plasma lipid absorption. The aim of the present study was to investigate whether, compared with an acid-unstable emulsion, an acid-stable fat emulsion would empty from the stomach more slowly, cause more rapid plasma lipid absorption and cause greater satiety. Eleven healthy male volunteers received on two separate occasions 500 ml of 15 % (w/w) [13C]palmitate-enriched olive oil-in-water emulsion meals which were either stable or unstable in the acid gastric environment. MRI was used to measure gastric emptying and the intragastric oil fraction of the meals. Blood sampling was used to measure plasma lipids and visual analogue scales were used to assess satiety. The acid-unstable fat emulsion broke and rapidly layered in the stomach. Gastric emptying of meal volume was slower for the acid-stable fat emulsion (P < 0·0001; two-way ANOVA). The rate of energy delivery of fat from the stomach to the duodenum was not different up to t = 110 min. The acid-stable emulsion induced increased fullness (P < 0·05), decreased hunger (P < 0·0002), decreased appetite (P < 0·0001) and increased the concentration of palmitic acid tracer in the chylomicron fraction (P < 0·04). This shows that it is possible to delay gastric emptying and increase satiety by stabilising the intragastric distribution of fat emulsions against the gastric acid environment. This could have implications for the design of novel foods.

Deficiency of oestrogen at menopause decreases intestinal Ca absorption, contributing to a negative Ca balance and bone loss. Mg deficiency has also been associated with bone loss. The purpose of the present investigation was to test the hypothesis that treatment with a spray-dried mixture of chicory oligofructose and long-chain inulin (Synergy1; SYN1) would increase the absorption of both Ca and Mg and alter markers of bone turnover. Fifteen postmenopausal women (72·2 (sd 6·4) years) were treated with SYN1 or placebo for 6 weeks using a double-blind, placebo-controlled, cross-over design. Fractional Ca and Mg absorption were measured using dual-tracer stable isotopes before and after treatment. Bone turnover markers were measured at baseline, 3 and 6 weeks. Fractional absorption of Ca and Mg increased following SYN1 compared with placebo (P < 0·05). Bone resorption (by urinary deoxypyridinoline cross-links) was greater than baseline at 6 weeks of active treatment (P < 0·05). Bone formation (by serum osteocalcin) showed an upward trend at 3 weeks and an increase following 6 weeks of SYN1 (P < 0·05). Closer examination revealed a variation in response, with two-thirds of the subjects showing increased absorption with SYN1. Post hoc analyses demonstrated that positive responders had significantly lower lumbar spine bone mineral density than non-responders (dual X-ray absorptiometry 0·887 ± 0·102 v. 1·104 ± 0·121 g/cm2; P < 0·01), and changes in bone turnover markers occurred only in responders. These results suggest that 6 weeks of SYN1 can improve mineral absorption and impact markers of bone turnover in postmenopausal women. Further research is needed to determine why a greater response was found in women with lower initial spine bone mineral density.

1. The thermic effect of a glucose load (50 g) was studied in ten control and eleven obese female subjects, using both direct and indirect calorimetry simultaneously. Experiments were done under conditions of thermal equilibrium (28° and 30% relative humidity)..

2. Thermal balance (heat production measured by indirect calorimetry minus heat losses measured directly) was negative in the control group during the fasting period (heat deficit – 14.2 ± 5.0 kJ/m2 per h), whereas that of the obese group was in equilibrium (+ 1.4 ± 4.8 kJ/m2 per h)..

3. After the glucose load, metabolic rate increased 13.0 ± 1.5 and 5.2 ± 1.3% in the control and obese groups respectively..

4. In contrast to the metabolic rate, total heat losses were not significantly altered in either group after the glucose load. Total heat losses of the obese group were significantly lower than those of the control group throughout the experimental period..

5. During the experiments the amount of heat stored was increased in both groups. Thermal balance in the control group became positive while that of the obese group remained positive..

6. During the fasting period, the control subjects oxidized more carbohydrates (90.4 mg/min) than lipids (68.8 mg/min), whereas obese subjects oxidized more lipids (103.7 mg/min) than carbohydrates (50.2 mg/min). After the glucose load, the oxidation rate of carbohydrates was increased in both groups to 158.1 mg/min in control subjects and 95.6 mg/min in obese subjects..

7. The mean skin temperature of the control subjects was significantly higher than that of the obese subjects and remained higher throughout the postprandial period..

8. These results indicate that: (a) during the fasting period, the energy sources utilized and the thermal balance of the two groups were different; (b) the thermic effect of glucose was less in the obese subjects and, therefore, might be a factor contributing to their low energy expenditure.

We examined the effect of dietary fats rich in n-3 polyunsaturated fatty acids (PUFA) on mRNA levels in white and brown adipose tissues in rats. Four groups of rats were fed on a low-fat diet (20 g safflower oil/kg) or a high-fat diet (200 g/kg) containing safflower oil, which is rich in n-6 PUFA (linoleic acid), or perilla (α-linolenic acid) or fish oil (eicosapentaenoic and docosahexaenoic acids), both of which are rich in n-3 PUFA, for 21 d. Energy intake was higher in rats fed on a high-safflower-oil diet than in those fed on low-fat or high-fish-oil diet, but no other significant differences were detected among the groups. Perirenal white adipose tissue weight was higher and epididymal white adipose tissue weight tended to be higher in rats fed on a high-safflower-oil diet than in those fed on a low-fat diet. However, high-fat diets rich in n-3 PUFA, compared to a low-fat diet, did not increase the white adipose tissue mass. High-fat diets relative to a low-fat diet increased brown adipose tissue uncoupling protein 1 mRNA level. The increases were greater with fats rich in n-3 PUFA than with n-6 PUFA. A high-safflower-oil diet, compared to a low-fat diet, doubled the leptin mRNA level in white adipose tissue. However, high-fat diets rich in n-3 PUFA failed to increase it. Compared to a low-fat diet, high-fat diets down-regulated the glucose transporter 4 mRNA level in white adipose tissue. However, the decreases were attenuated with high-fat diets rich in n-3 PUFA. It is suggested that the alterations in gene expression in adipose tissue contribute to the physiological activities of n-3 PUFA in preventing body fat accumulation and in regulating glucose metabolism in rats.

Cocoa flavanol (CF) intake improves endothelial function in patients with cardiovascular risk factors and disease. We investigated the effects of CF on surrogate markers of cardiovascular health in low risk, healthy, middle-aged individuals without history, signs or symptoms of CVD. In a 1-month, open-label, one-armed pilot study, bi-daily ingestion of 450 mg of CF led to a time-dependent increase in endothelial function (measured as flow-mediated vasodilation (FMD)) that plateaued after 2 weeks. Subsequently, in a randomised, controlled, double-masked, parallel-group dietary intervention trial (Clinicaltrials.gov: NCT01799005), 100 healthy, middle-aged (35–60 years) men and women consumed either the CF-containing drink (450 mg) or a nutrient-matched CF-free control bi-daily for 1 month. The primary end point was FMD. Secondary end points included plasma lipids and blood pressure, thus enabling the calculation of Framingham Risk Scores and pulse wave velocity. At 1 month, CF increased FMD over control by 1·2 % (95 % CI 1·0, 1·4 %). CF decreased systolic and diastolic blood pressure by 4·4 mmHg (95 % CI 7·9, 0·9 mmHg) and 3·9 mmHg (95 % CI 6·7, 0·9 mmHg), pulse wave velocity by 0·4 m/s (95 % CI 0·8, 0·04 m/s), total cholesterol by 0·20 mmol/l (95 % CI 0·39, 0·01 mmol/l) and LDL-cholesterol by 0·17 mmol/l (95 % CI 0·32, 0·02 mmol/l), whereas HDL-cholesterol increased by 0·10 mmol/l (95 % CI 0·04, 0·17 mmol/l). By applying the Framingham Risk Score, CF predicted a significant lowering of 10-year risk for CHD, myocardial infarction, CVD, death from CHD and CVD. In healthy individuals, regular CF intake improved accredited cardiovascular surrogates of cardiovascular risk, demonstrating that dietary flavanols have the potential to maintain cardiovascular health even in low-risk subjects.

The gastrointestinal (GI) microbiota differs between breast-fed and classic infant formula-fed infants. Breast milk is rich in prebiotic oligosaccharides (OS) and may also contain some probiotics, but scientific societies do not recommend the addition of prebiotic OS or probiotics to standard infant formula. Nevertheless, many infant formula companies often add one or the other or both. Different types of prebiotic OS are used in infant formula, including galacto-oligosaccharide, fructo-oligosaccharide, polydextrose and mixtures of these OS, but none adds human milk OS. There is evidence that the addition of prebiotics to infant formula brings the GI microbiota of formula-fed infants closer to that of breast-fed infants. Prebiotics change gut metabolic activity (by decreasing stool pH and increasing SCFA), have a bifidogenic effect and bring stool consistency and defecation frequency closer to those of breast-fed infants. Although there is only limited evidence that these changes in GI microbiota induce a significant clinical benefit for the immune system, interesting positive trends have been observed in some markers. Additionally, adverse effects are extremely seldom. Prebiotics are added to infant formula because breast milk contains human milk OS. Because most studies suggest a trend of beneficial effects and because these ingredients are very safe, prebiotics bring infant formula one step closer to the golden standard of breast milk.

The recovery of inulin, a naturally occurring β(2→l)-fructan isolated from Jerusalem artichoke (Helianthus tuberosus L.), in the small intestine of man was studied in ileostomy subjects. The ileostomists were given a low-dietary-fibre diet based on white wheat bread and virtually free of inulin, and the same diet with the addition of 10 g and 30 g inulin product respectively, and the recovery and mean transit time (MTT) of inulin were estimated by tracking inulin in ileal effluent. The recovery of inulin was approximately 87% at both ingestion levels. MTT was 4·9 (SE 0·6) h at an intake of 10 g inulin product decreasing to 3·4 (SE 0·3) h at an intake of 30 g Inulin product. A significant change in the fructose: glucose ratio of inulin from ingestion (4·1) to recovery in ileal effluent (4·5–4·7) and a lower recovery of the glucose residue than of the fructose residue of inulin indicate that the low-molecular-weight inulins are more sensitive to hydrolysis than the high-molecular-weight fragments. The loss of inulin during passage through the small intestine is presumably due to hydrolysis by either acids or enzymes and to microbial degradation by the microfiora permanently colonizing the distal small intestine. The concentrations of lactic acid (LA) and short-chain fatty acids (SCFA) in frequently collected ileal effluents on the control day were approximately 6 mmol/l and approximately 55 mmol/l respectively. During periods with inulin ingestion the concentration of LA increased to 18–26 mmol/l (P < 0·052), while the concentration of SCFA ran converse and decreased to 18–32 mmol/l (P < 0·023). The osmotic loads (68 and 204 mosmol/l) associated with the ingestion of inulin product caused minor malabsorption of low-molecular-weight sugars.

A number of vegetables have a high nitrate content which after ingestion can be reduced to nitrite by oral bacteria, and further to vasoprotective NO endogenously. In the present study, two separate randomly controlled, single-blind, cross-over, postprandial studies were performed in normotensive volunteers. Ambulatory blood pressure (BP) was measured over a 24 h period following consumption of either four doses of beetroot juice (BJ), 0, 100, 250 and 500 g (n 18), or three bread products, control bread (0 g beetroot), red beetroot- and white beetroot-enriched breads (n 14). Total urinary nitrate/nitrite (NOx) was measured at baseline, and at 2, 4 and 24 h post-ingestion. BJ consumption significantly, and in a near dose-dependent manner, lowered systolic BP (SBP, P < 0·01) and diastolic BP (DBP, P < 0·001) over a period of 24 h, compared with water control. Furthermore, bread products enriched with 100 g red or white beetroot lowered SBP and DBP over a period of 24 h (red beetroot-enriched bread, P <0·05), with no statistical differences between the varieties. Total urinary NOx significantly increased following the consumption of 100 g (P < 0·01), 250 g (P <0·001) and 500 g BJ (P <0·001) and after red beetroot-enriched bread ingestion (P <0·05), but did not reach significance for white beetroot-enriched bread compared with the no-beetroot condition. These studies demonstrated significant hypotensive effects of a low dose (100 g) of beetroot which was unaffected by processing or the presence of betacyanins. These data strengthen the evidence for cardioprotective BP-lowering effects of dietary nitrate-rich vegetables.

Non-alcoholic fatty liver disease (NAFLD) is usually associated with insulin resistance, central obesity, reduced glucose tolerance, type 2 diabetes mellitus and hypertriacylglycerolaemia. The beneficial effects of resveratrol on metabolic disorders have been shown previously. The aim of this study was to evaluate the effects of resveratrol supplementation on cardiovascular risk factors in patients with NAFLD. In this randomised double-blinded placebo-controlled clinical trial, fifty NAFLD patients were supplemented with either a 500-mg resveratrol capsule or a placebo capsule for 12 weeks. Both groups were advised to follow an energy-balanced diet and physical activity recommendations. resveratrol supplementation reduced alanine aminotransferase (ALT) and hepatic steatosis significantly more than placebo (P<0·05). BMI, waist circumference, serum aspartate aminotransferase, bilirubin, HDL-cholesterol and apo a1 were reduced significantly in both groups (P<0·05); however, there were no significant differences between the two groups (P>0·05). There were no significant changes in blood pressure, insulin resistance markers and TAG in either group (P>0·05). Our data have shown that 12-week supplementation of 500 mg resveratrol does not have any beneficial effect on anthropometric measurements, insulin resistance markers, lipid profile and blood pressure; however, it reduced ALT and hepatic steatosis in patients with NAFLD.

Many studies have been done on the hypocholesterolaemic effect of probiotic yoghurt. The results, however, are not conclusive. The aim of the present study was to test the effect of probiotic and conventional yoghurt on the lipid profile in women. In a randomised trial, ninety female volunteers aged 19–49 years were assigned to three groups. Subjects consumed daily 300 g probiotic yoghurt containing Lactobacillus acidophilus La5 and Bifidobacterium lactis Bb12 or 300 g conventional yoghurt or no yoghurt for 6 weeks. Fasting blood samples, 3 d dietary records and anthropometric measurements were collected at baseline (T1), end of week 3 (T2) and end of week 6 (T3). Lipid profile parameters were determined by enzymic methods. Results showed no significant difference in lipid profile within any group throughout the study. Comparing mean differences (T1 − T3) among the three groups showed: no difference in TAG and LDL-cholesterol, a decrease in cholesterol in both conventional (P < 0·05) and probiotic yoghurt groups (P < 0·005) compared with the control group, a decrease in total:HDL-cholesterol ratio for conventional (P < 0·05) and probiotic yoghurt groups (P < 0·001) compared with the control group, and an increase in HDL-cholesterol in the probiotic yoghurt group (P < 0·05) compared with the control group. Positive changes in lipid profile were observed in both yoghurt groups. Any added effect, therefore, is due to the consumption of fermented milk products.

Studies on animal and human subjects have shown that greatly increasing the amount of linseed (also known as flaxseed) oil (rich in the n−3 polyunsaturated fatty acid (PUFA) α-linolenic acid (ALNA)) or fish oil (FO; rich in the long-chain n−3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) in the diet can decrease a number of markers of immune function. The immunological effects of more modest doses of n−3 PUFA in human subjects are unclear, dose–response relationships between n−3 PUFA supply and immune function have not been established and whether ALNA has the same effects as its long-chain derivatives is not known. Therefore, the objective of the present study was to determine the effect of enriching the diet with different doses of FO or with a modest dose of ALNA on a range of functional responses of human monocytes and lymphocytes. In a randomised, placebo-controlled, double-blind, parallel study, forty healthy males aged 18–39 years were randomised to receive placebo or 3·5 g ALNA/d or 0·44, 0·94 or 1·9 g (EPA+DHA)/d in capsules for 12 weeks. The EPA:DHA ratio in the FO used was 1·0:2·5. ALNA supplementation increased the proportion of EPA but not DHA in plasma phospholipids. FO supplementation decreased the proportions of linoleic acid and arachidonic acid and increased the proportions of EPA and DHA in plasma phospholipids. The interventions did not alter circulating mononuclear cell subsets or the production of tumour necrosis factor-α, interleukin (IL) 1β, IL-2, IL-4, IL-10 or interferon-γ by stimulated mononuclear cells. There was little effect of the interventions on lymphocyte proliferation. The two higher doses of FO resulted in a significant decrease in IL-6 production by stimulated mononuclear cells. It is concluded that, with the exception of IL-6 production, a modest increase in intake of either ALNA or EPA+DHA does not influence the functional activity of mononuclear cells. The threshold of EPA+DHA intake that results in decreased IL-6 production is between 0·44 and 0·94 g/d.

There is increasing evidence suggesting that the cut-off values for defining obesity used in the Western countries cannot be readily applied to Asians, who often have smaller body frames than Caucasians. We examined the BMI and body fat (BF) as measured by bioelectrical impedance in 5153 Hong Kong Chinese subjects. We aimed to assess the optimal BMI reflecting obesity as defined by abnormal BF in Hong Kong Chinese. Receiver operating characteristic curve (ROC) analysis was used to assess the optimal BMI predicting BF at different levels. The mean age and SD OF THE 5153 SUBJECTS (3734 WOMEN AND 1419 MEN) WAS 51.5 (sd 16.3) years (range: 18.0–89.5 years, median: 50.7 years). Age-adjusted partial correlation (r) between BMI and BF in women and men were 0.899 (P<0.001) and 0.818 (P<0.001) respectively. Using ROC analysis, the BMI corresponding to the conventional upper limit of normal BF was 22.5–23.1 kg/m2, and the BMI corresponding to the 90 percentiles of BF was 25.4–26.1 kg/m2. Despite similar body fat contents, the BMI cut-off value used to define obesity in Hong Kong Chinese should be lower as compared to Caucasians. We suggest a BMI of 23 kg/m2 and 26 kg/m2 as the cut-off values to define overweight and obesity respectively in Hong Kong Chinese.

Epidemiological studies in humans show that size in early life is related to blood cholesterol concentrations in adult life, raising the hypothesis that early nutrition programs later lipid metabolism, affecting risk for later vascular disease. Here, we tested the hypothesis that nutrition during pregnancy or lactation in the rat programs lipid metabolism in the offspring, studied in adult life (mean 6 months). Rats (n 35) from normally-fed dams (controls) were compared with (1) rats (n 22) from dams protein-restricted in pregnancy and lactation; (2) rats (n 9) born to normally-fed mothers crossed to protein- restricted lactating dams and (3) those (n 9) born of protein-restricted dams and crossed to normally-fed lactating animals. In these latter three groups the offspring showed long-term reduction in plasma cholesterol, HDL-cholesterol and triacylglycerol concentrations compared with controls. The effects were predominantly in males. These findings suggest that in the rat the sensitive period for nutritional programming of cholesterol and triacylglycerol metabolism is both pre- and postnatal (pre-weaning) and that rats may be ‘indirectly’ programmed by altering the maternal nutritional milieu during gestation or lactation. whilst it has been hypothesized that early human undernutrition programs risk for vascular disease, one aspect of undernutrition, low maternal protein intake, in this rat model programmed lower plasma cholesterol and triacylglycerol concentrations.

Parkinson's disease (PD), one of the most common neurodegenerative disorders, is characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) to the striatum (ST), and involves oxidative stress. Mulberry fruit from Morus alba L. (Moraceae) is commonly eaten, and has long been used in traditional oriental medicine. It contains well-known antioxidant agents such as anthocyanins. The present study examined the protective effects of 70 % ethanol extract of mulberry fruit (ME) against neurotoxicity in in vitro and in vivo PD models. In SH-SY5Y cells stressed with 6-hydroxydopamine (6-OHDA), ME significantly protected the cells from neurotoxicity in a dose-dependent manner. Other assays demonstrated that the protective effect of ME was mediated by its antioxidant and anti-apoptotic effects, regulating reactive oxygen species and NO generation, Bcl-2 and Bax proteins, mitochondrial membrane depolarisation and caspase-3 activation. In mesencephalic primary cells stressed with 6-OHDA or 1-methyl-4-phenylpyridinium (MPP+), pre-treatment with ME also protected dopamine neurons, showing a wide range of effective concentrations in MPP+-induced toxicity. In the sub-acute mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), ME showed a preventative effect against PD-like symptoms (bradykinesia) in the behavioural test and prevented MPTP-induced dopaminergic neuronal damage in an immunocytochemical analysis of the SNpc and ST. These results indicate that ME has neuroprotective effects in in vitro and in vivo PD models, and that it may be useful in preventing or treating PD.