Using equations obtained in a previous analysis, results are computed numerically which illustrate the effects of diffusion and viscosity on faecal excretion patterns of markers in ruminants. Results are first given for plug flow, a velocity gradient produced by viscosity, and diffusion, each mechanism operating alone. Plug flow gives a period during which no marker appears in the faeces, then a sharp increase in faeces marker concentration, followed by rapid washout. A velocity gradient gives a more gradual appearance of marker in the faeces followed by a slower washout. DMusiou alone (although not realistic for ruminant marker kinetics) can give early appearance of marker followed by slow washout. Combining diffusion with a velocity gradient produced by viscosity can give a range of behaviour, depending on the effective diffusion coefficient, D'; an approximate method is used to compute these solutions. Because plug flow with no velocity gradient plus diffusion gives results similar to convective flow with a velocity gradient plus diffusion, we believe it will not be possible to determine the main mechanisms defining marker outtiow patterns from observations of marker kinetics alone, and more detailed investigations will be needed. Although estimates of quantities such as mean transit time are unaffected by detailed mechanism, the interpretations of measures such as sigmoidicity, sharpness of the faecal marker concentration v. time curve, and length and nature of the washout tail are highly dependent on mechanism.

The dietary patterns of sixty-four adolescents (thirty-seven young men and twenty-seven young women) between 15 and 17 years of age were examined by analysis of food, energy and nutrient ntakes, over a period of 5 d, including a Sunday. Adolescents were dentified for inclusion in two study groups: (1) overweight and obese subjects (O) with a BMI (kg/m2) ≥ 75th percentile, and (2) subjects of normal weight (NW) with BMI < 75th percentile. The study was designed to investigate the differences between the energy and nutrient intakes of NW and O adolescents. No differences were found in energy intake between NW and O adolescents. However, O subjects derived a greater proportion of their energy from proteins (19.8% v 16.4% for NW subjects) and fats (45.4% v. 38.7% for NW subjects), and less from carbohydrates (34.6% v. 44.6% for NW subjects). Also, O subjects consumed significantly larger amounts of cholesterol. In order to prevent obesity and avoid the disorders associated with this condition, it appears necessary not only to regulate energy intake, but also to control the composition of the diet. Given that it is during infancy that feeding habits are developed, it is important to ensure that correct habits are acquired. Special attention should be given to improving the dietary habits of overweight and obese children and adolescents.

The objective of the present study was to validate energy intake data, obtained by dietary history, in twelve elderly women aged 69–82 years. Energy and protein intakes were obtained using the dietary history method with a reference period of 30 d. Reported energy intake was compared with total energy expenditure (TEE) measured on two consecutive days in a respiration chamber. Reported protein intake was compared with mean N excretion from four 24 h urine collections. Mean reported energy intake was 7.2 (SD 1.5) MJ/d which was lower than TEE (P=0.059). Reported protein intake was 64 (SD 13) g/d and lower than estimated protein intake (P=0.053). The percentage underestimation was not related to body weight or percentage body fat. Subjects with a relatively high TEE or a relatively high estimated protein intake underestimated their energy intake to a greater extent. The discrepancy between reported energy intake and TEE was positively associated with the discrepancy between reported and estimated protein intakes. The results of this present study show an underestimation of energy intake of about 12% when using the dietary history method. Physical activity diaries completed in the chamber and during 4 d at home, as well as pedometer counts, indicated a higher level of physical activity in the free-living situation compared with the chamber situation. This suggests that the actual underestimation of energy intake may be even higher in this group of elderly women. These results have implications for the use of the dietary history method in, for example, epidemiological studies carried out in elderly subjects.

There is considerable evidence for the beneficial effects of dietary arginine, a conditionally essential amino acid that enhances anabolism and T-cell function. However, the safety and efficacy of higher doses of arginine supplementation following infection have not been investigated completely. These issues were explored therefore, in a murine model of malnutrition and infection. Severe protein malnutrition was induced by feeding mice for 6 weeks on an isoenergetic diet containing only 10 g protein/kg. Mice were then allowed to consume diets with normal amounts of protein (200 g/kg) with 50 g/kg provided as amino acid mixtures of glycine and arginine in which the arginine content ranged from 0 to 50 g/kg. During the repletion period a significant weight gain was noted in the groups fed on diets with either 10 or 20 g arginine/kg, but not in the group fed on the diet with 50 g arginine/kg, compared with the diet with 0 g arginine/kg. Mortality rates after infection with Salmonella typhimurium were not decreased by the addition of 10 or 20 g arginine/kg to the diet, and were in fact worsened by supplementation with 50 g arginine/kg. The results of the present study showed that not only are the beneficial effects of arginine supplementation after infection lost when high doses are administered, but also that these high doses become toxic. Mice fed on higher doses showed significant impairment of weight gain and an increase in mortality rates.

