Using percentage body fat (BF%) from a three-compartment (3C) model (body density from underwater weighing (UWW) and bone-mineral mass from dual-energy X-ray absorptiometry (DXA)) as a criterion, we studied the accuracy of UWW, DXA, two skinfold equations, and two bioimpedance (BIA) equations. Thirty-four women (aged 16–20 years) with BF% 13·5–31·1 volunteered. UWW underestimated BF% by −0·5 BF% (95 % CI: −1·0; −0·02), whereas DXA overestimated it by 7·3 BF% (95% CI5.8;8·8). Skinfolds underestimated and BIA overpredicted BF%. The differences between 3C and UWW, skinfolds (Durnin & Womersley, 1974) and BIA (Deurenberg et al. 1990) were dependent (range of r values: −0.63 to −0.79; P < 0·0001) on BF%, causing an overestimation of lean subjects' (UWW, BIA) or an underestimation of normal-weight subjects' (UWW, skinfolds) BF%. The 3C model and UWW gave comparable body-composition results for healthy young women with BF% of approximately 20–25. Based on a significant mean difference from the 3C model, and a large standard error of the estimate, we do not regard DXA as superior to skinfolds or BIA to assess BF%.

Dual-energy X-ray absorptiometry (DXA) is a novel, non-invasive technique for the measurement of gross body composition in small animals. In the present study the absolute accuracy of the Hologic QDR-lOOOW scanner was assessed by comparison with direct analysis in twelve rats with a range of body fat and bone mineral content (BMC) values. Fat masses measured by DXA and petroleumether extraction were significantly different (P<0·0023). The DXA technique consistently overestimated fat mass by approximately one third of the measured fatcontent. BMC derived from the measurement of Ca in asb gave a mean of 8·26 (range 1·57–15·71)g. BMC measured by DXA was not significantly different for the group as a whole. However, there was a trend for DXA to overestimate BMC in animals with low BMC and underestimate in those with higher BMC, compared with direct analysis, such that the 95% limits of agreement for the two techniques were +2·73 to −2·58g. These results suggest that the present small-animal software developed for use with currently available Hologic machines does not give an accurate measure of gross body composition compared with the results from classical direct analysis.

It has been reported that loss of ovarian oestrogen after menopause or by ovariectomy causes osteoporosis. In order to elucidate the effect of dietary protein restriction on bone metabolism after ovariectomy, we fed ovariectomized young female rats on a casein-based diet (50g/kg diet (protein restriction) or 200g/kg diet (control)) for 3 weeks and measured mRNA contents of bone-matrix proteins such as osteocalcin, osteopontin and α1 type I collagen, insulin-like growth factors (IGF) and IGF-binding proteins (IGFBP) in femur. Ovariectomy decreased the weight of fat-free dry bone and increased urinary excretion of pyridinium cross-links significantly, although dietary protein restriction did not affect them. Neither ovariectomy nor protein restriction affected the content of mRNA of osteopontin and osteocalcin; however, ovariectomy increased and protein restriction extensively decreased the α1 type I collagen mRNA content in bone tissues. Ovariectomy increased IGF-I mRNA only in the rats fed on the control diet. Conversely, protein rest riction increased and ovariectomy decreased the IGF-II mRNA content in femur. Furthermore, the contents of IGFBP-2, IGFBP-4 and IGFBP-5 mRNA increased, but the content of IGFBP-3 mRNA decreased in femur of the rats fed on the protein-restricted diet. In particular, ovariectomy decreased the IGFBP-2 mRNA content in the protein-restricted rats and the IGFBP-6 mRNA content in the rats fed on the control diet. These results clearly show that the mRNA for some of the proteins which have been shown to be involved in bone formation are regulated by both quantity of dietary proteins and ovarian hormones.

