We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to investigate the effect of adenosine administration on metabolic syndrome-related parameters in SHRSP fed a high-fat diet. Six-week-old rats were divided into three groups, and were administered either water (control) or adenosine (10 or 100 mg/l) for 8 weeks. During this period, the rats had free access to a high-fat diet based on AIN-93M. The results showed that hypertension, plasma lipid, NO, insulin, glucose and urinary 8-hydroxy-2′-deoxyguanosine levels improved significantly in both adenosine groups. The mRNA expression levels of genes involved in anti-oxidative activity and adenosine receptors were also altered in the adenosine groups. Administration of adenosine also increased plasma adiponectin levels, accompanied by upregulation of mRNA expression level of adiponectin and adiponectin receptor 1 in perirenal fat and adiponectin receptor 2 in the liver. In conclusion, oral administration of adenosine is effective for improving metabolic syndrome-related parameters in SHRSP, and accordingly it may prevent the progression of the metabolic syndrome.

The dietary methionine (Met) and total sulfur amino acid (TSAA) requirements of European sea bass (Dicentrarchus labrax) (initial body weight 13·4 (sd 0·2) g) were estimated in a 12-week dose–response experiment. Seven isonitrogenous (7·6 % DM) and isoenergetic (gross energy, 21·2 MJ/kg DM) diets, based on soya protein and crystalline l-amino acids containing graded levels of l-Met (1·6–16·2 g/kg) at a constant cysteine (4 g/kg) level and a fish meal-based diet, were fed each to triplicate groups of fifty fish kept in 250 litre tanks in a thermoregulated (23 ± 0·5°C) seawater system. The Met and TSAA-deficient diet resulted in higher mortality, impaired feed intake and growth relative to the other treatments (P < 0·01). No signs of lens opacity due to limiting Met intake were observed and no feed intake or growth depression occurred at the highest level of dietary TSAA. Met and TSAA requirements for optimal N deposition or weight gain as fitted with the broken-line model resulted in estimated values of 8·0 and 12·0 g/kg diet (for example, 1·8 and 2·7 % dietary protein) and 9·1 and 13·1 g/kg diet (for example, 2·0 and 3·0 % dietary protein), respectively. Plasma levels of Met, homocysteine and cysteine increased in response to excess dietary TSAA, corroborating requirement estimates from growth data. N gain resulted in a linear function of TSAA consumption at marginal Met (TSAA) intake. The TSAA intake needed to maintain N balance resulted in a value of 20·0 mg TSAA/kg average body weight0·75 per d, which represents 23 % of the total (maintenance+accretion) requirement.

Anthocyanins, phenolic acids and carotenoids are the predominant phytochemicals present in purple carrots. These phytochemicals could be useful in treatment of the metabolic syndrome since anthocyanins improve dyslipidaemia, glucose tolerance, hypertension and insulin resistance; the phenolic acids may also protect against CVD and β-carotene may protect against oxidative processes. In the present study, we have compared the ability of purple carrot juice and β-carotene to reverse the structural and functional changes in rats fed a high-carbohydrate, high-fat diet as a model of the metabolic syndrome induced by diet. Cardiac structure and function were defined by histology, echocardiography and in isolated hearts and blood vessels; liver structure and function, oxidative stress and inflammation were defined by histology and plasma markers. High-carbohydrate, high-fat diet-fed rats developed hypertension, cardiac fibrosis, increased cardiac stiffness, endothelial dysfunction, impaired glucose tolerance, increased abdominal fat deposition, altered plasma lipid profile, liver fibrosis and increased plasma liver enzymes together with increased plasma markers of oxidative stress and inflammation as well as increased inflammatory cell infiltration. Purple carrot juice attenuated or reversed all changes while β-carotene did not reduce oxidative stress, cardiac stiffness or hepatic fat deposition. As the juice itself contained low concentrations of carotenoids, it is likely that the anthocyanins are responsible for the antioxidant and anti-inflammatory properties of purple carrot juice to improve glucose tolerance as well as cardiovascular and hepatic structure and function.