Chickens fed on semi-purified low (7%) or high (61%) protein-energy diets for 14 or 17 d were used for determinations of oxidative phosphorylation and specific amounts of mitochondrial protein in liver. The ADP: oxygen (ADP:O) values obtained when pyruvate + malate were used as substrates were significantly reduced in the high-protein-fed group after the 4th day compared with those for the group fed the low-protein diet, while the differences in ADP:O values between the two treatments when L-glutamate was used as substrate were found to be significant on the 14th day. At any feeding period no significant differences in ADP:O values were observed between the two groups when α-ketoglutarate, malate, or octanoate + malate were used as substrates, nor in specific amounts of mitochondrial protein in liver. The dependency of the pyruvate + malate-supported respiration rate on the temperature in the reaction medium was also determined. The results of an Arrhenius plot showed that transition temperatures, and the lower and upper energies of activation, were similar for the groups fed on low- and high-protein diets. Furthermore, no morphological changes in mitochondria were observed among chickens fed on diets with various protein levels for 14 d. From these results we concluded that the reduction of ADP: O value with pyruvate + malate or L-glutamate substrates in chickens fed on a high-protein diet was substrate-specific, and was not due to functional damage to the respiratory chain for electron flow from NAD-linked substrates to the ubiquinone pool, nor to modulation of properties of the inner mitochondrial membrane.

Diets enriched in retrograded amylose (RS3) have been shown to lower serum cholesterol concentrations in rats. The possibility was tested that this hypocholesterolaemic effect of RS3 is caused by an increase in excretion of neutral steroids and/or bile acids. Six groups of ten rats were fed on purified diets containing either 12 or 140 g RS3/kg solid ingredients with and without added cholesterol (5 g/kg). Low-RS3 diets, with and without added cholesterol, to which the bile-acid-binding resin cholestvramine (20 g/kg) was added, were used as reference. The high-RS3 diets v. the low-RS3 diets tended to reduce the increase in the total serum cholesterol concentration during the course of the experiment (P = 0 067), decreased serum triacylglycerol concentrations, raised total neutral steroids and total bile acids in caecal contents and faecal excretion of total bile acids, but lowered faecal excretion of neutral steroids. In addition, the serum concentration of total 3α-bile acids was markedly raised by the high-RS3 diets. The high-RS3 diets raised the faecal excretion of lithocholic and muricholic acids, but lowered that of hyodeoxycholic acid, and increased the caecal amounts of lithocholic, ursodeoxycholic, β-muricholic and ω-muricholic acids. Apart from the stimulation of faecal bile acids excretion, the effects of cholestvramine on bile acid metabolism differed at various points from those of RS3. Cholesterol feeding had predictable effects on cholesterol metabolism and led to greater elevating effects of RS3 on the faecal and caecal amounts of muricholic acids. The results suggest that the serum-cholesterol-lowering effect of high-RS3 diets may be explained by an increased influx of neutral steroids and bile acids into the caecum, and increased faecal excretion of bile acids, and/or by an altered intestinal bile acid profile.

The effect of long-term sucrose intake on lipid metabolism and milk composition was examined in lactating mice and correlated with the development of their pups. Female mice were weaned onto semi-purified diets containing 685 g starch or sucrose/kg diet. Food intake was similar on the two diets. At mid-lactation, milk was collected and analysed. Milk from sucrose-fed dams had a lower percentage of linoleic acid (18:2n-6) and a higher percentage of oleic acid (18:ln-9), although milk fat content was similar. Hepatic fatty acid synthesis (as measured by 3H2O incorporation into fatty acid) was three times faster in sucrose-fed than in starch-fed dams. Dietary carbohydrate had no effect on fatty acid synthesis or functional lipoprotein lipase (EC 3.1.1.34) activity in mammary gland, nor on plasma triacylglycerol concentration. Pups from first litters were killed at 11–12 d and body composition analysed. Pups born to sucrose-fed dams were significantly heavier with increased body fat and higher levels of plasma glucose and triacylglycerol. Litters of sucrose- and starch-fed dams were cross-fostered at birth and killed at 10–12 d. Analysis of variance indicated that maternal sucrose intake, both during pregnancy and lactation, increased body fat of offspring. The increases in body weight and plasma triacylglycerol of pre-weaning offspring were caused primarily by maternal sucrose intake during lactation.

