A meta-analysis was carried out in order to establish the energy requirements of adult cats. Publications that identified cat body weight (BW) were used to generate allometric relationships between energy requirements and BW of healthy adult cats, using log-log linear regression. Energy requirements were expressed in kcal/kg BW to be consistent with those reported by the National Research Council. Mean maintenance energy requirements were 55·1 (se 1·2) kcal/kg BW (115 treatment groups). Three allometric equations were identified to predict the energy requirements for maintenance of BW in the cat based on BW: light (53·7 kcal/kg BW− 1·061), normal (46·8 kcal/kg BW− 1·115) and heavy (131·8 kcal/kg BW− 0 ·366). When reported on lean mass, the allometric equation revealed maintenance requirements were 58·4 kcal/kg lean mass− 1·140 (adjusted R2 0·694; thirty-six treatment groups). The present review suggests that values for maintenance energy requirements based on BW alone may not be an accurate prediction and more detailed information on the age, sex and neuter status, BW and composition would enhance the ability to interpret the maintenance energy requirements of cats.

Sucrose increases postprandial blood glucose concentrations, and diets with a high glycaemic response may be associated with increased risk of obesity, type 2 diabetes and CVD. Previous studies have suggested that polyphenols may influence carbohydrate digestion and absorption and thereby postprandial glycaemia. Berries are rich sources of various polyphenols and berry products are typically consumed with sucrose. We investigated the glycaemic effect of a berry purée made of bilberries, blackcurrants, cranberries and strawberries, and sweetened with sucrose, in comparison to sucrose with adjustment of available carbohydrates. A total of twelve healthy subjects (eleven women and one man, aged 25–69 years) with normal fasting plasma glucose ingested 150 g of the berry purée with 35 g sucrose or a control sucrose load in a randomised, controlled cross-over design. After consumption of the berry meal, the plasma glucose concentrations were significantly lower at 15 and 30 min (P < 0·05, P < 0·01, respectively) and significantly higher at 150 min (P < 0·05) compared with the control meal. The peak glucose concentration was reached at 45 min after the berry meal and at 30 min after the control meal. The peak increase from the baseline was 1·0 mmol/l smaller (P = 0·002) after ingestion of the berry meal. There was no statistically significant difference in the 3 h area under the glucose response curve. These results show that berries rich in polyphenols decrease the postprandial glucose response of sucrose in healthy subjects. The delayed and attenuated glycaemic response indicates reduced digestion and/or absorption of sucrose from the berry meal.

There have been reports of an inverse relationship between meal frequency (MF) and adiposity. It has been postulated that this may be explained by favourable effects of increased MF on appetite control and possibly on gut peptides as well. The main goal of the present study was to investigate whether using a high MF could lead to a greater weight loss than that obtained with a low MF under conditions of similar energy restriction. Subjects were randomised into two treatment arms (high MF = 3 meals+3 snacks/d or low MF = 3 meals/d) and subjected to the same dietary energy restriction of − 2931 kJ/d for 8 weeks. Sixteen obese adults (n 8 women and 8 men; age 34·6 (sd 9·5); BMI 37·1 (sd 4·5) kg/m2) completed the study. Overall, there was a 4·7 % decrease in body weight (P < 0·01); similarly, significant decreases were noted in fat mass ( − 3·1 (sd 2·9) kg; P < 0·01), lean body mass ( − 2·0 (sd 3·1) kg; P < 0·05) and BMI ( − 1·7 (sd 0·8) kg/m2; P < 0·01). However, there were NS differences between the low- and high-MF groups for adiposity indices, appetite measurements or gut peptides (peptide YY and ghrelin) either before or after the intervention. We conclude that increasing MF does not promote greater body weight loss under the conditions described in the present study.