Threonine oxidation to glycine was investigated in vivo in twelve growing pigs (27·4 kg live weight) fed on one of the following three diets with graded levels of threonine supply: a low-threonine diet (LT), a control well-balanced diet (C) or a high-threonine diet (HT), during 10h constant infusion of L-[1-13C]threonine and [2-3H]glycine in the cranial vena cava and [l-14C]glycine in the portal vein.13C-threonine and glycine enrichments and [3H]glycine and [14C]glycine specific radioactivities (SR) were determined at plateau in peripheral venous plasma, liver and pancreas. Glycine praduction rates calculated from plasma [2-3H]glycine or [1-14C]glycine SR gave similar values suggesting that [l-14C]glycine SR could be used in order to estimate whole-body glycine flux. The high pancreas [1-13C]glycine enrichment provided evidence that the pancreas may be, with the liver, a major site of threonine oxidation to glycine. Moreover, the present findings suggest that threonine transport into the Liver could be the limiting step of threonine oxidation in this tissue when dietary threonine supply is low. Total threonine oxidation to glycine, calculated from plasma values of enrichment and specific radioactivity, was low and constant when the estimated absorbed threonine was lower than 4 g/d and increased for higher amounts of absorbed threonine.

Male 1-d-old broilers (n 920) were given 0, 200, 400, 600, 800, 1000 and 1200 U microbial pbytase/kg diet in combination with 2·0, 2·7 or 3·4 g non-phytate P (nP)/kg or 4·0, 5·1 or 5·8 g total P (tP)/kg in a 21 d trial to assess the effectiveness of phytase in a maize–soyabean-meal diet. In addition to the above twenty-one diets, a positive control P diet supplied 4·5 g nP/kg, 6·9 g tP/kg and 10 g Ca/kg. The basal diet contained 230g crude protein/kg, 8·8 g Ca/kg, 4·4 g tP/Fg and 2/0 g nP/kg. Defluorinated phosphate and limestone were used to supply P and Ca. A Ca:tP ratio of 2:l was maintained except in the positive control diet which had a ratio of 1·45: 1. Phytase additions linearly increased (P < 0·01) body-weight (SW) gain, feed intake, toe ash percentage, and apparent retention (% of intake) or total amount (g/bird) of retained Ca and P, and linearly decreased (P < 0·01) P excretion (g/kg of DM intake) at each level of nP with the magnitude of the response inversely related to the level of nP. Above-normal mortality was only observed in the group receiving 2·0 g nP/kg diet without phytase. Adding nP linearly increased (P < 0·01) BW gain, feed intake, toe ash percentage, Ca retention, total amount (g/bird) of P retained, and P excretion, and iinearly decreased (P < 0·01) apparent retention (%) of P. Derived linear and non-linear equations for BW gain and toe ash percentage at the two lower nP levels, 2·0 and 2·7 g/kg, were used to calculate P equivalency value of microbial phytase. The results show that 939 U microbial phytase is equivalent to 1 g P from defluorinated phosphate in broilers fed on maize–soyabean-meal diets. The amount of P released per 100 U phytase decreased as the total amount of phytase increased.

We analysed the respective influences of age and lysine deficiency on skeletal muscle and liver protein turnover. Growing male broilers were fed ad libirum on isoenergetic diets containing 2OO g crude protein/kg which varied in their lysine content (7·7 or 10·1 g/kg). Fractional rates of protein synthesis (FSR) were measured in vivo in the liver and the pectoralis major muscle of 2-, 3- and 4-week-old chickens (flooding dose of l-[143H]phenylalanine). Fractional rates of proteolysis (FBR) were estimated for the same tissues as the difference between synthesis and growth. Over the 2-week period liver FSR and FBR were unchanged, whereas muscle FSR decreased with age. This developmental decline was related to the lower capacity for protein synthesis (Cs) without any modifications of the translational efficiency. Whatever the age, lysine deficiency resulted in significant decreases in body weight, tissue protein content and tissue protein deposition, apparently because of reduced amounts of proteins synthesized. We recorded a difference in the response of the two tissues to lysine deficiency, the pectoralis major being more sensitive than the liver. When comparing birds of the same age, liver FSR and FBR were not modified by the diet, where as muscle FSR, Cs and FBR were higher in chicks fed on a lysinc-deficient diet than in the controls. Conversely, when chicks of similar weights were compared, the main effect of the dietary deficiency was an increase in muscle FBR. The results suggest that lysine deficiency not only delayed chick development so that protein turnover was affected, but also induced greater changes in metabolism. Thus, the principal mechanism whereby muscle mass decreased appeared to be a change in FBR.