In balanced experiments with rats the influence of the period of adaptation on nutrient digestibility in diets containing cellulose (CEL), guar gum (GG), pectin (PEC) or retrograded high amylose maize starch (RS) was studied. Inclusion level was 80 g/kg diet DM except for the retrograded high-amylose maize starch, where the level was 316 g/kg diet DM. A diet containing normal maize starch only acted as a controi diet (FF). The apparent digestibilities of DM, NSP, starch and protein were determined after adaptation periods of 4 d and 2, 4, 6 and 8 weeks. The digestibility of nutrients was affected by diet (P < 0.001) as well as by the period of adaptation (P < 0.001). The digestibilities of DM, NSP and starch increased asymptotically during the course of the experiment. The asymptotic progress over time was most pronounced for the GG, PEC and RS diets. The estimated periods of adaptation required for stable DM digestibility were approximately 1 week for the GG, PEC and RS diets and < 4 d for the FF and CEL diets. The digestibility of NSP in the GG and PEC diets was also stable after approximately 1 week, while it was stable from < 4 d for the CEL diet. However, PEC increased the faecal content of uronic acids for at least 2 weeks. A stable starch digestibility required 1 month in the case of RS and 3–10 d for the other diets. The high faecal content of glucose for the RS diet decreased during all 8 weeks but was still high at the close of the experiment. The apparent protein digestibility changed over time in a parabolic rather than an asymptotic fashion. The GG, PEC and RS diets increased the amount of N excreted by the faecal route.

Given the current interest in the cardiovascular complications of Mg deficiency, the aim of the present experiment was to investigate the effect of Mg deficiency on the time-course of lipoprotein oxidation and to assess whether short-term Mg deficiency results in vitamin E depletion that predisposes lipoproteins and tissues to subsequent oxidation. Weanling rats were pair-fed for 8 d with control and Mg-deficient diets respectively. Plasma triacylglycerol and α-toeopherol levels were significantly greater in Mg-deficient rats compared with control animals. The increase in plasma apolipoprotein B concentration indicated that a corresponding increase in plasma triacylglycerol-rich lipoproteins (TGRLP) occurred in Mg-deficient animals. Hyperlipaemia was associated with modifications in the composition of TGRLP. The proportion of triacylglycerols was elevated whereas that of cholesterol and protein was reduced, and Mg deficiency resulted in a slight significant reduction in α-tocopherol content. When the TGRLP fractions were subjected to in vitro Cu-induced oxidation the lipoprotein fractions from Mg-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats. Mg deficiency did not modify the α-tocopherol content of liver, heart and skeletal muscle. However, after exposure of tissue homogenates to Fe-induced lipid peroxidation, thiobarbituric acid-reactive substances were significantly higher in tissues from Mg-deficient rats compared with those from control rats. These results complement previous findings, showing that Mg deficiency increases the susceptibility of TGRLP and tissues to peroxidation and suggest that oxidative damage is not the result of a decrease in vitamin E antioxidant status.

The present experiment was undertaken to verify if the demand of tissues for pteroylglutamic (folic) acid, evaluated by serum clearance and urinary excretion of folates, is different between multiparous dairy cows in late gestation (five gestating dry cows, 52.6 (SD 8.4) d before parturition), and in early lactation (four lactating non-gestating cows, 18.0 (SD 5.9) d after parturition). On day 1 the cows received one intravenous (i.v.) injection of 50 μg pteroylmonoglutamic acid/kg body weight (BW). Blood samples were taken at 0, 5, 15, 30 min, 1, 2, 4, 8 and 24 h after the i.v. injection. On day 3 the cows received one intramuscular (i.m.) injection of 0.3 mg pteroylmonoglutamic acid/kg BW. Blood and urine samples, as well as urine volume, were taken at 0, 1, 2, 4, 8, 12, 24, 36 and 48 h after the i.m. injection. On days 5, 6 and 7 a daily i.m. injection of 0.5 mg pteroylmonoglutamic acid/kg BW was given in an attempt to saturate tissues with folates. Then the cows received one i.v. (day 8) and one i.m. (day 10) injection of pteroylmonoglutamic acid according to the same procedures described previously for days 1 and 3. On day 12 plasma volume was determined. Before tissue saturation, serum clearance of folates during the 24 h following an i.v. injection was similar for gestating and lactating cows but after tissue saturation serum clearance was slower for lactating than gestating cows (stage x saturation, P = 0.04). The percentage of folates excreted in urine was not affected by the physiological stage (P ≥ 0.6) or the level of tissue saturation (P ≥ 0.5). In conclusion, serum clearance and urinary excretion of pteroylmonoglutamic acid seem to support the hypothesis that, in multiparous cows, although there are no deficiency symptoms, tissue demand for folic acid is high, especially during gestation.