Body composition was measured in nine healthy, normal-weight, weight-stable subjects in three different research centres. In each centre the usual procedures for the measurements were followed. It revealed that the measurement procedures in the three centres were comparable. Body composition was measured in each centre between 09.00 and 13.00 hours after a light breakfast by densitometry (underwater weighing) and bio-electrical impedance. A single, total-body-water determination by D2O dilution was used as a reference value. Body fat determined by densitometry was significantly lower in one centre, which, however, could be completely explained by a lower body weight, probably due to water loss (the subjects refrained for a longer time from food and drinks before the measurements in that centre) and, thus, by violation of the assumptions of Siri's (1961) formula. Also, body impedance was slightly higher in that centre, indicating a lower amount of body water. Mean body fat from densitometry was also slightly lower in that centre compared with body fat determined by D2O dilution. Individual differences between body fat from densitometry and from total body water were relatively large, up to 7% body fat. The relationship between fat-free mass from densitometry and bio-electrical impedance was not different between the centres. It is concluded that differences in the relationship between body composition and bio-electrical impedance, as reported in the literature, may be due to differences in standardization procedures and/or differences in reference population.

Knowledge about changes in body composition during gestation is of interest when estimating energy requirements during pregnancy, and relevant since reproduction is often surprisingly well maintained in malnourished females. Due to difficulties in conducting such studies in humans, studies in rats are of interest. Therefore, maternal retention of fat and fat-free weight was estimated in rats during the first 2 weeks of gestation and during a corresponding time period in virgin controls. Groups fed ad lib. or 70 % of ad lib. intake during the 4 weeks preceding conception and during gestation were studied. Retention was estimated by comparing pregnant and virgin rats with rats killed at the time of conception. Body fat was analysed chemically and fat-free weight was body weight minus body fat. Each rat was divided into twelve to fourteen parts and the fat content of each part was analysed. Pregnant ad lib.-fed rats retained more fat and fat-free weight than did virgin ad lib.-fed controls. In the energy-restricted group the pregnant rats retained more fat-free weight while virgin rats retained slightly more fat than did pregnant rats. The difference between pregnant and virgin rats with respect to the amount of fat in the different body parts was small in both feeding groups. Thus, the statement that fat stored at specific sites in the maternal body represents an important source of energy for use during lactation was not supported. The findings suggest that pregnancy stimulates growth of the maternal body and that chronic moderate energy restriction curtails this growth.

To investigate changes in the thermic effect of a meal (TEM) during pregnancy, metabolic rate was measured in the fasting state and during the first 180 min after consumption of a standardized test meal in twenty-seven women before, and in each trimester of pregnancy. Resting metabolic rate (RMR) showed a steady increase over pregnancy: values in weeks 24 and 35 of pregnancy were significantly higher than the prepregnancy baseline (Tukey's studentized range test). The pattern of changes of postprandial metabolic rate (PPMR) was similar to that of RMR. Consequently TEM, calculated as PPMR minus RMR, did not change over pregnancy; mean TEM values (kJ/180 min) before and in weeks 13, 24 and 35 of pregnancy were 117 3 (sd 19.4), 116.4 (sd 23.7), 111.6 (sd 24.4) and 111.5 (sd 26.7) respectively. We consider changes in TEM of less than 15% to be of little importance physiologically. If true changes in TEM over pregnancy are 15 % or more we would have had a 90 % chance of observing significant changes in TEM in the present study, given the number of subjects and the methods used. Therefore, we conclude that no substantial reduction in TEM occurs during pregnancy.

