To evaluate the extent to which daily oral Fe supplements may block Fe absorption from a subsequent dose, we compared effects of oral and intraperitoneal (i.p.) Fe supplementation on Fe status in anaemic rats (haemoglobin (Hb) 90 g/l). A ligated duodenal loop technique was used to assess the effects of the Fe supplements administered either orally or i.p. at different frequencies on Fe absorption from a subsequent test dose. Anaemic Sprague–Dawley rats were assigned to seven groups of eight rats each and received either oral or i.p. Fe supplements for 3 d as follows: (1) 4 mg oral supplement daily (three doses in 3 d); (2) 4 mg oral supplement once (one dose on day 1, low-Fe dose on days 2 and 3); (3) 12mg oral supplement once (one dose on day 1, low-Fe dose on days 2 and 3); (4) 3.2 mg i.p. supplement daily (three doses in 3d); (5) 3.2 mg i.p. supplement once (one dose on day 1); (6) 9.6 mg i.p. supplement once (one dose on day 1); (7) low-Fe diet (control). The effectiveness of the supplements in treating Fe deficiency on each of the two test-factors, i.e. route of administration and frequency of dose, was assessed by determining Hb-Fe gain and liver-Fe stores after the 3 d test period. Oral supplementation was as effective as i.p. in improving the Fe status of the anaemic animals. However, a 15 min absorption of a radio-Fe test dose from a ligated loop in i.p.-supplemented groups was significantly higher (11.68 (sd 1.70) %, 17.49 (sd 4.59) %, 16.71 (sd 3.39) %) than in orally supplemented groups (3.24 (sd 1.35) %, 2.45 (sd 1.05) %, 1.80 (sd 0.35) %) despite equal body Fe stores. No significant difference in intestinal Fe absorption efficiency was detected within the oral groups but those supplemented only once were more effective than or as effective as the group receiving daily supplements for 3d in improving Fe status as indicated by Hb-regeneration efficiency. We conclude that there is a mucosal block with the administration of oral Fe supplements but the extent of this blocking effect during oral Fe supplementation is not as dramatic as currently thought in the context of the poor efficacy of daily Fe supplementation programmes.

Indian River male broiler chickens growing from 7 to 28 d of age were fed on diets containing either 120 or 210 g crude protein and 0 or 1 mg triiodothyronine (T3)/kg diet to study in vitro lipogenesis (IVL). In addition, a carry-over period (180 g crude protein/kg diet from 28 to 40 d of age) was used to test the persistence of prior treatment effects. The higher protein level increased, but T3 decreased (P < 0.01) growth and feed consumption at 28 d of age. The lower protein level increased (P < 0.05) and T3 decreased IVL in 28-d-old chickens. These effects were only sustained for 6 d following the switch to a common diet at 28 d. IVL at 40 d of age was not affected by either crude protein or T3 fed during the 7–28 d period. The higher protein level increased plasma insulin-like growth factor-1 during the period from 7 to 28 d; however, this effect lasted for only 6 d following the switch to a common diet. Plasma growth hormone (GH) at 28 d of age was inversely related to dietary protein level. Changing to a common level of crude protein did not change plasma GH values at 12 d, indicating that the nutritional state of the young chicken may affect GH at a later period of life. Metabolic changes noted in this study were rapid and maintained for a short period of time following the feeding of a common diet.

Lipogenesis: Dietary protein: Triiodothyronine

While it is well established that the fatty acid composition of dietary fat is important in determining plasma lipoprotein cholesterol concentrations, the effects of changing the absolute quantities of the individual fatty acids are less clear. In the present study Golden Syrian hamsters were fed on isoenergetic, low cholesterol (0·05 g/kg) diets containing 100, 150 or 200 g added fat/kg. This consisted of triolein (TO) alone, or equal proportions of TO and either trimyristin (TM), tripalmitin (TP) or tristearin (TS). Each trial also included a control group fed on a diet containing 50g TO/kg. As the mass of TO in the diet increased, plasma VLDL-cholesterol concentrations rose. The TM-rich diets produced a concentration-dependent increase in total plasma cholesterol which was a result of significant increases in both VLDL and HDL levels. The TP-rich diets increased plasma LDL- and HDL-cholesterol levels in a concentration-dependent manner. TS-containing diets did not increase the cholesterol content of any of the major lipoprotein fractions. Hepatic LDL-receptor mRNA concentrations were significantly decreased in animals fed on TP, while apolipoprotein B mRNA concentrations were significantly increased. Thus, on a low-cholesterol diet, increasing the absolute amount of dietary palmitic acid increases LDL-cholesterol more than either myristic or stearic acid. These effects on lipoprotein metabolism may be exerted through specific modulation of the expression of the LDL receptor and apolipoprotein B genes.

Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC 1.11.1.9; GPx) and superoxide dismutase (EC 1.15.1.1; SOD) in rats infected with Plasmodium berghei malaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC 1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 × 106P. berghei parasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P = 0.004). GPx activity was higher in erythrocytes of rats parasitized with P. berghei than comparable non-infected rats regardless of riboflavin status (P < 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.

