Predicting the magnitude and rate of weight gain for a given increase of energy intake requires a model of whole-body energy expenditure that includes the energy cost of tissue deposition. Here, I introduce a mathematical framework for modelling energy expenditure that elucidates conceptual problems with the classical Kielanowski method for estimating the efficiencies of body fat and protein deposition. An alternative approach uses the theoretical biochemical efficiencies for protein and fat synthesis in combination with models of energy expenditure that include body fat and protein turnover costs. I illustrate this alternative approach using a simple mathematical model applied to previously published data from growing rats and human infants and compare the simple model results with the classical Kielanowski model. While both models fit the data reasonably well (R2>0·87 in rats and R2>0·67 in infants), the Kielanowski method resulted in parameter estimates that varied widely across experiments, had poor precision, and occasionally produced efficiency estimates greater than 1. In contrast, the new method provided precise parameter values and revealed consistencies across different experiments. The proposed mathematical framework has implications for interpreting studies of animal nutrition as well as providing a roadmap for future modelling efforts.

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.

Certain forms of dietary Se may have an advantage in improving Se status and reducing cancer risk. The present study compared the effects of an Se-enriched milk protein product (dairy-Se) with an Se yeast (yeast-Se) on selenoprotein activity and expression in the mouse colon. Mice were fed four diets for 4 weeks: a control milk protein diet (Se at 0·068 parts per million (ppm)), dairy-Se diets with Se at 0·5 and 1 ppm, and a yeast-Se diet with Se at 1 ppm. Cytosolic glutathione peroxidase-1 (GPx-1) activity, mRNA of selenoprotein P (SeP), GPx-1, gastrointestinal glutathione peroxidase-2 (GPx-2) and thioredoxin reductase-1 (TrxR-1) were examined in the mouse colon. Dairy-Se diets did not significantly affect GPx-1 mRNA and GPx-1 activity but produced a dose-dependent increase in SeP and GPx-2 mRNA, with a significantly higher level achieved at 1 ppm Se (P < 0·05). Yeast-Se at 1 ppm significantly increased GPx-1 mRNA and GPx-1 activity (P < 0·01) but not GPx-2 mRNA. Neither Se supplement had any effect on TrxR-1. The present study indicates that selenoprotein levels in the mouse colon are regulated differently depending on the Se supplement. As we have previously shown that dairy-Se at 1 ppm was protective against colorectal cancer (CRC) in an azoxymethane-induced CRC mouse model, this up-regulation of colonic GPx-2 and SeP with Se supplementation may be crucial to its chemopreventive action.

Older age, dietary folate and chronic alcohol consumption are important risk factors for the development of colon cancer. The present study examined the effects of ageing, folate and alcohol on genomic and p16-specific DNA methylation, and p16 expression in the murine colon. Old (aged 18 months; n 70) and young (aged 4 months; n 70) male C57BL/6 mice were pair-fed either a Lieber-DeCarli liquid diet with alcohol (18 % of energy), a Lieber-DeCarli diet with alcohol (18 %) and reduced folate (0·25 mg folate/l) or an isoenergetic control diet (0·5 mg folate/l) for 5 or 10 weeks. Genomic DNA methylation, p16 promoter methylation and p16 gene expression were analysed by liquid chromatography–MS, methylation-specific PCR and real-time RT-PCR, respectively. Genomic DNA methylation was lower in the colon of old mice compared with young mice (P < 0·02) at 10 weeks. Alcohol consumption did not alter genomic DNA methylation in the old mouse colon, whereas it tended to decrease genomic DNA methylation in young mice (P = 0·08). p16 Promoter methylation and expression were higher in the old mouse colon compared with the corresponding young groups. There was a positive correlation between p16 promoter methylation and p16 expression in the old mouse colon (P < 0·02). In young mice the combination of alcohol and reduced dietary folate led to significantly decreased p16 expression compared with the control group (P < 0·02). In conclusion, ageing and chronic alcohol consumption alter genomic DNA methylation, p16 promoter methylation and p16 gene expression in the mouse colon, and dietary folate availability can further modify the relationship with alcohol in the young mouse.

