Excessive deposition of Fe in the organs and tissues of Sub-Saharan Africans was first described in South Africa in 1929. Fe overload, or siderosis, was initially attributed to infections and to metallic poisoning (Cu, Sn, Zn), and then to malnutrition. In 1953 it was hypothesized that it was due primarily to excessive Fe intake derived from foods and drinks prepared in Fe vessels. Recently, in 1992 it was advanced that a gene distinct from any HLA-linked locus may also play a role. As to sequelae, in early research on series of hospital patients, the condition was linked to scurvy, osteoporosis, diabetes, cirrhosis, and latterly, to hepatocellular cancer and tuberculosis. Accordingly, many have concluded that Fe overload is responsible for considerable morbidity and mortality, that adventitious Fe intake should be reduced, and that phlebotomy be recommended for those severely affected. However, there are numerous limitations in the evidence. There are also problems in interpretation, since levels of Fe in the serum are affected additionally by a variety of factors: infection, inflammation, certain cancers and alcohol intake. These considerations complicate attempts to assess to what extent the associations described denote causation, and whether Fe overload has significant ramifications for ill in the general African population. While the adverse sequelae of overload may be less of significance than many believe, the precise pathogenicity of the phenomenon will remain uncertain until further investigations, including prospective studies, are undertaken.

The aim of the present study was to determine the reproducibility of measurement of resting metabolic rate (RMR) using a ventilated-hood indirect calorimeter in children using a short protocol suitable for the outpatient setting or home visit. The protocol consisted of an overnight (10–12 h) fast, 5–10 min supine rest, 5–10 min ‘settling in’ under the ventilated hood, and 12–16 min of measurement. Three measurements of RMR were made in eighteen healthy children (nine boys, nine girls, aged 6–11 years) on alternate days. Reproducibility of RMR was assessed using a reproducibility index and by calculating the CV for intra-individual measurements. The mean CV was 2·6 (sd 1·7)% and the reproducibility index was 95·0 %, indicating excellent reliability. The short protocol had higher reproducibility than more stringent protocols described in the literature. The new protocol has a number of practical advantages and should be adequate for most clinical or research purposes.

In two separate studies, the cholesterol-lowering efficacy of a diet high in monounsaturated fatty acids (MUFA) was evaluated by means of a randomized crossover trial. In both studies subjects were randomized to receive either a high-MUFA diet or the control diet first, which they followed for a period of 8 weeks; following a washout period of 4–6 weeks they were transferred onto the opposing diet for a further period of 8 weeks. In one study subjects were healthy middle-aged men (n 30), and in the other they were young men (n 23) with a family history of CHD recruited from two centres (Guildford and Dublin). The two studies were conducted over the same time period using identical foods and study designs. Subjects consumed 38 % energy as fat, with 18 % energy as MUFA and 10 % as saturated fatty acids (MUFA diet), or 13 % energy as MUFA and 16 % as saturated fatty acids (control diet). The polyunsaturated fatty acid content of each diet was 7 %. The diets were achieved by providing subjects with manufactured foods such as spreads, ‘ready meals’, biscuits, puddings and breads, which, apart from their fatty acid compositions, were identical for both diets. Subjects were blind to which of the diets they were following on both arms of the study. Weight changes on the diets were less than 1 kg. In the groups combined (n 53) mean total and LDL-cholesterol levels were significantly lower at the end of the MUFA diet than the control diet by 0·29 (sd 0·61) mmol/l (P < 0·001) and 0·38 (sd 0·64) mmol/l (P < 0·0001) respectively. In middle-aged men these differences were due to a mean reduction in LDL-cholesterol of – 11 (sd 12) % on the MUFA diet with no change on the control diet (−1·1 (sd 10) %). In young men the differences were due to an increase in LDL-cholesterol concentration on the control diet of +6·2 (sd 13) % and a decrease on the MUFA diet of −7·8 (sd 20) %. Differences in the responses of middle-aged and young men to the two diets did not appear to be due to differences in their habitual baseline diets which were generally similar, but appeared to reflect the lower baseline cholesterol concentrations in the younger men. There was a moderately strong and statistically significant inverse correlation between the change in LDL-cholesterol concentration on each diet and the baseline fasting LDL-cholesterol concentration (r – 0·49; P < 0·0005). In conclusion, diets in which saturated fat is partially replaced by MUFA can achieve significant reductions in total and LDL-cholesterol concentrations, even when total fat and energy intakes are maintained. The dietary approach used to alter fatty acid intakes would be appropriate for achieving reductions in saturated fat intakes in whole populations.