The ileal digestibility of tryptophan for growing pigs was determined for cottonseed, meat-and-bone and soya-bean meals. Tryptophan in the food and digesta was measured by two analytical procedures (NaOH hydrolysis and colorimetric estimation (method 1) and LiOH hydrolysis and HPLC determination (method 2)). The results were respectively: cottonseed meal 0.46, 0.81; meat-and-bone meal 0.55, 0.65; soya-bean meal 0.74, 0.90. In the first experiment the values for method 1 were shown to be inapplicable to pigs. In a second experiment three tryptophan-deficient diets (005 g ileal digestible tryptophan/MJ digestible energy (DE)) were formulated using values from method 2 for cottonseed meal, meat-and-bone meal plus L-tryptophan and soya-bean meal respectively as the only sources of tryptophan in the diets. This experiment was terminated after 28 d as overall growth performance of the pigs was very low. A third experiment was conducted in a similar manner to Expt 2 except that the diets were formulated to 0.065g ileal digestible tryptophan/MJ DE and growth responses and tryptophan retention were assessed over the 20–45 kg growth phase. Growth rates (g.d) of the pigs given the three diets were significantly different (P < 0.01): cottonseed meal 393, meat-and-bone meal plus L-tryptophan 531, soya-bean meal 437 (SED 39.0). Tryptophan retention (as a proportion of ileal digestible tryptophan intake) was significantly different (P < 0.05): cottonseed meal 0.51, meat-and-bone meal plus L-tryptophan 0.49, soya-bean meal 0.41. These results indicate (1) that the colorimetric technique for assessing tryptophan was inapplicable and (2) that ileal digestible values for tryptophan were not suitable for formulating diets containing heat-processed proteins, possibly due to absorption of some of the tryptophan in a form that was non-utilizable, and/or to underestimation of total tryptophan in the protein concentrates.

N metabolism was studied in young rats fed on lipid-rich, isonitrogenous, purified liquid diets, a convenient and easy technique for inducing voluntary overfeeding of energy and lipids under controlled nutritional conditions. Overfed rats showed a marked N retention at the expense of a reduced production of urea. The capacities of isolated hepatocytes to synthesize urea and glucose from added precursors were greatly diminished. The activities of the urea cycle enzymes and several enzymes involved in the availability of NH3, for this pathway were concomitantly reduced in overfed animals. Therefore, our results showed an improved N metabolism in overfed rats promoted by the overfeeding of lipids that could be due to an enhanced biosynthetic utilization and a reduced catabolism of amino acids. In addition, the versatile and accurate technique for inducing overfeeding in young rats used in the present study could have many advantages for nutritional studies.

The present study examines the effects of dietary saturated (hydrogenated coconut oil) and polyunsaturated (salmon oil) fats on the composition and metabolism of lipoproteins in growing rats fed on protein-deficient diets. Four groups of rats were fed on the following diets for 28 d: 200 g casein+50 g coconut oil (COC)/kg, 20 g casein+50 g coconut oil (COd)/kg, 200 g casein + 50 g salmon oil (SAC)/kg, 20 g casein+50 g salmon oil (SAd)/kg. Both protein-deficient groups exhibited low concentrations of protein and triacylglycerol (in serum, very-low-density lipoprotein (VLDL), low-density lipoprotein-high-density lipoprotein, (LDL-HDL1) and HDL2-3), of cholesterol (in LDL-HDL1) and of phospholipids (in VLDL). Furthermore, serum and VLDL cholesterol concentrations were also reduced in the SAd group. Compared with rats given 200 g casein/kg diets, those fed on low-protein diets presented lower linoleic and arachidonic acid levels, in serum phospholipids and a dramatic decrease in the polyunsaturated: saturated fatty acid value. Relative amounts of linoleic and arachidonic acids in phospholipids of VLDL and HDL2-3 were also lowered in the Cod group but not in the SAd group. However, proportions of 22:5n-6 and 22:6n-3 in VLDL and HDL2-3 phospholipid fractions were enhanced in the Cod and SAd groups respectively. The most affected apolipoproteins (apo) were apo B100 and apo B48 in rats fed on protein-deficient diets, apo A1 and apo E in the Cod group, and apo AIV, in the SAd group. Compared with rats fed hydrogenated coconut oil diets, those fed salmon oil diets had enhanced LDL-HDL1 and HDL2-3 but lower VLDL total apolipoproteins (mainly due to a fall in apo B100, and apo B48). Arachidonic and eicosapentaenoic acids, which are impaired by protein deficiency, are the precursors of prostaglandins, thromboxanes and leukotrienes which are implicated in a number of regulatory processes. Our results demonstrate that protein malnutrition is associated with impaired metabolism of arachidonic and eicosapentaenoic acids. Protein malnutrition and essential fatty acid (EFA) deficiency are characterized by many common clinical features and the Link between the two may be an impaired production of eicosanoids, since arachidonic and eicosapentaenoic acids are the precursors of these important metabolic regulators. Because of the apparent involvement of EFA deficiency in the aetiology of protein malnutrition, it may he prudent to include adequate amounts of EFA in diets of infants suffering from kwashiorkor.