The beneficial influence of three common spices was examined in experimental rats on: (i) the membrane fluidity of intestinal brush-border membranes (BBM), (ii) the activity of intestinal membrane-bound enzymes, and (iii) ultrastructural alterations in the intestinal epithelium. Groups of male Wistar rats were maintained on dietary black pepper (0·5 %), red pepper (3·0 %), ginger (0·05 %) and spice bioactive compounds piperine (0·02 %) and capsaicin (0·01 %) for 8 weeks. A membrane fluidity study using an apolar fluorescent probe showed increased BBM fluidity in all the spice-fed animals. This was corroborated by a decreased cholesterol:phospholipid ratio in the jejunal and ileal regions of the intestine. These dietary spices stimulated the activities of BBM enzymes (glycyl-glycine dipeptidase, leucine amino peptidase and γ-glutamyl transpeptidase) in the jejunal mucosa, suggesting a modulation in membrane dynamics due to the apolar spice bioactive compounds interacting with surrounding lipids and hydrophobic portions in the protein vicinity, which may decrease the tendency of membrane lipids to act as steric constraints to enzyme proteins and thus modify enzyme conformation. Scanning electronic microscopy of the intestinal villi in these spice treatments revealed alterations in the ultrastructure, especially an increase in microvilli length and perimeter which would mean a beneficial increase in the absorptive surface of the small intestine, providing for an increased bioavailability of micronutrients. Thus, dietary spices (black pepper, red pepper and ginger) were evidenced to induce alterations in BBM fluidity and passive permeability property, associated with the induction of an increased microvilli length and perimeter, resulting in an increased absorptive surface of the small intestine.

The beneficial influences of xylo-oligosaccharides (XOS) obtained from alkali-pretreated corncob and fructo-oligosaccharides (FOS) obtained from cane sugar were evaluated in experimental diabetes. These oligosaccharides were supplemented at 10 % (w/w) in the basal diet of streptozotocin-induced diabetic Wistar rats, while the control rats were fed with a basal diet for a period of 6 weeks. Both the oligosaccharides exerted favourable influences in diabetic rats by significantly improving body weight and reducing hyperglycaemia and cholesterol. The characteristic diabetic complications such as severe glucosuria, proteinuria and advanced glycation end products in renal tissue, diabetic nephropathy, and blood creatinine and urea concentrations were notably reduced. Besides, these oligosaccharide supplementations significantly increased the activity of antioxidant enzymes – catalase and glutathione reductase – in the blood of diabetic rats. Supplementation of XOS and FOS resulted in a significant increase in the bifidobacteria and lactobacilli population in the caecum. The present study indicates that XOS and FOS have an ameliorating influence on metabolic abnormalities associated with diabetes, besides conferring an optimal milieu of lactobacilli and bifidobacteria, thus suggesting their potential health benefit in diabetics.

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.

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.

Diets that ameliorate the adverse effects of uric acid (UA) on renal damage deserve attention. The effects of casein or soya protein combined with palm or safflower-seed oil on various serum parameters and renal histology were investigated on hyperuricaemic rats. Male Wistar rats administered with oxonic acid and UA to induce hyperuricaemia were fed with casein or soya protein plus palm- or safflower-seed oil-supplemented diets. Normal rats and hyperuricaemic rats with or without allopurinol treatment (150 mg/l in drinking water) were fed with casein plus maize oil-supplemented diets. After 8 weeks, allopurinol treatment and soya protein plus safflower-seed oil-supplemented diet significantly decreased serum UA in hyperuricaemic rats (one-way ANOVA; P < 0·05). In addition, soya protein and casein attenuated hyperuricaemia-induced decreases in serum albumin and insulin, respectively (two-way ANOVA; P < 0·05). Safflower-seed oil significantly decreased serum TAG and UA, whereas palm oil significantly increased serum cholesterol, TAG, blood urea N and creatinine. However, soya protein significantly decreased renal NO and nitrotyrosine and palm oil significantly decreased renal nitrotyrosine, TNF-α and interferon-γ and increased renal transforming growth factor-β. Casein with safflower-seed oil significantly attenuated renal tubulointerstitial nephritis, crystals and fibrosis. Comparing casein v. soya protein combined with palm or safflower-seed oil, the results support that casein with safflower-seed oil may be effective in attenuating hyperuricaemia-associated renal damage, while soya protein with safflower-seed oil may be beneficial in lowering serum UA and TAG.