Ellagic acid, a natural polyphenol found in certain fruits, nuts and vegetables, has in recent years been the subject of intense research within the fields of cancer and inflammation. Pain, fever and swelling, all typical symptoms of inflammation, are ascribed to elevated levels of PGE2. In the present study, we have investigated the effects of ellagic acid on PGE2 release and on prostaglandin-synthesising enzymes in human monocytes. Ellagic acid was found to inhibit Ca ionophore A23187-, phorbol myristate acetate- and opsonised zymosan-induced release of PGE2 from monocytes pre-treated with the inflammatory agent lipopolysaccharide. Ellagic acid suppressed the lipopolysaccharide-induced increase in protein expression of cyclo-oxygenase-2 (COX-2), microsomal PGE synthase-1 (mPGEs-1) and cytosolic phospholipase A2α (cPLA2α), while it had no effect on the constitutively expressed COX-1 protein. Ellagic acid had no apparent inhibitory effect on these enzymes when the activities were determined in cell-free assays. We conclude that the inhibitory effect of ellagic acid on PGE2 release from monocytes is due to a suppressed expression of COX-2, mPGEs-1 and cPLA2α, rather than a direct effect on the activities of these enzymes.

Grape antioxidant dietary fibre (GADF) is a grape product rich in dietary fibre and natural antioxidants. We showed previously that the GADF intake induced an epithelial hypoplasia in the rat colonic mucosa. In the present study, we propose that the antioxidant effect of GADF could modulate mucosal apoptosis via modulation of the cellular redox environment. Male Wistar rats (n 20) were fed with diets containing either cellulose (control diet group) or GADF (GADF diet group) as fibre for 4 weeks. The GSH:GSSG ratio, the redox state of the GSSG/2GSH couple (Ehc), the mitochondrial and/or cytosolic antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)), lipid peroxidation (LPO) and apoptosis were evaluated. GADF enhanced the cytosolic GSH:GSSG ratio, shifting the redox potential (Ehc) to a more pro-reducing status. Decreased Cu,ZnSOD:CAT, Cu,ZnSOD:GPx and MnSOD:GPx ratios could indicate an enhanced capacity for reducing H2O2, contributing to decreased cytosolic LPO. Reduced apoptosis in GADF-treated mucosa was inversely related to MnSOD activity. Furthermore, apoptosis increased directly as GSSG content increased. These results suggest that the reduction in apoptosis associated with GADF intake may be due to a modulation of the glutathione redox system and endogenous antioxidant enzymes.

Dietary beans and peas provide fibre, resistant starch and other nutrients that are often lacking in the human diet. The influence of native starches of beans and peas (and microwaved preparations) on N utilisation, biochemical indices in blood serum and caecal ecosystem state (SCFA, bacterial enzymes, micro-organisms) was studied in vivo. The native pea starch contained more resistant starch compared with its bean counterpart (31 v. 17 %); however, processing decreased these amounts to 25 v. 10 %. N digestibility was found to decrease considerably in all experimental groups. A considerable reduction was observed in glucose and total cholesterol concentration in rat blood serum as a result of feeding both dietary legume starch preparations under microwave treatment. This indicates that starch of bean origin activated glycolytic bacterial enzymes; however, all the analysed starches were found to reduce the activity of β-glucuronidase. In addition, both dietary bean starches significantly induced the formation of SCFA in the caecal digesta. As compared with the control group, a significant decrease in the pH of caecal and colonic digesta was demonstrated for both bean starch preparations. In comparison with the diet with native pea starch, its microwaved preparation reduced the concentrations of acetic, butyric and propionic acids among caecal SCFA and increased the pH of caecal and colonic digesta. The atherogenic index was significantly lower in rats fed microwaved pea starch. All investigated starch preparations increased the population of Bifidobacterium spp. in caecal digesta, but were also good substrates for opportunistic Enterococcus or Escherichia coli.