There is concern regarding the possible negative effects of ingestion of dietary fibre on growth and intestinal Fe absorption in infants. The aim of the present study was to compare the effect of a fibre mixture on the growth and the intestinal absorption of Fe in rats with Fe-deficiency anaemia with that of a diet without fibres. Faecal weight and caecal pH were also evaluated. According to the Hb depletion–repletion model, twenty-two male weaned Wistar rats were fed the AIN93-G diet without Fe until Fe-deficiency anaemia was induced with Hb < 70 g/l. The anaemic rats were divided into two groups: (1) fibre mixture group – fed 100 g of fibre mixture/kg of diet (soya polysaccharide, inulin, resistant starch, Arabic gum, fructo-oligossaccharide and cellulose) (n 11); (2) control group – fed without fibres (n 11). All diets had 157 mg of ferric citrate (30 mg of elemental Fe) added to lead to recovery from anaemia. Fe intestinal absorption was measured by Hb repletion efficiency (HRE) and apparent Fe intestinal absorption. The HRE was 44·8 (sd 9·5) % in the fibre mixture group and 43·0 (sd 9·5) % in the control group (P = 0·664). The apparent Fe absorption was 46·2 (sd 16·5) and 47·2 (sd 10·2) % (P = 0·861) in the fibre mixture and control groups, respectively. The faecal weight median was 6·17 g in the fibre mixture group and 2·11 g in the control group (P < 0·001). The caecal pH was in the same order: 6·11 (sd 0·59) and 7·07 (sd 0·34) (P < 0·001). Both the groups consumed similar quantities of diet, and growth was similar in both the groups. The fibre mixture had no influence either on growth or on Fe intestinal absorption in rats recovering from anaemia. This mixture favoured an increase in faecal weight and a decrease in caecal pH.

The present study was conducted to evaluate the effect of different dietary lipid sources, age and sex on the SFA and MUFA metabolism in broiler chickens using a whole body fatty acid balance method. Four dietary lipid sources (palm fat, Palm; soyabean oil, Soya; linseed oil, Lin; and fish oil, Fish) were added at 3 % to a basal diet containing 5 % Palm. Diets were fed to female and male chickens from day 1 to either day 21 or day 42 of age. The accumulation (percentage of net intake and ex novo production) of SFA and MUFA was significantly lower in broilers fed on Palm than in broilers fed on the other diets (85·7 v. 97·4 %). Conversely, β-oxidation was significantly higher in Palm-fed birds than the average of the other dietary treatments (14·3 v. 2·6 %). On average, 33·1 % of total SFA and MUFA accumulated in the body were elongated, and 13·8 % were Δ-9 desaturated to longer chain or more unsaturated metabolites, with lower proportions being elongated and desaturated for the Palm and Fish diets than for the Soya and Lin diets. Total in vivo apparent elongase activity decreased exponentially in relation to the net intake of SFA and MUFA, while it increased with age. Total in vivo apparent Δ-9 desaturase activity was not significantly affected by dietary treatment or age. Total ex novo production and β-oxidation of SFA and MUFA showed a negative and positive curvilinear relationship with net intake of SFA and MUFA, respectively. Sex had no effect on SFA and MUFA metabolism.