Inflammation plays an important role in diabetes mellitus and its complications. In this context, the negative cross-talk between adipose tissue and skeletal muscle leads to disturbances in muscle cell insulin signalling and induces insulin resistance. Because several studies have shown that energy restriction brings some benefits to diabetes, the aim of the present study was to evaluate the effects of dietary restriction on systemic and skeletal muscle inflammatory biomarkers, such C-reactive protein, adipokines and cytokines, and in insulin resistance in Goto-Kakizaki rats. This is an animal model of spontaneous non-obese type 2 diabetes with strongly insulin resistance and without dyslipidaemia. Animals were maintained during 2 months of dietary restriction (50 %) and were killed at 6 months of age. Some biochemical determinations were done using ELISA and Western blot. Data from the present study demonstrate that in Goto-Kakizaki rats the dietary restriction improved insulin resistance, NEFA levels and adipokine profile and ameliorated inflammatory cytokines in skeletal muscle. These results indicate that dietary restriction in type 2 diabetes enhances adipose tissue metabolism leading to an improved skeletal muscle insulin sensitivity.

Obesity is associated with complications during pregnancy and increased health risks in the newborn. The objective of the present study was to establish possible relationships between gut microbiota, body weight, weight gain and biochemical parameters in pregnant women. Fifty pregnant women were classified according to their BMI in normal-weight (n 34) and overweight (n 16) groups. Gut microbiota composition was analysed by quantitative real-time PCR in faeces and biochemical parameters in plasma at 24 weeks of pregnancy. Reduced numbers of Bifidobacterium and Bacteroides and increased numbers of Staphylococcus, Enterobacteriaceae and Escherichia coli were detected in overweight compared with normal-weight pregnant women. E. coli numbers were higher in women with excessive weight gain than in women with normal weight gain during pregnancy, while Bifidobacterium and Akkermansia muciniphila showed an opposite trend. In the whole population, increased total bacteria and Staphylococcus numbers were related to increased plasma cholesterol levels. Increased Bacteroides numbers were related to increased HDL-cholesterol and folic acid levels, and reduced TAG levels. Increased Bifidobacterium numbers were related to increased folic acid levels. Increased Enterobacteriaceae and E. coli numbers were related to increased ferritin and reduced transferrin, while Bifidobacterium levels showed the opposite trend. Therefore, gut microbiota composition is related to body weight, weight gain and metabolic biomarkers during pregnancy, which might be of relevance to the management of the health of women and infants.

Nutrition is a key element in geriatric health, and nutritional screening/assessment is a key component of comprehensive geriatric evaluation. The study aimed to validate the Mini Nutritional Assessment Taiwan version-1 (MNA-T1) which adopted population-specific anthropometric cut-points, and version-2 (MNA-T2) which replaced BMI with mid-arm and calf circumferences in the scale for predicting the nutritional status of elderly Taiwanese. Using data of a population-representative longitudinal study of 2802 Taiwanese aged 65 years or older, the study graded the nutritional status of each subject with the original and both modified versions at baseline, analysed their hospital length of stay, the Activities of Daily Living (ADL), the Center for Epidemiologic Studies Depression Scale (CES-D) and life-satisfaction scores at baseline and end of 4 years, and tracked their survival during the period. Results showed that both modified versions had superior predictive abilities compared with the original MNA, and their graded scores correlated better with hospital length of stay, and ADL, CES-D and life-satisfaction scores. Both modified versions were effective in predicting follow-up mortality risk. The relative mortality risk was about 7 times for those rated malnourished and 2·5 times for those rated at risk of malnutrition compared with those who were rated normal at baseline by the two modified versions. These results suggest that both of the modified versions are effective in predicting the nutrition and health statuses of Taiwanese elderly and would serve to validate the predictive ability of the two modified versions. The MNA-T2, which requires no BMI, can make routine nutritional screening/assessment an easier task.