Stable isotope breath tests offer a safe, repeatable non-invasive method of measuring fat digestion. They involve the ingestion of a substrate labelled with 13C followed by serial measurements of the 13C: 12C ratio in expired CO2, from which the percentage of the 13C dose recovered (PDR) can be calculated. However PDR depends on the CO2-production rate. Our aim was to compare results obtained using directly measured CO2-production rates with those calculated from two predicted values. Twelve normal healthy children and twenty-four children with cystic fibrosis (CF) (without or with the normal dose of enzyme supplementation) were studied with 1,3-distearyl, 2[carboxyl[13C]octanoyl glycerol. The volume of CO2 produced (litres/min) was measured at rest for 30 min approximately 3 h after substrate ingestion, and the results were converted to mmol/min. For each subject the expected BMR was calculated from the equation of Schofield (1985), based on sex, age, weight and height, and from these values, CO2-production rate was derived. Surface area was calculated and an estimated value of 5 mmol/m2 per min (Shreeve et al. 1970) was used. Using these three CO2-production rates, three different PDR were calculated and compared. In healthy children there was a close concordance between measured and predicted CO2-production rates, but children with CF had a mean measured CO2-production rate 39% higher than normal children. This use of normal data for predicted CO2-production rates in children with CF underestimates cumulative PDR. If direct measurements of CO2-production rate are not available or impossible to perform the Vco2 obtained from the BMR calculated using the equations of Schofield (1985) or Shreeve et al. (1970) can be used in normal children. However, if accurate results for PDR are to be obtained, CO2-production rates should be measured when performing breath tests in conditions where energy expenditure and/or CO2-production rate are not expected to be normal.

The effects of freeze-dried soya milk (SM) and Bifidobacterium-fermented soya milk (FSM) on plasma and liver lipids, and faecal steroid excretion were estimated in hamsters fed on a cholesterol-free or cholesterol-enriched diet. Hamsters fed on the cholesterol-free diet containing 300 g FSM/kg had lower levels of plasma VLDL + LDL cholesterol than the animals fed on the control diet. SM in the diet produced a similar pattern without significant differences. In the cholesterol-enriched diet group, SM and FSM decreased the levels of plasma total cholesterol and VLDL + LDL-cholesterol. SM and FSM decreased the plasma triacylglycerol level in both the cholesterol-free and -enriched diet groups. The liver total cholesterol contents in the SM and FSM groups were lower than that in the control group, for hamsters fed on the cholesterol-free diet. The liver triacylglycerol content was not modified by SM or FSM in hamsters fed on either the cholesterol-free or -enriched diet. SM and FSM increased the total bile acid excretion and the proportion of cholesterol entering the cholic acid biosynthesis pathway in both the cholesterol-free and -enriched diet groups. SM and FSM did not affect neutral steroid excretion in the cholesterol-free or -enriched diet group. There was an inverse relationship between VLDL + LDL-cholesterol and faecal bile acid excretion in hamsters fed on the cholesterol-free (r −0.670, P < 0.01) and cholesterol-enriched (r −0.761, P < 0.001) diets respectively. These results indicated that SM had an anti-atherogenic effect, and that this effect was not diminished by prior fermentation.

The uptake and metabolism of [14C]oleate-labelled chylomicron remnants derived from olive oil, maize oil, palm oil, fish oil or butter fat was investigated using perfused livers from rats fed on the corresponding fat-supplemented diet (providing 40 % of the dietary energy) or a low-fat diet for 21 d. The percentage of added [14C]oleate-labelled remnant removed from the perfusate was similar for livers from rats fed on the fat-supplemented diets irrespective of the type of fat fed, whereas livers from rats fed on the low-fat diet removed more labelled fish oil and butter fat remnants than olive, maize or palm oil remnants. Following hepatic uptake in the fat-supplemented groups, the oxidation of [14C]oleate-labelled remnant lipid from maize oil, fish oil, and butter fat remnants was greater than that of the lipids from olive and palm oil remnants, although only the oxidation of lipids from maize and palm oil remnants was increased by prior fat-supplementation of the diet. In addition, the livers from rats fed on the fish-oil-supplemented diet incorporated more [14C]oleate-labelled remnant lipid into phospholipid compared with the livers from rats fed on the other fat-supplemented diets or the low-fat diets. These investigations show that both prior fat feeding and the composition of the fat fed, as well as the fatty acid composition of the chylomicron remnant particles themselves, influence the uptake and metabolism of chylomicron remnants by the liver.

The effects of inclusion of different levels of raw kidney bean (Phaseolus vulgaris) of high lectin content (27 g/kg meal) in a high-quality (lactalbumin) control diet were tested in nutritional trials on the growth and metabolism of obese Zucker (fafa) rats and their lean littermates in comparison with pair-fed controls. All diets contained 100 g total protein/kg and either 50 g lipids/kg (low fat) or 150 g lipids/kg (moderate fat). The growth of both obese and lean rats on bean diets was retarded by the daily bean intake in a dose-dependent manner. However, most of this was because bean-fed rats contained less body fat than the controls after 10 d. Thus, after feeding low-fat diets containing up to 130 g kidney bean/kg (lectin intake ≤ 0·2 g/kg body weight (BW) per d) in both 10 d and 70 d trials, the bodies of obese rats contained less fat but not protein than their pair-fed controls. Moreover, by increasing the lipid content of the diet to 150 g/kg, the level of bean inclusion could be increased to 280 g/kg (lectin intake ≥ 0·4 g/kg BW per d) without loss of body protein and skeletal muscle. Although these rats contained more body fat than those which were fed on low-fat diets, their weight reduction could be accounted for exclusively by reduced lipid content. In contrast, significant body protein loss occurred when the same diet of high lectin content was fed to lean littermates. Plasma insulin levels were significantly depressed in the obese Zucker rats on bean diets but the pancreas was not significantly enlarged nor its insulin content changed in 10 d trials. However, significant pancreatic growth occurred on long-term (70 d) bean feeding compared with pair-fed controls. The results suggest that, in addition to animal nutrition, it may also be possible to use the bean lectin as a dietary adjunct or therapeutic agent to stimulate gut function and ameliorate obesity if a safe and effective dose-range can be established for human subjects.