In three experiments broiler chickens were inoculated with sporulated Eimeria acervulina oocysts at 18 d of age. Feed intake, body-weight gain, brush-border enzyme activities, fat digestion, protein digestion and protein retention were measured. Body-weight gain was reduced during the acute phase of the infection and increased during the recovery phase of the infection. Feed intake was decreased on day 4 and day 5 postinfection (PI) and increased from day 7 to day 11 PI. Maltase (EC 3.2.1.20) and sucrase (ECEC 3.2.1.48) activities were decreased on day 5 PI in all intestinal segments. In Expts 2 and 3, however, maltase activity was increased in the ileum. Fat digestion was decreased from day 2 to day 11 PI. N digestion and retention were decreased from day 2 to day 11 PI.

Previously an experimental infection model was developed in which broiler chickens were inoculated with sporulated Eimeria acervufina oocysts at an age of 18 d. The infection resulted in adverse performance results and reduced nutrient digestion. In two new experiments with the infection model effects of diet adjustments on fat digestion were investigated. In the first experiment addition of 0·4 g cholic acid/kg to a diet rich in animal fat resulted in increased fat digestion during the infection. In the second experiment replacing animal fat by coconut oil resulted in improved fat digestion during the coccidiosis infection. However, replacement of animal fat by soyabean oil did not improve fat digestion.

A colorimetric method was used on water-soluble much extracted from mucosal scrapings and contents of the caecum and the colon of five germ-free (GF) rats and five heteroxenic (HE) rats harbouring a hnmao flora (GF rats d a t e d with a human flora). These rats were fed on a diet containing either 100 g sucrose/kg or 100 g inulin/kg. Histological stains, periodic acid–Schiff, alcian blue pH 2·5 and alcian blue pH 0·5 were used to discriminate between neutral, acidic and acidic sulphated mucins respectively. Spectrocolorimetric assays led to a calculated absorbance value for 1 mg of the initial much extract. Each much type was compared between treatments. The caecal contents of GF rats contained more acidic mucin than sulphomucin, which was present in the same proportion as neutral mucin. Their colonic contents contained more acidic mucins than sulphomucin, which in turn was more abundant than neutral mucin. Their caecal mucosa mucin distribution differed from that of the contents: very little acidic much was present and neutral and dphomucin proportions were of the same order of magnitude. Inulin increased the amount of neutral much in the caecal contents and of sulphated mucios in the colonic contents and increased the amounts of neutral and acidic mucins in the caecal mucwa. Mucin distribution in the HE rats was very different from that in the GF rats: the caecal contents contained a high proportion of acidic much and very little sulphomucin. The same distribution of mucins was observed in the colonic contents. The caecal mucaw contained less acidic much and more sulphomucin than the caecal contents. Inulin decreased acidic mucins and increased sulphated much in the caecal contents and increased neutral and sulphated mucins in the colonic contents. Inulin increased sulphomucin in the caecal m u m and decreased acidic much in the caecal and colonic mucosas. The very low amount of mucin that was recovered in the colonic mucosa suggests that, in the presence of the bacterial flora and associated with inulin in the diet, much was extensively released from the mucosa to the colonic lumen. This might be related to the bacterial metabolites produced