Limited information is available on lignan metabolism and tissue distribution between sexes and the effects of prolonged lignan exposure on tissue concentrations. In the present study, excretion and tissue distribution of lignans were compared after 1 d and 7 d administration of flaxseed lignan secoisolariciresinol diglycoside (SDG) in male and female rats. Sprague–Dawley rats were daily gavaged per os with 3H-SDG (3·7 kBq/g body weight (bwt)) and unlabelled SDG (5·3 μg/g bwt). Urine, faeces, serum and tissues (liver, kidneys, bladder, spleen, lungs, brain, thymus, heart, muscle, adipose, mammary gland, ovaries, vagina, uterus, testis, seminal vesicles, coagulating glands and ventral prostate) were collected at 0, 12 and 24 h after a single lignan dose or after the last dose of 7 d exposure. The sample total lignan content was measured as radioactivity by liquid scintillation counting. In both sexes, majority of radioactivity was excreted in faeces (40–83 %) and urine (1·2–5·2 %). 3H-SDG administration increased radioactivity in all tissues at all time points, and the levels were further increased after prolonged SDG exposure. Liver contained majority of the tissue lignans (48–56 %) in both sexes after both exposure regimens. After prolonged SDG exposure, the serum lignan concentrations had reached a plateau which was approximately 4-fold of that of acute exposure, whereas in both sexes, concentrations in skin and kidneys still increased, indicating tissue accumulation. After prolonged exposure, females had higher lignan concentrations in heart and thymus at all time points, demonstrating sex-related differences in lignan tissue distribution and the possibility for sex-specific treatment responses. These findings facilitate identification of target tissues for local lignan actions in vivo.

An increased intestinal permeability is associated with several diseases. Nutrition can influence gut permeability. Previously, we showed that dietary Ca decreases whereas dietary short-chain fructo-oligosaccharides (scFOS) increase intestinal permeability in rats. However, it is unknown how and where in the gastrointestinal tract Ca and scFOS exert their effects. Rats were fed a Western low-Ca control diet, or a similar diet supplemented with either Ca or scFOS. Lactulose plus mannitol and Cr-EDTA were added to the diets to quantify small and total gastrointestinal permeability, respectively. Additionally, colonic tissue was mounted in Ussing chambers and exposed to faecal water of these rats. Dietary Ca immediately decreased urinary Cr-EDTA excretion by 24 % in Ca-fed rats compared with control rats. Dietary scFOS increased total Cr-EDTA permeability gradually with time, likely reflecting relatively slow gut microbiota adaptations, which finally resulted in a 30 % increase. The lactulose:mannitol ratio was 15 % higher for Ca-fed rats and 16 % lower for scFOS-fed rats compared with control rats. However, no dietary effect was present on individual urinary lactulose and mannitol excretion. The faecal waters did not influence colonic permeability in Ussing chambers. In conclusion, despite effects on the lactulose:mannitol ratio, individual lactulose values did not alter, indicating that diet did not influence small-intestinal permeability. Therefore, both nutrients affect permeability only in the colon: Ca decreases, while scFOS increase colonic permeability. As faecal water did not influence permeability in Ussing chambers, probably modulation of mucins and/or microbiota is important for the in vivo effects of dietary Ca and scFOS.

Linseed oil, being rich in 18 : 3n-3, represents an alternative source of n-3 PUFA in the maternal diet. However, little is known about the effect of this oil on the long chain n-3 PUFA composition of offspring, which are required for normal growth and maturation of numerous organs. The main objective of the experiment was therefore to investigate fatty acid composition of tissues from sows at the end of gestation and from piglets during the first week of postnatal life in response to maternal dietary linseed oil intake. Sows received either a lard (LAR)-based diet or a linseed oil (LSO)-based diet during gestation and lactation. Fatty acid composition was evaluated in sow plasma, placenta and milk, and in different tissues of piglets on days 0, 3, 7, 21 and 32. The LSO diet increased the proportions of n-3 PUFA and especially 22 : 6n-3 in the placenta. The carcass of LSO piglets at birth contained greater proportions of 20 : 5n-3, 22 : 5n-3 and 22 : 6n-3. The LSO sow milk exhibited greater proportions of 18 : 3n-3 compared with the LAR sow milk. The piglets suckling LSO sows had greater proportions of 18 : 3n-3, 20 : 5n-3 and 22 : 5n-3 in plasma and carcass. The proportions of 22 : 5n-3 and 22 : 6n-3 were greater in the brain of LSO piglets than in that of LAR piglets during the suckling period. In conclusion, LSO in the maternal diet during gestation and lactation increases 22 : 6n-3 concentrations in the placenta and in the foetus carcass, and it maintains 22 : 6n-3 concentrations in the brain during the first week of postnatal life.