Selective breeding of dogs has culminated in a large number of modern breeds distinctive in terms of size, shape and behaviour. Inadvertently, a range of breed-specific genetic disorders have become fixed in some pure-bred populations. Several inherited conditions confer chronic metabolic defects that are influenced strongly by diet, but it is likely that many less obvious breed-specific differences in physiology exist. Using Labrador retrievers and miniature Schnauzers maintained in a simulated domestic setting on a controlled diet, an experimental design was validated in relation to husbandry, sampling and sample processing for metabolomics. Metabolite fingerprints were generated from ‘spot’ urine samples using flow injection electrospray MS (FIE-MS). With class based on breed, urine chemical fingerprints were modelled using Random Forest (a supervised data classification technique), and metabolite features (m/z) explanatory of breed-specific differences were putatively annotated using the ARMeC database (http://www.armec.org). GC-MS profiling to confirm FIE-MS predictions indicated major breed-specific differences centred on the metabolism of diet-related polyphenols. Metabolism of further diet components, including potentially prebiotic oligosaccharides, animal-derived fats and glycerol, appeared significantly different between the two breeds. Analysis of the urinary metabolome of young male dogs representative of a wider range of breeds from animals maintained under domestic conditions on unknown diets provided preliminary evidence that many breeds may indeed have distinctive metabolic differences, with significant differences particularly apparent in comparisons between large and smaller breeds.

African catfish (Clarias gariepinus) were fed four isonitrogenous diets (34 % crude protein), each containing one of two lipid (100 or 180 g/kg) and two l-carnitine (15 or 1000 mg/kg) levels. After 81 d of feeding, thirty-two fish (body weight 32 g) from each dietary group were randomly selected, sixteen fish were induced to a 3-h swim (speed of 1·5 body length (BL)/s), while the other sixteen fish were kept under resting condition. Fish fed 1000 mg l-carnitine accumulated 3·5 and 5 times more l-carnitine in plasma and muscle, respectively, than fish fed the 15 mg l-carnitine. Muscle l-carnitine content was significantly lower in exercised fish than in rested fish. High dietary lipid level (fish oil) led to an increase in muscle n-3 PUFA content and a decrease in SFA and MUFA content. In liver, the increase in dietary lipid level resulted in an increased levels of both n-6 and n-3 PUFA. l-carnitine supplementation significantly decreased n-3 PUFA content. Exercise decreased n-3 PUFA in both muscle and liver. Plasma lactate and lactate dehydrogenase, normally associated with increased glycolytic processes, were positively correlated with exercise and inversely correlated with dietary l-carnitine level. l-carnitine supplementation reduced significantly the RQ from 0·72 to 0·63, and an interaction between dietary l-carnitine and lipid was observed (P < 0·03). Our results indicate that an increase in fatty acids (FA) intake may promote FA oxidation, and both carnitine and exercise might influence the regulation of FA oxidation selectivity.

Endurance training improves exercise performance and insulin sensitivity, and these effects may be in part mediated by an enhanced fat oxidation. Since n-3 and n-9 unsaturated fatty acids may also increase fat oxidation, we hypothesised that a diet enriched in these fatty acids may enhance the effects of endurance training on exercise performance, insulin sensitivity and fat oxidation. To assess this hypothesis, sixteen normal-weight sedentary male subjects were randomly assigned to an isoenergetic diet enriched with fish and olive oils (unsaturated fatty acid group (UFA): 52 % carbohydrates, 34 % fat (12 % SFA, 12 % MUFA, 5 % PUFA), 14 % protein), or a control diet (control group (CON): 62 % carbohydrates, 24 % fat (12 % SFA, 6 % MUFA, 2 % PUFA), 14 % protein) and underwent a 10 d gradual endurance training protocol. Exercise performance was evaluated by measuring VO2max and the time to exhaustion during a cycling exercise at 80 % VO2max; glucose homeostasis was assessed after ingestion of a test meal. Fat oxidation was assessed by indirect calorimetry at rest and during an exercise at 50 % VO2max. Training significantly increased time to exhaustion, but not VO2max, and lowered incremental insulin area under the curve after the test meal, indicating improved insulin sensitivity. Those effects were, however, of similar magnitude in UFA and CON. Fat oxidation tended to increase in UFA, but not in CON. This difference was, however, not significant. It is concluded that a diet enriched with fish- and olive oil does not substantially enhance the effects of a short-term endurance training protocol in healthy young subjects.

