The post-genomic technologies are generating vast quantities of data but many nutritional scientists are not trained or equipped to analyse it. In high-resolution NMR spectra of urine, for example, the number and complexity of spectral features mean that computational techniques are required to interrogate and display the data in a manner intelligible to the researcher. In addition, there are often multiple underlying biological factors influencing the data and it is difficult to pinpoint which are having the most significant effect. This is especially true in nutritional studies, where small variations in diet can trigger multiple changes in gene expression and metabolite concentration. One class of computational tools that are useful for analysing this highly multivariate data include the well-known ‘whole spectrum’ methods of principal component analysis and partial least squares. In this work, we present a nutritional case study in which NMR data generated from a human dietary Cu intervention study is analysed using multivariate methods and the advantages and disadvantages of each technique are discussed. It is concluded that an alternative approach, called feature subset selection, will be important in this type of work; here we have used a genetic algorithm to identify the small peaks (arising from metabolites of low concentration) that have been altered significantly following a dietary intervention.

It is unclear whether postprandial blood glucose or insulin exerts a regulatory function in short-term appetite regulation in humans. The aim of this study was to investigate, by use of meta-analysis, the role of blood glucose and insulin in short-term appetite sensation and energy intake (EI) in normal weight and overweight participants. Data from seven test meal studies were used, including 136 healthy participants (ALL) (92 normal weight (NW) and 44 overweight or obese (OW)). All meals were served as breakfasts after an overnight fast, and appetite sensations and blood samples were obtained frequently in the postprandial period. Finally, an ad libitum lunch was served. Data were analysed by fixed effects study level (SL) meta-regression analysis and individual participant data (IPD) regression analysis, using STATA software. In SL analysis, postprandial insulin response was associated with decreased hunger in ALL, NW and OW (P < 0·019), and with increased satiety in NW (P = 0·004) and lower subsequent EI in OW (P = 0·022). Multivariate IPD analysis showed similar associations, but only in NW for hunger, satiety and EI (P < 0·028), and in ALL for EI (P = 0·016). The only association involving blood glucose was the multivariate IPD analysis showing an inverse association between blood glucose and EI in ALL (P = 0·032). Our results suggest that insulin, but not glucose, is associated with short-term appetite regulation in healthy participants, but the relationship is disrupted in the overweight and obese. We conclude that the postprandial insulin response may be an important satiety signal, and that central nervous system insulin resistance in overweight might explain the blunted effect on appetite.

Personalised, genotype-based nutrition is a concept that links genotyping with specific nutritional advice in order to improve the prevention of nutrition-associated, chronic diseases. This review describes the current scientific basis of the concept and discusses its problems. There is convincing evidence that variant genes may indeed determine the biological response to nutrients. The effects of single-gene variants on risk or risk factor levels of a complex disease are, however, usually small and sometimes inconsistent. Thus, information on the effects of combinations of relevant gene variants appears to be required in order to improve the predictive precision of the genetic information. Furthermore, very few associations between genotype and response have been tested for causality in human intervention studies, and little is known about potential adverse effects of a genotype-derived intervention. These issues need to be addressed before genotyping can become an acceptable method to guide nutritional recommendations.

One of the challenges in type 2 diabetes treatment is to ensure pancreas functionality with gut peptides such as glucagon-like peptide-1 (GLP-1). We have recently shown that the endogenous GLP-1 production is promoted by dietary non-digestible carbohydrates (oligofructose), the higher GLP-1 secretion could participate in the control of obesity and associated disorders. This experimental study was designed to highlight the mechanisms of endogenous increase of GLP-1 following non-digestible carbohydrate feeding. Male Wistar rats were fed a standard diet (70·4 g/100 g total carbohydrates; controls) or the same diet supplemented with oligofructose (10 g/100 g diet) for 4 weeks. GLP-1-producing L-cells of the colon were quantified by immunohistochemistry. GLP-1 was quantified by ELISA, and proglucagon, neurogenin 3 and NeuroD mRNA were measured in the colon by quantitative RT–PCR. The number of GLP-1-expressing cells was doubled in the proximal colon of oligofructose-treated rats, a phenomenon correlated with the increase in proglucagon mRNA and peptide content in the tissue. Moreover, oligofructose increased the number of enteroendocrine L-cells in the proximal colon by a mechanism involving up-regulation of two differentiation factors: neurogenin 3 and NeuroD. It is the first demonstration that nutrients fermented in the gut may promote L-cell differentiation in the proximal colon, a phenomenon contributing to a higher endogenous GLP-1 production. These results suggest a new mechanism by which dietary fibres may lower food intake and fat mass development.