Seven men and seven women participated in a randomized crossover trial to study the effect of intake of parsley (Petroselinum crispum), containing high levels of the flavone apigenin, on the urinary excretion of flavones and on biomarkers for oxidative stress. The subjects received a strictly controlled diet low in flavones and other naturally occurring antioxidants during the 2 weeks of intervention. This basic diet was supplemented with parsley providing 3·73–4·49 mg apigenin/MJ in one of the intervention weeks. Urinary excretion of apigenin was 1·59–409·09 μg/MJ per 24 h during intervention with parsley and 0–112·27 μg/MJ per 24 h on the basic diet (P < 0·05). The fraction of apigenin intake excreted in the urine was 0·58 (se 0·16) % during parsley intervention. Erythrocyte glutathione reductase (EC 1.6.4.1; GR) and superoxide dismutase (EC 1.15.1.1; SOD) activities increased during intervention with parsley (P < 0·005) as compared with the levels on the basic diet, whereas erythrocyte catalase (EC 1.11.1.6) and glutathione peroxidase (EC 1.11.1.9) activities did not change. No significant changes were observed in plasma protein 2-adipic semialdehyde residues, a biomarker of plasma protein oxidation. In this short-term investigation, an overall decreasing trend in the activity of antioxidant enzymes was observed during the 2-week study. The decreased activity of SOD was strongly correlated at the individual level with an increased oxidative damage to plasma proteins. However, the intervention with parsley seemed, partly, to overcome this decrease and resulted in increased levels of GR and SOD.

The contribution of the total splanchnic tissue (TSP; portal-drained viscera (PDV) plus liver) to whole-body protein metabolism was estimated in relation to intake (0·6, 1·0 and 1·6 × maintenance requirements), in six multicatheterized growing beef steers used in a double 3 × 3 Latin square design. At the end of each 21 d experimental period, [1-13C]leucine was infused into a jugular vein (1·05 mmol/h for 5 h, preceded by a priming dose of 1·05 mmol). Arterial, portal and hepatic blood samples were collected hourly during the infusion. The increment in TSP leucine irreversible loss rate (ILR) observed with increasing intake reached significance (P < 0·10) only for PDV, while whole-body ILR increased markedly (P < 0·001) with intake. The relative contribution of TSP to whole-body leucine ILR averaged 44 % (25 % from PDV and 19 % from the liver). Although these proportions were not affected by intake, on an incremental basis more than 70 % of the increase of whole-body leucine ILR between the 0·6 and 1·0 × maintenance originated from the changes in TSP ILR, while the corresponding value was below 13 % between 1·0 and 1·6 × maintenance. Total whole-body leucine oxidation and fractional oxidation increased (P < 0·05) with intake. Protein retention increased with intake (P < 0·01), as a result of a greater increase in protein synthesis compared with protein degradation. Protein breakdown had a major impact on protein turnover as 65 % of the protein synthesized was degraded when intake varied from 1·0 to 1·6 × maintenance. Net leucine portal absorption increased (P < 0·001) with intake and represented 1, 16 and 23 % of whole body leucine ILR, for 0·6, 1·0 and 1·6 × maintenance, respectively. Although leucine oxidation was not a major component of whole body ILR (9·3–19·9 %), it represented 69 % of the net available leucine (portal absorption) even at 1·6 × maintenance. The lower relative contribution of the TSP to whole-body leucine ILR at higher intake indicates the proportional increase in the metabolic activity of peripheral tissues as the animals moved into positive protein balance.