The erythrocyte and plasma fatty acid compositions of children with autism were compared in a case–control study with typically developing (TD) children and with children showing developmental delay (DD). Forty-five autism subjects were age-matched with TD controls and thirty-eight with DD controls. Fatty acid data were compared using paired t tests. In addition, blood fatty acids from treatment-naive autism subjects were compared with autism subjects who had consumed fish oil supplements by two-sample t tests. Relatively few differences were seen between erythrocyte fatty acids in autism and TD subjects although the former had an increased arachidonic acid (ARA):EPA ratio. This ratio was also increased in plasma samples from the same children. No changes in n-3 fatty acids or ARA:EPA ratio were seen when comparing autism with DD subjects but some SFA and MUFA were decreased in the DD subjects, most notably 24 : 0 and 24 : 1, which are essential components of axonal myelin sheaths. However, if multiple comparisons are taken into account, and a stricter level of significance applied, most of these values would not be significant. Autism subjects consuming fish oil showed reduced erythrocyte ARA, 22 : 4n-6, 22 : 5n-6 and total n-6 fatty acids and increased EPA, 22 : 5n-3, 22 : 6n-3 and total n-3 fatty acids along with reduced n-6:n-3 and ARA:EPA ratios. Collectively, the autism subjects did not have an underlying phospholipid disorder, based on erythrocyte fatty acid compositions, although the increased ARA:EPA ratio observed suggested that an imbalance of essential highly unsaturated fatty acids may be present in a cohort of autism subjects.

Epidemiological studies have suggested an inverse correlation between red wine consumption and the incidence of CVD. However, Champagne wine has not been fully investigated for its cardioprotective potential. In order to assess whether acute and moderate Champagne wine consumption is capable of modulating vascular function, we performed a randomised, placebo-controlled, cross-over intervention trial. We show that consumption of Champagne wine, but not a control matched for alcohol, carbohydrate and fruit-derived acid content, induced an acute change in endothelium-independent vasodilatation at 4 and 8 h post-consumption. Although both Champagne wine and the control also induced an increase in endothelium-dependent vascular reactivity at 4 h, there was no significant difference between the vascular effects induced by Champagne or the control at any time point. These effects were accompanied by an acute decrease in the concentration of matrix metalloproteinase (MMP-9), a significant decrease in plasma levels of oxidising species and an increase in urinary excretion of a number of phenolic metabolites. In particular, the mean total excretion of hippuric acid, protocatechuic acid and isoferulic acid were all significantly greater following the Champagne wine intervention compared with the control intervention. Our data suggest that a daily moderate consumption of Champagne wine may improve vascular performance via the delivery of phenolic constituents capable of improving NO bioavailability and reducing matrix metalloproteinase activity.

The purpose of the present study was to determine the effects of dietary antioxidant restriction on plasma concentrations of carotenoids and inflammatory markers at rest and in response to exercise in endurance-trained males. Seventeen males performed two exercise trials 2 weeks apart. Participants followed their habitual antioxidant diet (H-AO) before the first exercise test, then a restricted antioxidant diet (R-AO) for 2 weeks before the second exercise test. Blood was collected pre- and post-exercise. Dietary intakes of fibre, ascorbic acid and β-carotene were lower (P < 0·05) on the R-AO diet, but no other differences were observed. Pre-exercise plasma β-carotene concentrations were lower (H-AO, 195 (sd 92); R-AO, 123 (sd 54) ng/ml; P < 0·05), and TNF-α concentrations were higher (H-AO, 16 (sd 7); R-AO, 613 (sd 325) pg/ml; P < 0·01) on the R-AO diet compared to the H-AO diet. Most plasma carotenoid concentrations decreased with exercise, but this effect was more consistent on the H-AO diet. No differences in plasma IL-6 concentrations were observed pre-exercise, whereas post-exercise plasma IL-6 concentrations (H-AO, 30·3 (sd 16); R-AO, 15·3 (sd 5) pg/ml; P < 0·05) were lower following the R-AO diet. Post-exercise TNF-α concentrations were higher on the R-AO diet. Ratings of perceived effort during submaximal exercise were higher (P < 0·05) on the R-AO diet, but there was no difference in the time to exhaustion between diets. In conclusion, lower dietary intakes of carotenoids alter the plasma concentrations of antioxidants and markers of inflammation at rest and in response to exercise.