Carotenoids have been shown to have potential beneficial effects on human health which has led to an increasing interest in the study of their bioavailability. A Caco-2 cell model, as previously described, was employed to examine the percentage transfer of the carotenoids α-carotene, β-carotene, lycopene, astaxanthin, β-cryptoxanthin, lutein and zeaxanthin through an intact, highly differentiated Caco-2 cell monolayer at a range of different amounts. Our results show that astaxanthin, a carotenoid with powerful antioxidant capacity, had the highest percentage transfer overall. We examined the cellular uptake and secretion of lutein and zeaxanthin to compare two structurally similar carotenoids. Both were efficiently transported through the monolayer with a range between 5·1 (sem 1·2) % to 20·2 (sem 3·3) % and 5·5 (sem 2·5) % to 13·4 (sem 4) % for lutein and zeaxanthin, respectively. These carotenoids were compared to each other at each added amount and no significant difference was observed between the two xanthophylls. The carotene carotenoids α-carotene, β-carotene and lycopene and the xanthophyll β-cryptoxanthin were also examined and had lower uptake and secretion values when compared to lutein, zeaxanthin and astaxanthin. The xanthophyll β-cryptoxanthin was also not significantly different when compared to the carotene carotenoids. Data generated from this study compares well with in vivo bioavailability studies. Furthermore, the model provides comparative data on the relative absorption and transfer of seven different carotenoids. Our data indicate that lower amounts of carotenoids were absorbed and transferred more efficiently than higher amounts suggesting a saturation effect at higher exposure.

One aim of the EC Framework V project, ’Rumen-up’ (QLK5-CT-2001-00 992), was to find plants or plant extracts that would inhibit the nutritionally wasteful degradation of protein in the rumen. A total of 500 samples were screened in vitro using 14C-labelled casein in a 30-min incubation with ruminal digesta. Eight were selected for further investigation using a batch fermentation system and soya protein and bovine serum albumin as proteolysis substrates; proteolysis was monitored over 12 h by the disappearance of soluble protein and the production of branched SCFA and NH3. Freeze-dried, ground foliage of Peltiphyllum peltatum, Helianthemum canum, Arbutus unedo, Arctostaphylos uva-ursi and Knautia arvensis inhibited proteolysis (P < 0·05), while Daucus carota, Clematis vitalba and Erica arborea had little effect. Inhibition by the first four samples appeared to be caused by the formation of insoluble tannin–protein complexes. The samples were rich in phenolics and inhibition was reversed by polyethyleneglycol. In contrast, K. arvensis contained low concentrations of phenolics and no tannins, had no effect in the 30-min assay, yet inhibited the degradation rate of soluble protein (by 14 %, P < 0·0001) and the production of branched SCFA (by 17 %, P < 0·05) without precipitating protein in the 12-h batch fermentation. The effects showed some resemblance to those obtained in parallel incubations containing 3 μm-monensin, suggesting that K. arvensis may be a plant-derived feed additive that can suppress growth and activity of key proteolytic ruminal micro-organisms in a manner similar to that already well known for monensin.

Digestibility is the result of two competing processes: digestion and digesta transit. To develop or parameterise mechanistic models of digestion, both processes have to be quantified. The aim of this study was to determine the effect of insoluble dietary fibre on the transit in the gastrointestinal tract of pigs. Six barrows (33 kg initial body weight and fitted with two simple T-cannulas at the proximal duodenum and distal ileum) were used in a double 3 × 3 Latin square design. Pigs were offered diets differing in total dietary fibre content (170, 220 and 270 g/kg DM) at 4 h intervals. A single meal marked with YbO2 and Cr-EDTA was used to determine the kinetics of markers concentrations of the solid and liquid phases, respectively. The mean retention time (MRT), calculated by the method of the moments, averaged 1, 4 and 38 h in the stomach, small intestine and large intestine, respectively. Increasing the insoluble fibre content in the diet had no effect on MRT in the stomach and decreased the MRT of both phases in the small intestine (P < 0·05). In the large intestine, increasing the insoluble fibre content decreased the MRT of the liquid phase (P = 0·02) and tended to decrease the MRT of the solid phase (P = 0·06). Transit of the solid phase in the large intestine was 4–8 h slower than transit of the liquid phase. Analysis of marker excretion curves indicated that the small and large intestine should be represented mathematically to have both a tubular (propulsion) and compartmental (mixing) structure.