Broiler chickens were fed on a control diet based on maize or a diet containing sugar-beet-pulp fibre (Beeffiber) at an inclusion level of 46 g/kg. Diets were provided ad lib. or at a restricted level either once daily or three times daily. On days 13 and 20, chickens fed on the ad lib. control and sugar-beet-pulp-containing diets generally weighed more and had poorer feed conversion ratios than chickens given the restricted control and sugar-beet-pulp-containing diets respectively. Furthermore, chickens given the restricted diets once daily had greater body weights and generally improved feed conversion efficiencies compared with chickens given the restricted diets three times daily. Generally, elevated plasma Lipid concentrations were observed amongst chickens given the restricted diets once daily compared with chickens fed ad lib. as well as the restricted diets three times daily, while chickens fed on restricted diets three times daily had plasma lipid concentrations intermediate between those fed ad lib. and once daily. In a plasma triacylglycerol response study on day 22, feeding of sugar-beet-pulp-containing diets generally reduced postprandial triacylglycerol concentrations and delayed triacylglycerol response relative to chickens given the control diets either ad lib. or restricted, which may indicate gastrointestinal adaptation to feeding of a fibre-rich diet. Postprandial triacylglycerol concentrations observed for chickens receiving restricted diets were increased compared with chickens given the respective ad lib. diets, indicating adaptation of chickens to reduced feed frequency. On day 25, feeding of sugar-beet-pulp-containing diets decreased digesta dry matter content and ileal organic matter digestibility. Chickens given sugar-beet-pulp-containing diets generally had, on day 25, increased caecal short-chain fatty acid (SCFA) concentrations in comparison with chickens given the ad lib. control diet, indicating increased fermentation of dietary components. It is also noteworthy that the greatest SCFA concentrations were observed amongst chickens given the control diet once daily, suggesting enhanced caecal fermentation capacity. This may have been a consequence of increased bacterial activity and caecal hypertrophy due to infrequent feeding of a low-fibre diet.

The present study has examined the possibility that the positional distribution of fatty acids on dietary triacylglycerol (TAG) influences the postprandial response to a liquid meal in adult subjects. Postprandial TAG, non-esterified fatty acids (NEFA), ketones, glucose, insulin and gastric inhibitory polypeptide (GIP) responses were monitored in sixteen normal adult male subjects over 6 h following consumption of test meals containing dietary TAG in which palmitic acid was predominantly on the sn-1 (Control) or sn-2 positions (Betapol). Plasma total TAG, chylomicron-rich TAG and chylomicron-poor TAG concentrations were identical in response to the two test meals. The peak increase (mean (sd)) in chylomicron TAG was 0 85 (0 46) mmol/l after the Control meal and 0 85 (0 42) mmol/l after the Betapol meal. Plasma glucose, insulin, GIP, NEFA and ketone concentrations were also very similar following the two meals. It is concluded that dietary TAG containing saturated fatty acids on the sn-2 position appear in plasma at a similar level and over a similar timescale to TAG in which saturated fatty acids are predominantly located on sn-1 or sn-3 positions. The results reported in the present study demonstrate that the positional distribution of fatty acids on dietary TAG is not an important determinant of postprandial lipaemia in adult male subjects, but do not exclude the possibility that different responses may occur when these dietary TAG are given long term.

A stable isotope technique has been developed which uses 57Fe and 58Fe as labels and which enables the simultaneous measurement of Fe absorption from two test meals in infants. The method was evaluated by measuring Fe absorption from a commercial whey-adjusted infant formula in nine healthy infants aged 13–25 weeks. Each infant was fed 210 ml formula, labelled with either 57Fe or 58Fe, on four consecutive mornings, in random order. The total Fe content in each feed was 2.5 mg Fe; either as 2.5 mg 57Fe, or 0 6 mg 58Fe plus 1.9 mg Fe with normal isotopic composition. Isotopic enrichment of Fe in erythrocytes was measured by thermal ionization mass spectrometry 14 d after the last administration, and Fe absorption was calculated based on isotope ratio shifts, total circulating Fe and intake of each isotope. Geometric mean absorption for the 57Fe and 58Fe labels was 6.72 and 658% respectively, and the absorption of the two isotopes was not significantly different (Student's paired t test). By this technique, paired comparisons of Fe absorption can be obtained and systematic studies of the influence of dietary factors on Fe absorption during infancy can he conducted.