In the present study, we evaluated the cholesterol-lowering effects of different oat bran (OB) preparations, differing regarding their peak molecular weight (MWp) of β-glucans (2348, 1311, 241, 56, 21 or < 10 kDa), in C57BL/6NCrl mice. The diets were designed to be atherogenic (0·8 % cholesterol and 0·1 % cholic acid), and they reflected the Western diet pattern (41 % energy fat). All OB preparations that were investigated significantly reduced plasma cholesterol when compared with a cellulose-containing control diet, regardless of the molecular weight of β-glucan. Moreover, the difference in viscous properties between the processed OB (from 0·11 to 17·7 l/g) did not appear to play a major role in the cholesterol-lowering properties. In addition, there was no correlation between the molecular weight of β-glucan and the amount of propionic acid formed in caecum. Interestingly, however, there was a significant correlation between the ratio of (propionic acid+butyric acid)/acetic acid and the MWp of β-glucans: the ratio increased with increasing molecular weight. The results of the present study suggest that the molecular weights and viscous properties of β-glucan in oat products may not be crucial parameters for their cholesterol-lowering effects.

Taurine (TAU) supplementation increases insulin secretion in response to high glucose concentrations in rodent islets. This effect is probably due to an increase in Ca2+ handling by the islet cells. Here, we investigated the possible involvement of the cholinergic/phospholipase C (PLC) and protein kinase (PK) A pathways in this process. Adult mice were fed with 2 % TAU in drinking water for 30 d. The mice were killed and pancreatic islets isolated by the collagenase method. Islets from TAU-supplemented mice showed higher insulin secretion in the presence of 8·3 mm-glucose, 100 μm-carbachol (Cch) and 1 mm-3-isobutyl-1-methyl-xanthine (IBMX), respectively. The increase in insulin secretion in response to Cch in TAU islets was accompanied by a higher intracellular Ca2+ mobilisation and PLCβ2 protein expression. The Ca2+ uptake was higher in TAU islets in the presence of 8·3 mm-glucose, but similar when the islets were challenged by glucose plus IBMX. TAU islets also showed an increase in the expression of PKAα protein. This protein may play a role in cation accumulation, since the amount of Ca2+ in these islets was significantly reduced by the PKA inhibitors: N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) and PK inhibitor-(6–22)-amide (PKI). In conclusion, TAU supplementation increases insulin secretion in response to glucose, favouring both influx and internal mobilisation of Ca2+, and these effects seem to involve the activation of both PLC–inositol-1,4,5-trisphosphate and cAMP–PKA pathways.

Based on the potential benefits to human health, there is interest in developing sustainable nutritional strategies to enhance the concentration of long-chain n-3 fatty acids in ruminant-derived foods. Four Aberdeen Angus steers fitted with rumen and duodenal cannulae were used in a 4 × 4 Latin square experiment with 21 d experimental periods to examine the potential of fish oil (FO) in the diet to enhance the supply of 20 : 5n-3 and 22 : 6n-3 available for absorption in growing cattle. Treatments consisted of total mixed rations based on maize silage fed at a rate of 85 g DM/kg live weight0·75/d containing 0, 8, 16 and 24 g FO/kg diet DM. Supplements of FO reduced linearly (P < 0·01) DM intake and shifted (P < 0·01) rumen fermentation towards propionate at the expense of acetate and butyrate. FO in the diet enhanced linearly (P < 0·05) the flow of trans-16 : 1, trans-18 : 1, trans-18 : 2, 20 : 5n-3 and 22 : 6n-3, and decreased linearly (P < 0·05) 18 : 0 and 18 : 3n-3 at the duodenum. Increases in the flow of trans-18 : 1 were isomer dependent and were determined primarily by higher amounts of trans-11 reaching the duodenum. In conclusion, FO alters ruminal lipid metabolism of growing cattle in a dose-dependent manner consistent with an inhibition of ruminal biohydrogenation, and enhances the amount of long-chain n-3 fatty acids at the duodenum, but the increases are marginal due to extensive biohydrogenation in the rumen.