Oxidised frying oil (OFO) and fish oil have been shown to be peroxisome proliferator-activated receptor (PPAR)α activators and their ingestion results in pleotropic peroxisome proliferator responses in rats. To examine the effect of dietary OFO on adiposity, four groups of weanling Sprague–Dawley rats were fed isoenergetically with, respectively, a low fat basal diet containing 5 g/100 g of fresh soybean oil (LSB) or a high fat diet containing 20 g/100 g of fresh soybean oil (HSB), OFO (HO) or fish oil (HF). The tissue mass, cell size and lipid/DNA ratio in the retroperitoneal fat pad and serum leptin levels were lowest in the HO group (P < 0·05), indicating that dietary OFO has a greater anti-adipogenic action than dietary fish oil. However, a tendency to hyperglycaemia was observed in the HO group (P = 0·0528). To examine the effect of dietary OFO on glucose tolerance, three groups of rats and three groups of mice were fed, respectively, the LSB, HSB or HO diet, and an oral glucose tolerance test was performed. After oral glucose load, the area under the curve for blood glucose (AUCglu) over 2 h was significantly higher, and that for serum insulin (AUCins) over 90 min was significantly lower, in the HO group than in the other two groups (P < 0·05). These results demonstrate that, in rats and mice, a high OFO diet is less adipogenic, but induces glucose intolerance.

Potassium (K) organic anion salts, such as potassium citrate or potassium malate in plant foods, may counteract low-grade metabolic acidosis induced by western diets, but little is known about the effect of other minor plant anions. Effects of K salts (chloride, citrate, galacturonate or tartrate) were thus studied on the mineral balance and digestive fermentations in groups of 6-week-old rats adapted to an acidogenic/5 % inulin diet. In all diet groups, substantial amounts of lactate and succinate were present in the caecum, besides SCFA. SCFA were poorly affected by K salts conditions. The KCl-supplemented diet elicited an accumulation of lactate in the caecum; whereas the lactate caecal pool was low in rats fed the potassium tartrate-supplemented (K TAR) diet. A fraction of tartrate (around 50 %) was recovered in urine of rats fed the K TAR diet. Potassium citrate and potassium galacturonate diets exerted a marked alkalinizing effect on urine pH and promoted a notable citraturia (around 0·5 μmol/24 h). All the K organic anion salts counteracted Ca and Mg hyperexcretion in urine, especially potassium tartrate as to magnesuria. The present findings indicate that K salts of unabsorbed organic anions exert alkalinizing effects when metabolizable in the large intestine, even if K and finally available anions (likely SCFA) are not simultaneously bioavailable. Whether this observation is also relevant for a fraction of SCFA arising from dietary fibre breakdown (which represents the major organic anions absorbed in the digestive tract in man) deserves further investigation.

The guinea-pig was previously reported as being sensitive to a niacin-deficient (ND), high-protein diet, suggesting that it is a suitable model for the low tryptophan to NAD+ conversion observed in human subjects. However, these studies were based on growth rates and mortality. The objective of the present study was to determine whether guinea-pigs are suitable for ND studies based on measurements of blood and bone marrow NAD+. Using a 20 % casein diet, ND decreased blood NAD+ after 4 weeks, but this parameter returned to normal after 9 weeks of feeding, while bone marrow was decreased by 35 % at this time point. Using a 15 % casein diet, 7 weeks of ND caused 44 and 42 % decreases in blood and bone marrow NAD+. Using a 10 % casein diet, ND decreased NAD+ by 32 % in blood and 62 % in bone marrow at 7 weeks. Growth rates were directly related to the dietary tryptophan content, with the lowest growth rates seen with the 10 % casein diet. Changes in guinea-pig NAD+ are comparable with the rat model at similar levels of dietary tryptophan, while mortality rates were dramatically higher in the guinea-pig model. The present study concludes that mortality in ND guinea-pigs is not indicative of poor tryptophan conversion, but is due to environmental stresses in guinea-pigs that are not observed with rats. We conclude that guinea-pigs are not suitable for research on niacin deficiency and they present challenges for any study requiring purified diets and wire-bottomed cages.