The aims of this work were to quantify the requirements of Zn for wool growth in growing male Merino lambs, and to describe the histological lesions of Zn deficiency in skin and wool follicles. Four groups of male Merino lambs (n 4) weighing 22 kg were fed ad lib. for 96 d on diets that contained 4 (basal diet), 10, 17 or 27 mg Zn/kg. Sheep in a fifth group were fed on the diet containing 27 mg Zn/kg, but were pair-fed to sheep on the 4 mg Zn/kg diet. Zn was added to the basal diet as ZnSO4 to give the respective treatment concentrations. Sheep fed on the diet containing 4 mg Zn/kg showed clinical signs of Zn deficiency and lower feed intakes and wool growth than sheep in the other groups. Their wool fibres were improperly keratinized and the wool follicles contained a higher proportion of apoptotic bodies than other groups. There was no evidence of parakeratosis and the rate of bulb-cell production was not affected. Sheep from other groups showed no clinical signs of Zn deficiency, and mean feed intakes and growth rates did not differ significantly between sheep fed on diets containing 10, 17 or 27 mg Zn/kg. However, wool growth was reduced in sheep fed on the diet containing 10 mg Zn/kg compared with those fed on diets containing 17 or 27 mg/kg. The mean concentration of Zn in the plasma at which wool growth was 90 % of maximum was 0.5 mg/l. The equivalent value for the diet was 12 mg/kg, with 95 % confidence intervals of 8 to 16 mg/kg. The results suggest that Zn deficiency reduces wool growth through a specific mechanism, perhaps involving impaired protein synthesis.

The effect of fasting for 12, 36 and 72 h was studied in twenty-nine healthy subjects (seventeen women and twelve men). Measurements were made of cardiovascular variables, metabolic rate, respiratory exchange ratio, plasma metabolites, insulin, thyroid hormones and catecholamines. During starvation there were no significant changes in blood pressure, whilst heart rate (beatslmin) increased at 36 h and remained elevated after 72 h (12 h 625 (SE 1.8), 36 h 68.0 (SE 1.9), 72 h 69 2 (SE 1.8); P< 0.001). Forearm blood flow (FBF), increased progressively from 3.32 (SE 0.20) to 6.21 (SE 0.46) m1/100 ml per min (P < 0.001). Resting metabolic rate (kJ/min) was significantly increased after 36 h of starvation (12 h 4 60 (SE 0.14), 36 h 4 88 (SE 0.13), P < 0.001), but was not significantly different from the 12 h value after 72 h (72 h 4.72 (SE 0.15) P = 0.06). The respiratory exchange ratio fell progressively from 0.80 to 076 to 0.72 (P < 0.001). Blood glucose fell, whilst plasma glycerol and β-hydroxybutyrate rose and plasma lactate did not change. Plasma insulin and free triiodothyronine fell during starvation. Plasma adrenaline and noradrenaline were unchanged at 36 h, but were significantly increased after 72 h. Both sexes showed a similar pattern of response to starvation, although absolute values of blood pressure, forearm blood flow, metabolic rate and plasma catecholamines were higher in men than women. Acute starvation produces profound cardiovascular and metabolic changes which are not explained by the accompanying hormonal changes.

Alcohol accounts for 4-6% of the average energy intake in most Western countries. Alcohol-induced hypoglycaemia is a well-known and feared complication in insulin-dependent diabetic subjects, but little attention has been paid to the impact of alcohol on carbohydrate metabolism in non-insulin-dependent diabetes. The aim of the present study was to investigate in non-insulin-dependent diabetic subjects the acute metabolic effects of a moderate amount of alcohol taken with a light meal, conditions chosen to mimic an everyday situation. The patients received 500 ml non-alcoholic beer with an alcohol content (ml/l) of 0 (treatment A) and 54 (treatment B) together with a light meal, implying identity of the contents of ingredients except for alcohol. We found similar serum glucose, insulin, free fatty acid and triacylglycerol responses irrespective of addition of a modern amount of alcohol. In conclusion, a moderate amount of alcohol can be taken with a meal without eliciting hypoglycaemia in non-insulin-dependent diabetic subjects.