The concept of diet-induced ‘acidosis’ as a cause of disease has been a subject of interest for more than a century. The present article reviews the history of our evolving understanding of physiological pH, the physiological support for the concept of ‘acidosis’, the causes of acidosis, how it is recognised, its short-term effects as well as the long-term clinical relevance of preventative measures, and the research support for normalisation of pH. Further, we suggest differentiation of the terms ‘acidosis’ and ‘acidaemia’ as a way to resolve the conflation of these topics which has led to confusion and controversy. The available research makes a compelling case that diet-induced acidosis, not diet-induced acidaemia, is a real phenomenon, and has a significant, clinical, long-term pathophysiological effect that should be recognised and potentially counterbalanced by dietary means.

Danish legislation regarding food fortification has been very restrictive resulting in few fortified food items on the Danish market. Folate and vitamin B12 deficiency is thought to be common due to inadequate intakes but little is known about the actual prevalence of low serum folate and vitamin B12 in the general population. The aim of the present study was to evaluate the folate and vitamin B12 status of Danish adults and to investigate associations between vitamin status and distinct lifestyle and genetic factors. The study included a random sample of 6784 individuals aged 30–60 years. Information on lifestyle factors was obtained by questionnaires and blood samples were analysed for serum folate and vitamin B12 concentrations and several genetic polymorphisms. The overall prevalence of low serum folate ( < 6·8 nmol/l) was 31·4 %. Low serum folate was more common among men than women and the prevalence was lower with increasing age. Low serum folate was associated with smoking, low alcohol intake, high coffee intake, unhealthy diet, and the TT genotype of the methylenetetrahydrofolate reductase (MTHFR)-C677T polymorphism. The overall prevalence of low serum vitamin B12 ( < 148 pmol/l) was 4·7 %. Low serum vitamin B12 was significantly associated with female sex, high coffee intake, low folate status, and the TT genotype of the MTHFR-C677T polymorphism. In conclusion, low serum folate was present in almost a third of the adult population in the present study and was associated with several lifestyle factors whereas low serum concentrations of vitamin B12 were less common and only found to be associated with a few lifestyle factors.

The present study has explored mother–child relationships in the intake of different food groups and the sex differences in these relationships. A population-based sample of 471 mother–child pairs from Stockholm completed a dietary questionnaire to assess habitual dietary intake. Girls showed overall stronger correlations with their mothers' diet than boys did. The strongest correlations found, in both girls and boys, were for the intakes of fruit juice and sweet bakery goods (r 0·30–0·37, P < 0·001). There was a wide range in correlation strength between food groups. Milk/yoghurt and desserts showed no mother–child relationship at all. Breakfast cereals was the only food group with a significant sex interaction (P = 0·01; mothers–girls, r 0·30, P < 0·001; mothers–boys, r0·05, NS). There were significant positive correlations between mothers and daughters in the intake of all macronutrients, whereas none between mothers and sons (sex interactions: protein, P = 0·001; fat, P = 0·004; carbohydrates, P = 0·001). Mothers and daughters (r 0·29, P < 0·001), but not mothers and sons, showed significant correlation in total energy intake, (P = 0·001 for sex interaction). There were generally more differences between mothers and children than between boys and girls in the relative intake (percentage of energy) of different food groups. Since teenaged children have a similar intake of especially snack foods as their mothers, it could be meaningful to educate mothers when aiming at improving the diet of teenaged children, both boys and girls.