Most of the P in oilseed meal is in the form of phytate P, and phytate forms complexes with protein. Phytate P has been considered to be absorbed easily in ruminants because of phytate degradation in the rumen. Treatment of oilseed meals with formaldehyde improves the nutritional value of protein through suppressing its ruminal degradation. The present experiment was conducted to study the effects of formaldehyde treatment on phytate degradation in the rumen. The ruminal degradation of phytate in formaldehyde-treated soyabean meal or rapeseed meal was determined by a nylon-bag technique in sheep. Soyabean meal and rapeseed meal were treated with formaldehyde at levels of 3, 5 or 10 g/kg. Treatment with formaldehyde suppressed phytate and protein degradation in both the oilseed meals. Compared with the regular soyabean meal, the regular rapeseed meal showed lower degradability of phytate in the rumen. These results suggest that treatment with formaldehyde suppresses ruminal degradation of phytate in oilseed meal. Thus, the absorption of P from oilseed meal is probably decreased by this treatment in ruminants.

Using cytofluorimetric and biochemical methods, the content of glycogen and its labile and stable fractions, as well as activities of glucose-6-phosphatase (EC 3.1.3.9), glycogen phosphorylase (EC 2.4.1.1) and glycogen synthase (EC 2.4.1.11) were determined in the rat liver for 6 months after chronic poisoning of the animals with CCl4 and then at 1, 3, and 6 months after the end of the poisoning. One group of rats was given a standard diet, the other, a high-carbohydrate diet. The 6-month long chronic intoxication with CCl4 was shown to produce development of typical liver cirrhosis characterized by a 2·8-fold increase in the total glycogen content in hepatocytes as compared with normal cells, by a fall in the glycogen labile fraction (from 85 to 53 % of the total glycogen) as well as by decreases in the activities of glycogen phosphorylase and glucose-6-phosphatase by 25 and 82% respectively. The structural rehabilitation occurred faster and more completely at the cellular level than at the tissue level. Functional variables of the cirrhotic liver tissue also recovered, after cessation of poisoning, faster and more completely than the liver structure at the tissue level: glycogen levels in hepatocytes fell dramatically, the labile: stable glycogen fraction ratio recovered completely, and the activity of glycogen phosphorylase rose to the level characteristic of the normal liver. Use of the high-carbohydrate diet promoted a somewhat faster and more complete recovery of hepatic structure and function.

Poor early nutrition may elicit long-term detrimental effects on adult health, including susceptibility to non-insulin-dependent diabetes mellitus. We investigated the impact of moderate maternal protein restriction during pregnancy and lactation on the action of insulin on adipocyte glucose uptake in female offspring during their own pregnancies. Offspring of dams provided with diets containing either 200 g protein/kg or 80 g protein/kg during pregnancy and lactation (termed C and EPR groups respectively) were weaned on to 200 g protein/kg diet at 24 d of age. At 9–12 weeks of age both groups were time-mated and studied at day 19 of gestation. Rates of glucose utilization (assessed using the 2-deoxy-d-- [1-3H- ]glucose technique) measured in five distinct adipose tissue depots (parametrial (PM), mesenteric (MES), perirenal (PR), subcutaneous (SC), interscapular (IS)) in vivo in the post-absorptive state were consistently lower in early-protein-restricted (EPR) pregnant rats compared with control (C) pregnant rats. In C pregnant rats, insulin significantly increased glucose utilization only in the IS depot. In contrast, significantly increased glucose utilization rates in response to hyperinsulinaemia were evident in all five adipose-tissue depots of the EPR pregnant group. Consequently, glucose utilization rates in PM and SC depots during hyperinsulinaemia were significantly higher in EPR pregnant rats compared with C pregnant rats. Adipocytes were isolated from PM and MES depots to determine whether altered responses to insulin in vivo were retained in vitro. Rates of insulin-stimulated glucose uptake at sub-maximal (15 μU/ml) and maximal (15 mU/ml) insulin concentrations were significantly higher in both MES and PM adipocytes from EPR pregnant rats, but the sensitivity of glucose uptake to insulin at low concentrations was blunted compared with adipocytes from C pregnant rats. The results demonstrate that early protein restriction enhances the capacity for adipocyte glucose uptake at high insulin concentrations, but dampens the response to insulin at low physiological concentrations.