Low dietary Ca intake and vitamin D insufficiency have been implicated as part of the aetiology leading to osteoporosis. The aim of the present study was to examine the effects of a 30-month dietary intervention that combined supplementation of dairy products fortified with Ca and vitamin D3 and lifestyle and nutrition counselling sessions on bone mineral density (BMD) of postmenopausal women. Sixty-six postmenopausal women (aged 55–65 years) were randomised into a dietary group (DG; n 35), receiving daily and for the first 12 months 1200 mg Ca and 7·5 μg vitamin D3, while for the next 18 months of intervention 1200 mg Ca and 22·5 μg vitamin D3 through fortified dairy products, and a control group (CG; n 31) receiving neither counselling nor dairy products. The DG was found to have more favourable changes in arms (P < 0·001), total spine (P = 0·001) and total body BMD (P < 0·001) compared with the CG. Furthermore, a significant increase was observed for the DG in lumbar spine BMD (0·056; 95 % CI 0·009, 0·103), which was not found to differentiate significantly compared with the change observed in the CG (P = 0·075). In conclusion, the present study showed that intakes of vitamin D of about 22·5 μg/d and of Ca close to the recommended level of 1200 mg from fortified dairy foods for 30 months, with compliance ensured by lifestyle and nutrition counselling sessions, can induce favourable changes in arms, total spine and total body BMD of postmenopausal women.

Low vitamin D levels during pregnancy may account for reduced fetal growth and for altered neonatal development. The present study explored the association between maternal vitamin D status measured early in pregnancy and birth weight, prevalence of small-for-gestational-age (SGA) infants and postnatal growth (weight and length), as well as the potential role of vitamin D status in explaining ethnic disparities in these outcomes. Data were derived from a large multi-ethnic cohort in The Netherlands (Amsterdam Born Children and their Development (ABCD) cohort), and included 3730 women with live-born singleton term deliveries. Maternal serum vitamin D was measured during early pregnancy (median 13 weeks, interquartile range: 12–14), and was labelled ‘deficient’ ( ≤ 29·9 nmol/l), ‘insufficient’ (30–49·9 nmol/l) or ‘adequate’ ( ≥ 50 nmol/l). Six ethnic groups were distinguished: Dutch, Surinamese, Turkish, Moroccan, other non-Western and other Western. Associations with neonatal outcomes were analysed using multivariate regression analyses. Results showed that compared with women with adequate vitamin D levels, women with deficient vitamin D levels had infants with lower birth weights ( − 114·4 g, 95 % CI − 151·2, − 77·6) and a higher risk of SGA (OR 2·4, 95 % CI 1·9, 3·2). Neonates born to mothers with a deficient vitamin D status showed accelerated growth in weight and length during the first year of life. Although a deficient vitamin D status influenced birth weight, SGA risk and neonatal growth, it played a limited role in explaining ethnic differences. Although vitamin D supplementation might be beneficial to those at risk of a deficient vitamin D status, more research is needed before a nationwide policy on the subject can be justified.