Non-alcoholic fatty liver disease (NAFLD) has been deeply associated with visceral adiposity, adipose tissue inflammation and a variety of adipocytokines. We reported previously that genistein inhibited NAFLD by enhancing fatty acid catabolism. However, this molecular approach focused on hepatic metabolism. Thus, we have attempted to determine whether this anti-steatotic effect of genistein is linked to visceral adipocyte metabolism. C57BL/6J mice were fed on normal-fat (NF) diet, high-fat (HF) diet and HF diet supplemented with genistein (1, 2 and 4 g/kg diet) for 12 weeks. Mice fed on the HF diet gained body weight, exhibited increased visceral fat mass and elevated levels of serum and liver lipids, and developed NAFLD, unlike what was observed in mice fed on the NF diet. However, genistein supplementation (2 and 4 g/kg diet) normalised these alternations. In the linear regression analysis, visceral fat (R 0·77) and TNFα (R 0·62) were strongly correlated with NAFLD among other NAFLD-related parameters. Genistein supplementation suppressed the hypertrophy of adipocytes via the up-regulation of genes involved in fatty acid β-oxidation, including PPARα, 5′-AMP-activated protein kinase and very long-chain acyl CoA dehydrogenase, as well as through the down-regulation of genes associated with adipogenesis or lipogenesis, including liver X receptor-α, sterol-regulatory element-binding protein-1c, PPARγ, retinoid X receptor-α and acetyl CoA carboxylase 2. Moreover, genistein supplementation augmented an anti-steatohepatitic adiponectin TNF and reduced a steatohepatitic TNFα. Collectively, these findings show that genistein may prevent NAFLD via the regulation of visceral adipocyte metabolism and adipocytokines.

In the present study, the immune-modulating efficacy of a polyphenol-rich beverage on symptoms associated with the common cold was evaluated. For this purpose, ninety-eight patients reporting common cold symptoms that began no longer than 24 h before the study intervention were randomly assigned to consume either the test beverage or placebo twice per d for 10 d. The severity of the disease was expressed as the total score of the five cold symptoms ‘general feeling of sickness’, ‘headache and/or joint aches’, ‘sore throat and/or difficulty swallowing’, ‘hoarseness and/or cough’ and ‘stuffy nose/sniffle’. Consequently, the decrease from 10·2 (sd 3·1) points at the beginning to 2·1 (sd 2·7) points by the end of the study in the verum group demonstrated a clear improvement, whereas in the placebo group only a reduction from 10·5 (sd 3·0) to 6·3 (sd 3·8) points could be observed. The mean difference between the groups (primary efficacy criterion) of 3·9 points was highly significant (P < 0·01). At the end of the study there were highly significantly (P < 0·01) more patients in the verum group complaint free than in the placebo group (secondary efficacy criterion). In addition to these self-reported values, several local findings of the physical examination were also significantly improved in the verum group.

Malnutrition during foetal life can induce modifications in the phenotype of an individual. The present study aimed to observe effects of low foetal life protein provision on modifications of the phenotype and changes in the progeny of 1-year-old female mink (F1 generation) offspring of mothers fed a low-protein diet. Traits studied included reproductive performance, energy and protein metabolism, and key hepatic enzymes associated with glucose homeostasis and metabolic hormones. The F0 generation offspring were fed either a low-protein (14 % of metabolisable energy (ME) from protein – FLP1) or an adequate-protein (29 % of ME from protein – FAP1) diet for the last 17·9 (sd 3·6) d of gestation. The F1 dams were studied at birth and at 1 year of age, during their first reproductive cycle, after maintenance on an adequate diet from birth and thereafter. Metabolic traits during gestation and lactation were largely unaffected by foetal life protein provision, but birth weight in the F2 generation was higher (P = 0·003) among FLP2 kits than among FAP2 kits. Furthermore, the relative abundance of pyruvate kinase mRNA was significantly (P = 0·007) lower, and fructose-1,6-bisphosphatase mRNA tended (P = 0·08) to be lower in FLP2 foetuses than in FAP2 foetuses, showing some similar difference in the F2 generation and F1 generation foetuses, suggesting an effect on some hepatic enzymes affecting glucose homeostasis being transmitted from the F1 to the F2 generation. These findings indicate that even though energy and nitrogen metabolism displayed no effect of protein provision during early life, programming effects still appeared at the molecular level in the following generation.