True fractional Ca absorption from six foods was measured in twelve normal healthy women, aged 20–29 years. The tested foods were commercially available fresh cheese, fresh cheese prepared by new technology and rich in Ca, similar cheese with added Fe, enteral food, mineral water alone and combined with a spaghetti meal. The aim of the study was to investigate: (1) Ca absorption from a new Ca-rich fresh cheese and to compare it with that from the traditional commercial type of fresh cheese; (2) the effect of Fe enrichment of the new cheese on Ca absorption; (3) Ca absorption from the mineral water and the enteral product and to compare it with that from the dairy products; (4) the effect of a meal combined with the mineral water on Ca absorption. All test foods were consumed by all subjects according to a design with two Latin squares. Each treatment of 2 d was followed by a wash-out period of 2 weeks. Ca absorption was measured using a double stable-isotope (44Ca and 48Ca) extrinsic labelling technique. Mean fractional Ca absorption from the new fresh cheese was not significantly different from that from the traditional type (37·7 (SD 10·2)% v. 42·2 (SD 11·6)%). The addition of Fe to the new cheese did not significantly influence Ca absorption. Ca-absorption values from the mineral water (37·0 (SD 98) %) and from the enterd product (42·6 (SD 11·4)%) were not significantly different from those from the dairy products (37·7–42·2%, SD 10·2–11·6%). The co-ingestion of a spaghetti meal with the mineral water significantly enhanced Ca absorption from 37 (SD 9·8)% to 46·1 (SD 11·7)%. It is concluded that a new process leading to a fresh cheese with a higher Ca concentration does not alter Ca bioavailability compared with the standard technology and for a constant Ca supply. Thus this new fresh cheese would probably provide more Ca than the standard one. The fractional Ca-absorption values for mineral water and the enteral product indicate that these products can make an interesting contribution to Ca supply for populations with a low Ca intake and patients with specilic diseases respectively.

Several studies have failed to demonstrate an association between Fe status and intake of dietary Fe. However, in the long term, it Seems logical to presume that body Fe reserves are, fundamentally, dependent on the intake of bioavailpble dietary Fe. This discrepancy may depend on several factors(1)interindividual variation in biological availability of dietary Fe (differences in intestinal absorption),(2) interactions between dietary Fe and absorption enhancers and inbibitors, (3) variatiom in physiological (menstruation, childbirth) or unphysiological (blood donation) Fe losses, (4) the failure to adjust dietary intake data for Fe supplements, (5) uncertain food composition data (discrepancies between calculated and chemically measured Fe content inthe diet), and (6) diet reporting error (reported intake of dietary Fe may deviate considerably from the true intake). The present study examined associations between dietary intake of Fe (assessed by diet history interview) and Fe status (assessed by femtin status) among 167 Danish women aged 35–65 years, who were not blood donors, by taking into account diet reporting error (assessed from p-amino benzoic acid-validated urinary N), physiological blood losses (menstruation, Childbirth, abortions), and Fe supplementation. Our results indicate that the lack of a general association between Fe status and dietary Fe intake may, in part, be caused by selective dietreporting error.

The purpose of the present study was to determine the effects of feeding nutritionally adequate and increased levels of vitamin A (retinyl acetate at 1·4, 34·4, and 206·4 mg/kg diet) in combination with adequate or increased Zn (12 and 240 mg/kg) and Cu (5 and 50mg/kg) on serum and tissue concentrations of retinol and retinyl palmitate and on indices of Cu and Zn status in female Sprague–Dawley rats, and to measure interactive effects of such nutrient imbalances. Rats fed on diets containing 34·4 and 206·4 mg vitamin A/kg had higher feed intakes and relative Liver weights than those fed on diets containing 1.4mg vitamin A/kg. An interaction between dietary Cu and Zn and an independent effect of vitamin A affected serum ceruloplasmin oxidase (EC 1.16.3.1) activity. Rats fed on high Zn, adequate-Cu diets (240 and 5 mg Zn and Cu/kg respectively) had lower serum ceruloplasmin oxidase levels than rats fed on adequate-Zn, adequate-Cu diets (12 and 5 mg Zn and Cu/kg respectively). This effect was not observed in rats fed on high-Zn, high-Cu diets (240 and 50mg Zn and Cu/kg respectively). Alterations in dietary levels of Cu and vitamin A independently affected haemoglobin levels. Serum cholesterol concentration was affected by interactions between Zn and vitamin A and Cu and vitamin A. Levels of retinol and retinyl palmitate in liver and kidney were significantly higher in rats fed on diets with increased dietary vitamin A than in those fed on diets with adequate vitamin A. Three-way interactions among Cu, Zn, and vitamin A affected levels of retinol in serum and liver. Two-way interactions between Cu and vitamin A affected liver retinyl palmitate and the sum of liver retinol + retinyl palmitate. An independent effect of dietary Zn on these variables was also observed. Interactions between Cu and vitamin A affected levels of Cu in liver and kidney, while Fe and Zn in kidney were affected by interactions between Cu and Zn. This study demonstrates that differing interactions among variables of vitamin A metabolism and mineral status occur with higher dietary levels of vitamin A, Zn and Cu in the rat

To clarify the relationship between intracellular concentrations of methylmalonic acid and metabolic and growth inhibition in vitamin B12-deficient rats, hepatic methylmalonic acidlevels were assayed and inhibition of glucose and glutamic acid metabolism by methylmalonic acid was studied in isolated hepatocytes. Vitamin B12-deficient rats (14 weeks old) excreted more urinary methylmalonic acid and had lower body weights than the control rats. Hepatic methylmalonic acid levels (3·6 (SD 1·30)–5·3 (SD 0·51) µmol/g tissue; 7·9 (SD 2·90)–11·8 (SD 1·14) mM) were increased and correlated with the extent of the growth retardation during vitamin B12-deficiency. Isolated hepatocytes and mitochondria from normally fed rats were labelled with [14C(U)]glucose and [14C(U)]glutamic acid respectively, in the presence or absence of 5mM-methylmalonic acid. Although methylmalonic acid did not affect the incorporation of 14C into protein and organic acid fractions in the hepatocytes, it inhibited 14CO2 formation (an index of glucose oxidation by the Krebs cycle) by 25% and incorporation of 14C into the amino acid fractionby 30%. In the mitochondria, methylmalonic acid inhibited 14CO2, formation (indicating glutamic acid oxidation by the Krebs cycle) by 70%, but not the incorporation of 14C into the protein fraction. The incorporation of 14C into the organic acid fraction was significantly stimulated by the addition of methylmalonic acid. These results indicate that the unusual accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal glucose and glutamic acid metabolism in rat liver, probably by inhibiting the Krebs cycle.

Vegetable fats and oils are major sources of dietary vitamin E. Consequently the current trend to reduce fat consumption is accompanied by a reduction of the intake of vitamin E. In addition, the absorption of vitamin E is thought to be dependent on the hydroiysis of dietary lipids in the small intestine. It is therefore conceivable that a lower dietary fat intake also diminishes the intestinal absorption of vitamin E. The present 3-week feeding study in young male rats was designed to investigate whether different concentrations of vitamin E added to a very-low-fat product (0, 330 or 1350mg dl-α-tocopheryl acetate/kg product) were absorbed. We therefore incorporated these products into a very-low-fat meal (final fat concentration: 7 g/kg) or a low-fat meal containing 52 g fat/kg. The magnitude of vitamin E absorption from these meals was compared with that from meals containing similar amounts of vitamin E, but a high fat concentration of 190 g/kg. Apparent vitamin E absorption was defined as intake of α- tocopherol equivalents (αTE) minus faecal αTE excretion over 4 d during week 3 of the experimental period. The results of this study showed that apparent absorption of vitamin E from a very-low-fat meal varied, depending on the vitamin E concentration, from 73 to 83%. The magnitude of this vitamin E absorption was not significantly different from that from meals containing a high amount of fat. Liver vitamin E status was equal in rats fed on the very-low-fat meals compared with those fed on the high- fat meals. We conclude that, when very-low-fat or low-fat products are used as a replacement for full- fat products, addition of vitamin E to these products, as dl-α-tocopheryl acetate, might be useful in meeting the vitamin E requirements.