Previous studies have suggested that daidzein's metabolites, equol and O-desmethylangolensin (O-DMA), rather than daidzein itself may contribute to the beneficial effects of soya foods in the prevention of CVD. The present study aims to assess the proportion of equol and O-DMA producers, and to compare differences in anthropometric factors, serum lipids, glucose and uric acid between producers and non-producers in Chinese adults aged 20–69 years. For the present cross-sectional study, 202 subjects (100 women and 102 men) were recruited. Twenty-four-hour urinary daidzein and its metabolites were determined in these subjects while on their usual diet and again after a 3-d isoflavone challenge. Fasting serum lipids, glucose and uric acid were examined on their usual diet. Three days of 24 h dietary recalls were used to assess dietary intakes. Of the 202 subjects, 27 (13·4 %) and 27 (13·4 %) excreted equol and O-DMA on their usual diet, and 101 (50 %) and 94 (46·5 %) produced equol and O-DMA after a load of 80 mg/d isoflavones. Equol producers showed lower serum uric acid ( − 10·2 %, P = 0·001), TAG ( − 29·5 %, P = 0·007) and waist:hip ratio ( − 2·6 %, P = 0·032), and tended to have higher HDL cholesterol (6·3 %, P = 0·069) compared with equol non-producers. There were no significant differences in serum lipids, glucose and uric acid between O-DMA producers and non-producers. In conclusion, equol phenotypes might influence cardiovascular risk.

Recommendations for whole-grain (WG) intake are based on observational studies showing that higher WG consumption is associated with reduced CVD risk. No large-scale, randomised, controlled dietary intervention studies have investigated the effects on CVD risk markers of substituting WG in place of refined grains in the diets of non-WG consumers. A total of 316 participants (aged 18–65 years; BMI>25 kg/m2) consuming < 30 g WG/d were randomly assigned to three groups: control (no dietary change), intervention 1 (60 g WG/d for 16 weeks) and intervention 2 (60 g WG/d for 8 weeks followed by 120 g WG/d for 8 weeks). Markers of CVD risk, measured at 0 (baseline), 8 and 16 weeks, were: BMI, percentage body fat, waist circumference; fasting plasma lipid profile, glucose and insulin; and indicators of inflammatory, coagulation, and endothelial function. Differences between study groups were compared using a random intercepts model with time and WG intake as factors. Although reported WG intake was significantly increased among intervention groups, and demonstrated good participant compliance, there were no significant differences in any markers of CVD risk between groups. A period of 4 months may be insufficient to change the lifelong disease trajectory associated with CVD. The lack of impact of increasing WG consumption on CVD risk markers implies that public health messages may need to be clarified to consider the source of WG and/or other diet and lifestyle factors linked to the benefits of whole-grain consumption seen in observational studies.

The diet quality index (DQI) for preschool children is a new index developed to reflect compliance with four main food-based dietary guidelines for preschool children in Flanders. The present study investigates: (1) the validity of this index by comparing DQI scores for preschool children with nutrient intakes, both of which were derived from 3 d estimated diet records; (2) the reproducibility of the DQI for preschoolers based on a parentally reported forty-seven-item FFQ DQI, which was repeated after 5 weeks; (3) the relative validity of the FFQ DQI with 3 d record DQI scores as reference. The study sample included 510 and 58 preschoolers (2·5–6·5 years) for validity and reproducibility analyses, respectively. Increasing 3 d record DQI scores were associated with decreasing consumption of added sugars, and increasing intakes of fibre, water, Ca and many micronutrients. Mean FFQ DQI test–retest scores were not significantly different: 72 (sd 11) v. 71 (sd 10) (P = 0·218) out of a maximum of 100. Mean 3 d record DQI score (66 (sd 10)) was significantly lower than mean FFQ DQI (71 (sd 10); P < 0·001). The reproducibility correlation was 0·88. Pearsons correlation (adjusted for within-person variability) between FFQ and 3 d record DQI scores was 0·82. Cross-classification analysis of the FFQ and 3 d record DQI classified 60 % of the subjects in the same category and 3 % in extreme tertiles. Cross-classification of repeated administrations classified 62 % of the subjects in the same category and 3 % in extreme categories. The FFQ-based DQI approach compared well with the 3 d record approach, and it can be used to determine diet quality among preschoolers.

Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects.