1. The relative rates of passage of polyethylene glycol (PEG) and lignin through the alimentary tracts of sheep were examined through the ratio of these two markers in the fodder and in the contents of various segments of the gut. A much faster turnover of PEG than of lignin in the stomach compartments suggested that samples from these organs could not be representative of the digesta flowing through them. Average PEG:lignin ratios in the small and large intestines were close to the ratio in the fodder, indicating that sampling from the duo-denum in the living animal could possibly yield material representative of that flowing from the stomach to the small intestine. Similar results were obtained for high and low levels of fodder intake.

2. A procedure was developed for automatic sampling from the duodenum for prolonged periods, and the material collected was shown to be representative of digesta flow. Simpler methods of sampling from the duodenum were shown to be liable to relatively large errors.

3. The amount of nitrogen reaching the duodenum in sheep given lucerne hay pellets was found to be equivalent to practically 100 % of the dietary N, whether the intake of fodder was 600 g/d or 1500 g/d.

The present results are the last part of a series of experiments conducted in this laboratory on metabolism of major individual rumen ciliate protozoa species and their combinations in sheep. These species were inoculated into the rumen of fauna-free (FF) sheep to study digestibility of dietary fibre and duodenal flow of N. Sixteen rumen- and duodenum-cannulated FF sheep were divided into four equal groups and used in the present experiment. One group remained FF, while the other three were each inoculated intraruminally with the Holotrich protozoa sp. (HT), Entodinium sp. (EN) or total mixed fauna (TF). In comparison with the FF group, the HT did not affect (P>0·05) the duodenal flow of non-NH3-N and bacterial-N, while the flow was decreased (P < 0·05) by both the EN and TF populations. The digestibility of fibre was increased (P < 0·05) by both the EN and TF populations, but the results for the HT group were mostly similar to those for the FF sheep. The fibre digestibility in the stomach for TF was intermediate between that for EN and FF. It was concluded that except when fed high-carbohydrate diets, the presence in the rumen of the HT protozoa are of no significant value or major detriment to ruminant production.

The growth of broiler chickens on diets containing various levels of Lemna gibba was evaluated. Groups of broiler chicks were fed on diets containing 0-400 g Lemna gibba/kg for 3 weeks. These chickens were then changed to standard diets for a further 2 weeks. As the level of Lemna gibba increased, feed consumption and weight gain decreased. However, when diets were changed to the standard diet, compensatory growth was observed. In a second experiment, diets were formulated with a metabolizable energy of 5.02 MJ (1200 kcal)/kg Lemna gibba and included a finer-milled Lemna gibba. Chickens were fed on diets containing 0-300 g Lemna gibba/kg for 4 weeks. Each group was then divided into two subgroups. For the next 2 weeks one of these sub-groups was maintained on the experimental (Lemna gibba) diets (LL), while the other sub-group was changed to a standard diet (LS). Bird fed at levels above 150 g Lemna gibba/kg had decreased consumption and weight gain. These birds when changed to a standard diet tended to have increased weight gain compared with chickens continuously fed standard rations. LS birds had significantly higher weight gains and feed consumption and lower feed conversion than LL birds. In contrast to older birds, chicks fed on Lemna gibba at high concentrations showed growth retardation. When changed back to a standard diet they demonstrated normal or compensatory growth.

Flaxseed oil is rich in α-linolenic acid (ALA), which is the metabolic precursor of EPA and DHA. The present study investigated the effect of flaxseed oil supplementation on lipopolysaccharide (LPS)-induced muscle atrophy and carbohydrate oxidation impairment in a piglet model. Twenty-four weaned pigs were used in a 2 × 2 factorial experiment including dietary treatment (5 % maize oil v. 5 % flaxseed oil) and LPS challenge (saline v. LPS). On day 21 of treatment, the pigs were injected intraperitoneally with 100 μg/kg body weight LPS or sterile saline. At 4 h after injection, blood, gastrocnemius muscle and longissimus dorsi muscle were collected. Flaxseed oil supplementation increased ALA, EPA, total n-3 PUFA contents, protein:DNA ratio and pyruvate dehydrogenase complex quantity in muscles (P < 0·05). In addition, flaxseed oil reduced mRNA expression of toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) 2 and their downstream signalling molecules in muscles and decreased plasma concentrations of TNF-α, IL-6 and IL-8, and mRNA expression of TNF-α, IL-1β and IL-6 (P < 0·05). Moreover, flaxseed oil inclusion increased the ratios of phosphorylated protein kinase B (Akt) 1:total Akt1 and phosphorylated Forkhead box O (FOXO) 1:total FOXO1 and reduced mRNA expression of FOXO1, muscle RING finger (MuRF) 1 and pyruvate dehydrogenase kinase 4 in muscles (P < 0·05). These results suggest that flaxseed oil might have a positive effect on alleviating muscle protein loss and carbohydrates oxidation impairment induced by LPS challenge through regulation of the TLR4/NOD and Akt/FOXO signalling pathways.

Nine ‘large-eating’ (approximately 12 MJ/d) and nine ‘small-eating’ (approximately 5.3 MJ/d) women were selected from the population on the basis of diet and activity diaries. At rest and in the post-absorptive state the rate of oxygen consumption (Vo2)/kg fat-free mass (FFM) and rate of carbon dioxide production (Vco2)/kg FFM were 9–17% higher (P < 0.05) in the ‘large-eaters’ than in the ‘small-eaters’. As energy expenditure was increased by walking at 2.4, 3.9 and 5.4 km/h the differences between the two experimental groups for both Vo2/kg FFM and Vco2/kg FFM were decreased to negligible values, but energy expended on a body-weight basis (MJ/kg per min) remained significantly higher (5–10%) in ‘large-eaters’. Oral temperature was also consistently higher (up to 0.5°) in this group both at rest and during sitting, standing and walking activities. Although the average thermic effect of a standardized liquid meal tended to be higher (27%; not significant) in the ‘small-eaters’, the other results demonstrate that the ‘large-eating’ females had a markedly higher rate of energy expenditure at rest and during light physical activities.

The scientific literature contains evidence suggesting that women who have been treated for breast cancer may, as a result of their diagnosis, increase their phyto-oestrogen (PE) intake. In the present paper, we describe the creation of a dietary analysis database (based on Dietplan6) for the determination of dietary intakes of specific PE (daidzein, genistein, glycitein, formononetin, biochanin A, coumestrol, matairesinol and secoisolariciresinol), in a group of women previously diagnosed and treated for postmenopausal breast cancer. The design of the database, data evaluation criteria, literature data entry for 551 foods and primary analysis by LC–MS/MS of an additional thirty-four foods for which there were no published data are described. The dietary intake of 316 women previously treated for postmenopausal breast cancer informed the identification of potential food and beverage sources of PE and the bespoke dietary analysis database was created to, ultimately, quantify their PE intake. In order that PE exposure could be comprehensively described, fifty-four of the 316 subjects completed a 24 h urine collection, and their urinary excretion results allowed for the description of exposure to include those identified as ‘equol producers’.

Dietary protein has been shown to increase urinary Ca excretion in randomised controlled trials, and diets high in protein may have detrimental effects on bone health; however, studies examining the relationship between dietary protein and bone health have conflicting results. In the present study, we examined the relationship between dietary protein (total, animal and vegetable protein) and lumbar spine trabecular volumetric bone mineral density (vBMD) among participants enrolled in the Multi-Ethnic Study of Atherosclerosis (n 1658). Protein intake was assessed using a FFQ obtained at baseline examination (2000–2). Lumbar spine vBMD was measured using quantitative computed tomography (2002–5), on average 3 years later. Multivariable linear and robust regression techniques were used to examine the associations between dietary protein and vBMD. Sex and race/ethnicity jointly modified the association of dietary protein with vBMD (P for interaction = 0·03). Among white women, higher vegetable protein intake was associated with higher vBMD (P for trend = 0·03), after adjustment for age, BMI, physical activity, alcohol consumption, current smoking, educational level, hormone therapy use, menopause and additional dietary factors. There were no consistently significant associations for total and animal protein intakes among white women or other sex and racial/ethnic groups. In conclusion, data from the present large, multi-ethnic, population-based study suggest that a higher level of protein intake, when substituted for fat, is not associated with poor bone health. Differences in the relationship between protein source and race/ethnicity of study populations may in part explain the inconsistent findings reported previously.

A high Ca intake has been recommended for osteoporosis prevention; however, little research has examined the relationship between dietary Ca and bone health in men. We examined associations between dietary Ca intake, bone mineral density (BMD) and change in BMD at the total body, hip and spine over 2 years in a cohort of men (mean age 57 years, BMI 26 kg/m2) from a trial. Data from the total cohort (n 323) were used in the analysis of Ca intake and BMD at baseline, and data from the placebo group (n 99) were used in the longitudinal analysis of Ca intake and change in BMD. Parathyroid hormone (PTH) and the markers of bone turnover serum total alkaline phosphatase activity, serum C-telopeptide and serum procollagen type-1 N-terminal propeptide were measured in a subset of participants at baseline (n 150), and associations with dietary Ca at baseline were examined. Mean Ca intake was 870 mg/d. Baseline BMD was not related to dietary Ca intake at any site, before or after adjustment for covariables. Similarly, bone loss over 2 years was not related to Ca intake at any site, before or after adjustment. Dietary Ca intake was inversely correlated with PTH at baseline (r −0·19, P=0·02), but was not associated with the markers of bone turnover. BMD and rates of bone loss were unrelated to Ca intake in these men. This suggests that strategies to increase Ca intake are unlikely to impact on the prevalence of and morbidity from male osteoporosis.

Cu has long been known to influence immune responses. An in vitro model system was established in which human myeloid(HL-60), B-lymphoid (Raji) and T-lymphoid (Molt-3) cell lines could be grown in culture media of varying Cu levels. Initially Cu was removed from the medium by dialysisof fetal calf serum against a metal-ion chelator, minor depletion of other trace metals being obviated by repletion with appropriate metal salts. The growth rate of HL-60 was significantly (P<0·05) inhibited by 72 h Cu depletion. Molt-3 cells required a longer period, up to 144 h, in Cudepleted medium before growth was impaired. Raji-cell growth was not affected. These results confirmed clinical observations that T-cell functions were more sensitive to Cu deprivation than B cells. Analysis of intracellular metal levels in Molt-3 cells showed that Cu levels had been significantly lowered (P <0·05) although Ca2+ levels were raised. Intracellular activity of the antioxidant enzyme superoxide dismutase (EC 1. 15. 1. 1) was significantly impaired (P<0·05) in Molt-3 cells grown in Cudepleted medium. Activity of the mitochondria1 enzyme cytochrome c oxidase (EC 1. 9. 3. 1) was also significantly impaired (P <0·05) by Cu depletion. Each of these findings indicates an increase in the potential for cellular damage by reduced antioxidant activity, impairment of normal mitochondrial activity and excessive Ca2+influx. A major consequence of the type of damage occurring under these circumstances is membrane disruption. This was confirmed by scanning electron microscopy of Molt-3 cells grown under varying Cu levels.

Sleep hygiene recommendations discourage eating before bedtime; however, the impact of mealtime on sleep has been inconsistent. We examined gender-stratified associations between eating or drinking <1, <2 and <3 h before bedtime, sleep duration and wake after sleep onset (WASO >30 min). This study utilised 2003–2018 data from the American Time Use Survey, a nationally representative sample of USA residents aged ≥15 years. Participants recorded weekday/weekend activities during a 24-h period. Age-specific sleep duration and WASO were estimated categorically and continuously. Eating or drinking were identified from all activities recorded <1, <2 and <3 h before bedtime. Mean ± se sleep duration was 8·0 ± 0·006 h, and 6% of participants ate or drank <1 h prior to weekdays bedtime. Overall, eating or drinking <1 h prior to bedtime was associated with longer weekdays sleep duration. Women and men who ate or drank <1 h before bedtime, v. those who did not, had 35 min (95% CI (30,39)) and 25 min (95 % CI (21,29)) longer sleep duration, respectively, as well as increased odds of WASO; women (OR=2·03, 95% CI (1·66,2·49)) and men (OR=2·64, 95% CI (2·08,3·36)). As the interval of eating or drinking prior to bedtime expanded, odds of short and long sleep durations and WASO decreased. This population-based data linked eating or drinking <1 h before bedtime to longer sleep duration, but increased WASO. Eating or drinking further from bedtime lowers the odds of short and long sleep duration and WASO. Causal pathways are difficult to discern, though inefficient sleep after late-night eating could increase WASO and trigger compensatory increases in sleep duration.

In goats, the combination of dietary N and Ca reduction caused hypocalcaemia and further changes in Ca homeostasis. The aim of the present study was to characterise the effects of dietary N reduction under normocalcaemia on mineral and bone metabolism in young goats. Young male goats of the Saanen breed were fed a diet reduced in N (8 %) for about 7 weeks (ten animals per group) and were compared with goats fed with an adequate N (14 %) diet. When N intake was reduced in young goats, plasma urea concentrations as well as renal elimination of urea were reduced. This was inversely related to creatinine in plasma and urine, which increased during a dietary N reduction as a function of reduced renal activity to save urea during N scarcity. During this decrease in renal function, associated with declined insulin-like growth factor 1 concentrations, a reduction in calcidiol and calcitriol concentrations could be observed. Meanwhile, carboxyterminal cross-linked telopeptide of type I collagen values and activity of total alkaline phosphatase were both elevated, indicating some bone remodelling processes taking place during a reduced N diet in young goats. The concentrations of inorganic phosphate (Pi) and total Ca were changed in several body fluids, indicating that Pi and Ca homeostasis was perturbed in goats fed a reduced N diet. Therefore, more research is needed to find the balance between reduction of environmental N pollution by reducing dietary N in ruminant feeding and maintaining the animal's health.

Chickens were fed on diets containing either 12.8 MJ, 150 g crude protein (nitrogen x 6.25)/kg or 12.8 MJ, 200 g crude protein/kg to determine differences in metabolism. The diet containing 12.8 MJ, 150 g crude protein/kg contained either 8 or 12 g lysine/kg. Treatment variables examined in vitro were lipogenesis, glucose production and hepatic enzyme activities to compare metabolism in chicks fed on a low-protein, lysine-supplemented diet and a diet formulated to contain the required amount of lysine from intact protein. Growth was similar in chicks fed on diets containing either 12.8 MJ, 154 g crude protein with 12 g lysine/kg or 12.8 MJ, 200 g crude protein/kg. Net glucose production was greater (p < 0.05) in liver explants from chickens fed on diets containing either 12.8 MJ, 154 g crude protein with 12 g lysine/kg or 12.8 MJ, 200 g crude protein/kg than in explants from chickens fed on 12.8 MJ, 150 g crude protein with 8 g lysine/kg. Pyruvate use for glucose production was greater (p < 0.05) in chickens fed on a diet containing 12.8 MJ, 150 g crude protein with 8 g lysine/kg. The findings from the present study suggest that crystalline and ‘natural’ lysine additions to chick diets may influence metabolism differently.