The present study evaluated the pharmacokinetics of three different grapefruit flavanone forms in dog plasma and demonstrated their absorption after an oral intake of a grapefruit extract; pharmacokinetic parameters of these forms were also determined. Ten healthy beagles were administered 70 mg citrus flavonoids as a grapefruit extract contained in capsules, while two additional dogs were used as controls and given an excipient. The grapefruit flavanone naringin, along with its metabolites naringenin and naringenin glucuronide, was detected in dog plasma. Blood samples were collected between 0 and 24 h after administration of the extract. Naringin reached its maximun plasma concentration at around 80 min, whereas naringenin and naringenin glucuronide reached their maximun plasma concentrations at around 20 and 30 min, respectively. Maximum plasma concentrations of naringin, naringenin and naringenin glucuronide (medians and ranges) were 0·24 (0·05–2·08), 0·021 (0·001–0·3) and 0·09 (0·034–0·12) μmol/l, respectively. The areas under the curves were 23·16 l (14·04–70·62) min × μmol/for nariningin, 1·78 (0·09–4·95) min × μmol/l for naringenin and 22·5 (2·74–99·23) min × μmol/l for naringenin glucuronide. The median and range values for mean residence time were 3·3 (1·5–9·3), 2·8 (0·8–11·2) and 8·0 (2·3–13·1) h for naringin, naringenin and naringenin glucuronide, respectively. The results of the present study demonstrate the absorption of grapefruit flavanones via the presence of their metabolites in plasma, thus making an important contribution to the field since the biological activities ascribed to these compounds rely on their specific forms of absorption.

Rats exposed to protein restriction as fetuses develop hypertension as adults. Hypertension increases the risk of myocardial ischaemia and infarction. We investigated whether rats exposed to low-protein diets in utero are more susceptible to myocardial ischaemia–reperfusion (IR) injury. Pregnant Wistar rats were fed control or low-protein (MLP) diets throughout pregnancy. At 4 and 8 weeks postnatal age systolic blood pressure was determined in the offspring using tail-cuff plethysmography. At 6 months of age, rats were treated with saline or N-acetylcysteine (NAC) for 48 h. Rapidly excised hearts were retro-perfused (Langendorff) to assess isolated cardiac function before (baseline), during 30 min ischaemia (no coronary perfusion) and for 60 min after reinstating coronary perfusion (reperfusion). Hearts were then harvested and treated appropriately for analysis of infarct size. Exposure to the MLP diet in utero significantly increased systolic blood pressure at 4 and 8 weeks of age (6–13 mmHg increase; P < 0·001) and significantly impaired recovery of left ventricular developed pressure after ischaemia at 6 months of age in male offspring only (P < 0·003). Pre-treatment with NAC prevented this impairment of recovery in MLP male offspring and improved recovery in all females. Myocardial infarct size was not different between dietary groups after IR, but NAC pre-treatment significantly reduced the degree of infarction (P < 0·001). In conclusion, an MLP diet throughout gestation significantly impairs recovery of the 6-month-old adult rat heart to IR-induced injury in a sex-specific manner. Undernutrition during development may increase susceptibility to CHD by impairing recovery from coronary events.

Dietary fibre consumption is associated with improved glucose homeostasis. In contrast, dietary polyphenols have been suggested to exert both beneficial and detrimental effects on glucose and insulin metabolism. Recently, we reported that a polyphenol-rich insoluble dietary fibre preparation from carob pulp (carob fibre) resulted in lower postprandial acylated ghrelin levels after a liquid meal challenge test compared with a control meal without supplementation. The effects may, however, differ when a different food matrix is used. Thus, we investigated the effects of carob fibre on glucose, insulin and ghrelin responses in healthy humans in combination with a glucose load. In a randomized single-blind cross-over study involving twenty healthy subjects (aged 22–62 years), plasma glucose, total and acylated ghrelin, and serum insulin were repeatedly assessed before and after the ingestion of 200 ml water with 50 g glucose and 0, 5, 10 or 20 g carob fibre over a period of 180 min. The intake of 5 and 10 g carob fibre increased the plasma glucose by 47 % and 64 % (P < 0·001), and serum insulin by 19·9 and 24·8 % (P < 0·001), compared with the control. Plasma acylated ghrelin concentrations did not change significantly after the consumption of carob-enriched glucose solution. Total ghrelin decreased only after 10 g carob fibre (P < 0·001) compared with control. In conclusion, we showed that polyphenol-rich carob fibre, administered within a water–glucose solution, increases postprandial glucose and insulin responses, suggesting a deterioration in glycaemic control.