The present study was conducted to determine whether provision of preformed dietary docosapentaenoic acid (DPAn-6) can replace DHA for normal long bone growth as assessed by dual-energy X-ray absorptiometry for mineral content (BMC). A newly modified artificial rearing method was employed to generate n-3 fatty acid-deficient rats. Except the dam-reared (DR; 3·1 % α-linolenic acid) group, newborn pups were separated from their mothers at age 2 d and given artificial rat milk containing linoleic acid (LA), or LA supplemented with 1 % DHA (22 : 6n-3; DHA), 1 % DPAn-6 (DPA), or 1 % DHA plus 0·4 % DPAn-6 (DHA/DPA). The rats were later weaned onto similar pelleted diets. At adulthood, the rats were euthanised and bones (femur, tibia, and lumbar vertebrae) collected for tissue fatty acid analysis and bone mineral density (BMD) determination. The analyses showed that long bones such as femur and tibia in DPAn-6-treated rats contained higher DPAn-6 content and generally had the lowest BMC and BMD values. Hence, DPAn-6 did not replace DHA for normal bone growth and maximal BMC in femur, indicating an indispensible role of DHA in bone health. In conclusion, DHA accumulates in the osteoblast-rich and nerve-abundant periosteum of femur; DHA but not EPA appears to be a vital constituent of marrow and periosteum of healthy modelling bone; and both DHA and total n-3 PUFA strongly correlate to BMC.

Finger millet (Eleusine coracana) is extensively cultivated and consumed in India and Africa. The millet seed coat is a rich source of dietary fibre and phenolic compounds. The effect of feeding a diet containing 20 % finger millet seed coat matter (SCM) was examined in streptozotocin-induced diabetic rats. Diabetic rats maintained on the millet SCM diet (diabetic experimental (DE) group) for 6 weeks exhibited a lesser degree of fasting hyperglycaemia and partial reversal of abnormalities in serum albumin, urea and creatinine compared with the diabetic control (DC) group. The DE group of rats excreted comparatively lesser amounts of glucose, protein, urea and creatinine and was accompanied by improved body weights compared with their corresponding controls. Hypercholesterolaemia and hypertriacylglycerolaemia associated with diabetes were also notably reversed in the DE group. Slit lamp examination of the eye lens revealed an immature subcapsular cataract with mild lenticular opacity in the DE group of rats compared to the mature cataract with significant lenticular opacity and corneal vascularisation in the DC group. Lower activity of lens aldose reductase, serum advanced glycation end products and blood glycosylated Hb levels were observed in the DE group. The millet SCM feeding showed pronounced ameliorating effects on kidney pathology as reflected by near normal glomerular and tubular structures and lower glomerular filtration rate compared with the shrunken glomerulus, tubular vacuolations in the DC group. Thus, the present animal study evidenced the hypoglycaemic, hypocholesterolaemic, nephroprotective and anti-cataractogenic properties of finger millet SCM, suggesting its utility as a functional ingredient in diets for diabetics.