Examining the relationship between glucose intolerance and dietary intake in genetically similar populations with different dietary patterns and rates of type 2 diabetes may provide important insights into the role of diet in the pathogenesis of this disease. The objective of the present study was to assess the relationship between dietary variables and dysglycaemia/type 2 diabetes among three populations of African origin. The study design consists of a cross-sectional study of men and women of African descent aged 24–74 years from Cameroon (n 1790), Jamaica (n 857) and Manchester, UK (n 258) who were not known to have diabetes. Each participant had anthropometric measurements and underwent a 2 h 75 g oral glucose tolerance test. Habitual dietary intake was estimated with quantitative FFQ, developed specifically for each country. The age-adjusted prevalence of undiagnosed type 2 diabetes in Cameroon was low (1·1 %), but it was higher in Jamaica (11·6 %) and the UK (12·6 %). Adjusted generalised linear and latent mixed models used to obtain OR indicated that each 1·0 % increment in energy from protein, total fat and saturated fats significantly increased the odds of type 2 diabetes by 9 (95 % CI 1·02, 1·16) %, 5 (95 % CI, 1·01, 1·08) % and 16 (95 % CI 1·08, 1·25) %, respectively. A 1 % increase in energy from carbohydrates and a 0·1 unit increment in the PUFA:SFA ratio were associated with significantly reduced odds of type 2 diabetes. The results show independent effects of dietary factors on hyperglycaemia in African origin populations. Whether modifying intake of specific macronutrients helps diabetes prevention needs testing in randomised trials.

1. Sulphur amino acid metabolism in livers from rats which had been fed ad lib. on a restricted diet (malnourished) or a Zn-deficient diet was investigated. Perfusion of normal livers with different amounts of L-methionine revealed that homocysteine was recycled four to five times before being eliminated via the transsulphuration pathway.

2. From the perfusion experiments, we found no evidence that any of the enzymes involved in recycling homocysteine back to methionine (methylation pathway) were adversely effected by Zn deficiency or malnutrition.

3. The intracellular concentration of cystathionine and S-adenosylmethionine increased in all livers in response to increased concentrations of L-methionine (L-Met) in the perfusate.

4. The intracellular concentration of S-adenosylhomocysteine remained the same in all livers regardless of the concentration of perfusate methionine.

5. Although homocysteine did not accumulate in the cell, it was excreted into the perfusate. The amount of homocysteine in the perfusate of livers from Zn-deficient rats was higher than either ad lib. or pair-fed rats.

6. The breakdown of homocysteine, via the transsulphuration pathway, was augmented by Zn deficiency. This was apparent from the greater amount of α-ketobutyrate excreted by livers from Zn-deficient rats compared with pair-fed or ad lib.-fed controls.

7. The increase in metabolism of L-Met, via the transsulphuration pathway, in the livers from Zn-deficient rats appears to reflect the lack of demand for this compound in protein synthesis and methylation reactions (Wallwork & Duerre, 1985).

Fluctuations in Zn metabolism throughout gestation and lactation might affect Zn requirements. However, scientific data on Zn requirements for breeding sows are limited. The objective of the present study was to assess the Zn status of primiparous and multiparous sows using different Zn status biomarkers, to identify periods of critical Zn status throughout the reproductive cycle at different parities. Blood samples were taken after overnight fasting before feeding in the morning from five primiparous and ten multiparous sows at fixed time intervals during gestation (days − 5, 0 (insemination), 21, 42, 63 and 84), around parturition (days 108, 112, 115 (parturition) and 118) and during lactation (days 122, 129 and 143 (weaning)). At parturition, blood samples were collected from two randomly selected piglets per sow before colostrum intake. Plasma was analysed for Zn and Cu contents, whereas serum was analysed for alkaline phosphatase, metallothionein and albumin concentrations. Independently of parity, all biomarkers fluctuated differently during gestation and lactation (P< 0·050). This reflects their different roles in Zn metabolism, and suggests that the choice of a Zn status biomarker necessitates careful consideration. Low average plasma Zn concentration at the end of gestation and throughout lactation seem to be replenished towards weaning.