Circulating leptin is regulated by food intake in the long, medium and short term; however, little is known about putative remnant effects of these successive regulations at any given time. To clarify this, two experiments were conducted in adult sheep, during which body condition parameters and plasma leptin were measured. During experiment 1, twenty ewes with normal body condition were either well fed (101 % of maintenance energy requirements (MER)) or underfed (41 % MER) for 166 d, then rapidly re-fed (at a mean of 208 % MER) for 3 d. Leptinaemia decreased after 14 d of underfeeding, remained depressed until day 166 and did not increase after 3 d re-feeding, whereas it was increased (+153 %; P < 0·05) by re-feeding the previously well-fed ewes. During experiment 2, twenty-four fat or lean ewes were either well fed (114 % MER) or underfed (52 % MER) for 94 d, and gradually re-fed for 2 d and maintained at a high feeding level (235 % MER) for 9 d. Underfeeding decreased leptinaemia in fat (from 4·19 to 2·63 ng/ml) but not lean ewes, and re-feeding increased leptinaemia after 5 d in lean previously well-fed (+123 %; P < 0·05) but not underfed ewes. In fat ewes, the impact of re-feeding was rapid (+144 %; P < 0·001 at 5 d) in previously well-fed ewes, whereas it was more gradual with a maximum at 11 d (+162 %; P < 0·01) in previously underfed ewes. In conclusion, leptinaemia is modulated by short-term energy intake level in interaction with long-term regulations involving nutritional history and body fatness, suggesting that a biological threshold of adiposity (about 20 %) is necessary to allow short- and medium-term leptin regulation.

Excessive iodine induces thyroid dysfunction. However, the effect of excessive iodine exposure on maternal–fetal thyroid hormone metabolism and on the expression of genes involved in differentiation, growth and development is poorly understood. Since a thyroid hormone receptor response element was found in the Hoxc8 promoter region, Hoxc8 expression possibly regulated by excessive iodine exposure was firstly investigated. In the present study, Balb/C mice were given different doses of iodine in the form of potassium iodate (KIO3) at the levels of 0 (sterile water), 1·5, 3·0, 6·0, 12·0 and 24·0 μg/ml in drinking water for 4 months, then were mated. On 12·5 d postcoitum, placental type 2 and type 3 deiodinase activities and fetal Hoxc8 expression were determined. The results showed that excessive iodine exposure above 1·5 μg/ml resulted in an increase of total thyroxine and a decrease of total triiodothyronine in the serum of maternal mice, which was mainly associated with the inhibition of type 1 deiodinase activity in liver and kidney. Placental type 2 deiodinase activity decreased, showing an inverse relationship with maternal thyroxine level. Hoxc8 mRNA and protein expression at 12·5 d postcoitum embryos were down regulated. Because Hoxc8 plays an important role in normal skeletal development, this finding provides a possible explanation for the skeletal malformation induced by excessive iodine exposure and also provides a new clue to study the relationship between iodine or thyroid hormones and Hox gene expression pattern.

Dietary fibre has been proposed to decrease risk for colon cancer by altering the composition of intestinal microbes or their activity. In the present study, the changes in intestinal microbiota and its activity, and immunological characteristics, such as cyclo-oxygenase (COX)-2 gene expression in mucosa, in pigs fed with a high-energy-density diet, with and without supplementation of a soluble fibre (polydextrose; PDX) (30 g/d) were assessed in different intestinal compartments. PDX was gradually fermented throughout the intestine, and was still present in the distal colon. Irrespective of the diet throughout the intestine, of the four microbial groups determined by fluorescent in situ hybridisation, lactobacilli were found to be dominating, followed by clostridia and Bacteroides. Bifidobacteria represented a minority of the total intestinal microbiota. The numbers of bacteria increased approximately ten-fold from the distal small intestine to the distal colon. Concomitantly, also concentrations of SCFA and biogenic amines increased in the large intestine. In contrast, concentrations of luminal IgA decreased distally but the expression of mucosal COX-2 had a tendency to increase in the mucosa towards the distal colon. Addition of PDX to the diet significantly changed the fermentation endproducts, especially in the distal colon, whereas effects on bacterial composition were rather minor. There was a reduction in concentrations of SCFA and tryptamine, and an increase in concentrations of spermidine in the colon upon PDX supplementation. Furthermore, PDX tended to decrease the expression of mucosal COX-2, therefore possibly reducing the risk of developing colon cancer-promoting conditions in the distal intestine.