The present study assessed the effect of separate reduction of each energy-delivering nutrient – protein, fat and carbohydrate – on glucose tolerance and insulin response in a strict carnivore: the domestic cat (Felis catus). Three isoenergetic, home-made diets with the following energetic distribution, low protein (LP): protein 28 % of metabolisable energy; fat 43 %; nitrogen-free extract 29 %; low fat: 47, 27 and 25 %; low carbohydrate (LC): 45, 48 and 7 %, were tested in a 3 × 3 Latin square design. Nine healthy normal-weight cats were randomly assigned to each of the diets in a random order at intervals of 3 weeks. At the end of each testing period, intravenous glucose tolerance tests were performed. Plasma glucose concentrations and area under the glucose curve showed no differences. Area under the insulin curve was lower when cats were fed the LP diet, and the second insulin peak tended to be delayed when the LC diet was fed. In contrast to other studies, in which energy sources were elevated instead of being reduced, the present trial contradicts the often suggested negative impact of carbohydrates on insulin sensitivity in carnivores, and shows that reducing the dietary carbohydrate content below common amounts for commercial foods evokes an insulin-resistant state, which can be explained by the cats' strict carnivorous nature. It even points to a negative effect of protein on insulin sensitivity, a finding that corresponds with the highly gluconeogenic nature of amino acids in strict carnivores.

The objective of the present study was twofold: first to compare the degradation patterns of caprine whey proteins digested with either human digestive juices (gastric or duodenal) or commercial porcine enzymes (pepsin or pancreatic enzymes) and second to observe the effect of gastric pH on digestion. An in vitro two-step assay was performed at 37°C to simulate digestion in the stomach (pH 2, 4 or 6) and the duodenum (pH 8). The whey proteins were degraded more efficiently by porcine pepsin than by human gastric juice at all pH values. Irrespective of the enzyme source, gastric digestion at pH 2 followed by duodenal digestion resulted in the most efficient degradation. Lactoferrin, serum albumin and the Ig heavy chains were highly degraded with less than 6 % remaining after digestion. About 15, 56 and 50 % Ig light chains, β-lactoglobulin (β-LG) and α-lactalbumin remained intact, respectively, when digested with porcine enzymes compared with 25, 74 and 81 % with human digestive juices. For comparison, purified bovine β-LG was digested and the peptide profiles obtained were compared with those of the caprine β-LG in the digested whey. The bovine β-LG seemed to be more extensively cleaved than the caprine β-LG in the whey. Commercial enzymes appear to digest whey proteins more efficiently compared with human digestive juices when used at similar enzyme activities. This could lead to conflicting results when comparing human in vivo protein digestion with digestion using purified enzymes of non-human species. Consequently the use of human digestive juices might be preferred.

Maternal nutritional status, e.g. body weight and composition, is associated with fetal growth. It has been suggested that the insulin-like growth factor (IGF) system may be a mediator of this relationship. In twenty-three healthy Swedish women, we studied (1) the relationships before and during pregnancy between maternal serum concentrations of IGF-I and IGF binding protein-1 (IGFBP-1) and maternal body weight and composition; (2) interactions between serum concentrations of IGF-I (before and in early pregnancy) and maternal nutritional status in relation to infant birth weight. We found that serum IGF-I during pregnancy was positively correlated with maternal body weight (r 0·47–0·56) and fat-free body weight (r 0·61–0·65), whereas serum IGFBP-1 was negatively correlated with maternal body weight (r − 0·44 to − 0·69) and body fat (r − 0·64 to − 0·76) before and during pregnancy. Women with a lower body fat content (%) before pregnancy had greater increases in serum IGFBP-1 during pregnancy than women with a higher prepregnant body fat content (%). In addition, significant fractions of the variation in corrected infant birth weight were explained by variables related to the maternal nutritional status when these were combined with serum concentrations of IGF-I in gestational week 14 (adjusted r2 0·25–0·44, P = 0·001–0·021), but not when they were combined with such concentrations before pregnancy (adjusted r2 0·11–0·12, P = 0·105–0·121). These results suggest mechanisms by which the IGF system may be a mediator between maternal nutritional status and fetal growth.