Epidemiological evidence shows an inverse relationship between dietary fibre intake and body weight gain. Oat β-glucan, a soluble fibre alters appetite hormones and subjective satiety in acute meal test studies, but its effects have not been demonstrated with chronic consumption. The present study aimed to test the effects in women of two different doses of oat β-glucan on weight loss and hormones associated with appetite regulation. In a 3-month parallel trial, sixty-six overweight females were randomised into one of three 2 MJ energy-deficit diets: a control and two interventions including 5–6 g or 8–9 g β-glucan. Anthropometric and metabolic variables (blood glucose level, insulin, total cholesterol (TC), LDL, HDL, TAG and leptin), together with markers of appetite regulation (cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), ghrelin, peptide YY (PYY) and PYY3-36) were measured at baseline and at 3 months. After 3 months, all groups lost weight (P < 0·001) and showed a reduced waist circumference (P < 0·001). The study sample also showed reductions in TC, LDL, HDL, leptin, PYY, GLP-1 values (all P < 0·001) and an increase in CCK levels (P < 0·001). No significant differences were noted between the groups for all outcome values except PYY levels (P = 0·018). In broad terms, the addition of oat β-glucan did not enhance the effect of energy restriction on weight loss in mildly overweight women, although wide variations in observed results suggests that individual responsiveness may be an issue.

Obesity affects one in three American adult women and is associated with overall mortality and major morbidities. A composite diet index to evaluate total diet quality may better assess the complex relationship between diet and obesity, providing insights for nutrition interventions. The purpose of the present investigation was to determine whether diet quality, defined according to the previously validated Framingham nutritional risk score (FNRS), was associated with the development of overweight or obesity in women. Over 16 years, we followed 590 normal-weight women (BMI < 25 kg/m2), aged 25 to 71 years, of the Framingham Offspring and Spouse Study who presented without CVD, cancer or diabetes at baseline. The nineteen-nutrient FNRS derived from mean ranks of nutrient intakes from 3 d dietary records was used to assess nutritional risk. The outcome was development of overweight or obesity (BMI ≥ 25 kg/m2) during follow-up. In a stepwise multiple logistic regression model adjusted for age, physical activity and smoking status, the FNRS was directly related to overweight or obesity (P for trend = 0·009). Women with lower diet quality (i.e. higher nutritional risk scores) were significantly more likely to become overweight or obese (OR 1·76; 95 % CI 1·16, 2·69) compared with those with higher diet quality. Diet quality, assessed using a comprehensive composite nutritional risk score, predicted development of overweight or obesity. This finding suggests that overall diet quality be considered a key component in planning and implementing programmes for obesity risk reduction and treatment recommendations.

The objective of the present study was to examine anthropometric, metabolic, psychosocial and dietary factors associated with dropout in a 6-month weight loss intervention aimed at reducing body weight by 10 %. The study sample included 137 sedentary, overweight and obese postmenopausal women, participating in a weight loss intervention that consisted of either energy restriction (ER) or ER with resistance training (ER+RT). Anthropometric (BMI, percent lean body mass, percent fat mass, visceral adipose tissue and waist circumference), metabolic (total energy expenditure, RMR, insulin sensitivity and fasting plasma levels of leptin and ghrelin), psychosocial (body esteem, self-esteem, stress, dietary restraint, disinhibition, hunger, quality of life, self-efficacy, perceived benefits for controlling weight and perceived risk) and dietary (3-d food record) variables were measured. Thirty subjects out of 137 dropped out of the weight loss programme (22 %), with no significant differences in dropout rates between those in the ER and the ER+RT groups. Overall, amount of weight loss was significantly lower in dropouts than in completers ( − 1·7 (sd 3·5) v. − 5·6 (sd 4·3) kg, P < 0·05); weekly weight loss during the first 4 weeks was also significantly lower. Dropouts consumed fewer fruit servings than completers (1·7 (sd 1·1) v. 2·7 (sd 1·53), P < 0·05) and had higher insulin sensitivity levels (12·6 (sd 3·8) v. 11·1 (sd 2·8) mg glucose/min per kg fat-free mass, P < 0·05). The present results suggest that the rate of weight loss during the first weeks of an intervention plays an important role in the completion of the programme. Thus, participants with low rates of initial weight loss should be monitored intensely to undertake corrective measures to increase the likelihood of completion.