The objective was to determine the effects of the National Cholesterol Education Program (NCEP) step II diet on LDL and HDL particle size in dyslipidaemic adolescents. Forty-four dyslipidaemic adolescents, aged 10–18 years, participated in this case-control study. The control diet was a diet similar to what most Tehranian adolescents eat. NCEP step II diet was a diet with 30 % of energy as total fat, less than 7 % saturated fat, less than 200 mg cholesterol/d, less than 15 % of energy as MUFA and less than 10 % as PUFA. Lipoprotein particle size was the major outcome variable, which was measured after 3 months of intervention. Comparison was made by the repeated measurement ANOVA. The mean BMI was 26·3 (sd 4·2) kg/m2. There were no significant changes in weight or physical activity in the two groups during the study. The NCEP diet resulted in higher reduction in total cholesterol ( − 13 (sd 4) v. − 2 (sd 0·3) mg/dl, P < 0·001) and LDL ( − 9 (sd 2) v. 3 (sd 0·6) mg/dl, P < 0·01), and higher increase in size of the LDL (1·7 (sd 0·4) v. 0·1 (sd 0·4) nanometer, P < 0·001). HDL particle size did not change significantly. NCEP step II diet had a favourable effect on the LDL particle size. The related mechanism needs to be studied in future experimental designs.

Lycopene is present mainly as cis-isomers in human serum and tissues whereas all-trans-lycopene predominates in tomato products, suggesting that all-trans-lycopene is isomerised in the body or is less bioavailable. The objectives of the present study were to develop processing conditions for tomatoes to obtain products with different cis-trans-lycopene isomer distribution and to assess their bioavailability. Healthy adult subjects (n 12) were recruited for this randomised cross-over trial. Each intervention was preceded by a 2-week washout period. Two tomato sauces, one rich in all-trans-lycopene (32·5 mg total lycopene/100 g sauce; 5 % cis-isomers), the other high in cis-lycopene (26·4 mg total lycopene/100 g sauce; 45 % cis-isomers), were produced by different heat-processing techniques. Each sauce (150 g) was served in a standardised meal at 08.00 hours after overnight fasting. Plasma TAG-rich lipoprotein fractions over 9.5 h following test-meal consumption as a measure of lycopene absorption were obtained and expressed as baseline-corrected area under the concentration v. time curves (AUC), using HPLC-electrochemical detection. AUC values adjusted for the amount lycopene consumed showed that total, total cis-, and all-trans-lycopene responses were significantly higher from the cis-isomer-rich sauce, compared with the all-trans-rich sauce, being 7·30 (sem 1·45) v. 4·74 (sem 1·08) nmol × h/l (P = 0·002), 3·80 (sem 0·76) v. 1·98 (sem 0·37) nmol × h/l (P = 0·0005) and 3·50 (sem 0·76) v. 2·76 (sem 0·76) nmol × h/l (P = 0·01), respectively. The present study demonstrates significant lycopene bioavailability from cis-lycopene-rich tomato sauce and highlights the importance of considering isomer-distribution for lycopene bioavailability. Furthermore, processing parameters can be controlled to alter isomer patterns of tomato products and influence lycopene bioavailability.

There is currently an increased global interest in the published glycaemic index (GI) values of foods. The aim of the present work was to supplement a previous study on the glycaemic response of 140 foods available in the UK by studying a further forty-four foods. One hundred and twenty-two healthy subjects, with a mean age of 32·4 (sd 11·4) years and a mean BMI of 23·6 (sd 3·6) kg/m2, were recruited to the study. Subjects were served equivalent available carbohydrate amounts (50 or 30 g) of test foods (cereal products and weight-management meals) and a standard food (glucose) on separate occasions. Capillary blood glucose was measured from finger-prick samples in fasted subjects (0 min) and at 15, 30, 45, 60, 90 and 120 min after starting to eat each test food. For each test food, the GI value was determined, and the glycaemic load was calculated as the product of the GI and the amount of available carbohydrate in a reference serving size. The GI values of the foods tested ranged from 23 to 83. Of the forty-four foods tested, thirty-three were classified as low-GI, eight as medium-GI and three as high-GI foods. Most GI values of the foods tested compared well with previously published values for similar foods. In summary, this study provides reliable GI and glycaemic load values for a range of foods, further advancing our understanding of the glycaemic response of different foods. The data reported here make an important addition to published GI values.