The metabolism of maltitol (4-α-D-glucosylsorbitol) was assessed in fasting conventional (C) rats, C mice and germ-free (GF) mice, using [U-14C]maltitol. The radiorespirometric patterns of 14CO2 collected for 48 h after the administration of labelled maltitol were characterized by a constant rate of 14CO2 production lasting 4 h for both C rats and mice. The pattern for the GF mice showed a peak at the second hour followed immediately by a slow decrease. The percentage recovery of 14CO2 was significantly lower for the GF mice (59%) compared with C animals (72–74%). Urine, faeces and intestinal contents after 48 h totalled 19% of the administered radioactivity in the C rats and mice and 39% in the GF mice. The digestibility of maltitol and the absorption of sorbitol in GF mice was also assessed. The caecum and small intestine of GF mice, 3 h after administration of equimolar quantities of maltitol (140 mg/kg body-weight) or sorbitol (70 mg/kg body-weight), contained 39 and 51 % of the ingested dose respectively, present mostly in the caecum as sorbitol. The α-glucosidase (maltase) (EC 3.2.1.20) activity of the small intestine was appreciably higher (1·5–1·7 times) in the GF mice than in the C mice. These results suggest that the enzymic activities in the small intestine of mice and rats are sufficient to hydrolyse maltitol extensively. Consequently, the slow absorption of sorbitol seems to be an important factor limiting the overall assimilation of maltitol in the small intestine.

An in vitro faecal incubation system was used to study the metabolism of complex carbohydrates by intestinal bacteria. Homogenates of human faeces were incubated anaerobically with added lactulose, pectin, the hemicellulose arabinogalactan, and cellulose, both before and after subjects had been pre-fed each carbohydrate. Fermentation of added substrate was assessed by the production of short-chain fatty acids (SCFA) and suppression of net ammonia generation over 48 h of incubation. Control faecal homogenates to which carbohydrate was not added yielded an average increment of SCFA of 43 mmol/l, equivalent to 172 mmol/kg in the original stool. The addition of lactulose, pectin and arabinogalactan each increased the yield of SCFA by a similar amount, averaging 6·5 mmol/g carbohydrate or 1·05 mol/mol hexose equivalent; organic acid yield was not increased by pre-feeding these substances for up to 2 weeks. Acetate was the major SCFA in all samples at all times and, after pre-feeding with extra carbohydrate, butyrate concentrations exceeded propionate in all samples. Faecal homogenates incubated with cellulose showed no greater SCFA production than controls over the first 48 h, but there was a slight increase when samples from two subjects pre-fed cellulose were incubated for 14 d. Net ammonia generation was markedly suppressed by addition of lactulose to faecal incubates with an initial period of net bacterial uptake of ammonia. Pectin and arabinogalactan also decreased ammonia generation, but the reductions were not significant unless subjects were pre-fed these materials; cellulose had no effect on ammonia generation.

Vitamin B6 deficiency was induced in mice by maintenance for 4 weeks on a vitamin B6-free diet. Tryptophan metabolism was assessed by determining the urinary excretion of tryptophan metabolites, the metabolism of [14C]tryptophan in vivo and the formation of tryptophan and niacin metabolites by isolated hepatocytes. The vitamin B6-deficient animals excreted more xanthurenic acid and 3-hydroxykynurenine, and less of the niacin metabolites N1-methyl nicotinamide and methyl-2-pyridone-4-carboxamide, than did control animals maintained on the same diet supplemented with 5 mg vitamin B6/kg. After intraperitoneal injection of [14C]tryptophan, vitamin B6-deficient mice showed lower liberation of14CO2 from [methylene-14C]tryptophan and [U-14C]tryptophan than did controls, indicating impairment of kynureninase (EC 3.7.1.3) activity. There was no difference between the two groups of animals in the metabolism of [ring-2-14C]tryptophan. Hepatocytes isolated from the vitamin B6-deficient animals formed more 3-hydroxykynurenine and xanthurenic acid than did cells from control animals, but also formed more NADP and free niacin.

Healthy male volunteers consumed hot lunches consisting of cooked white rice, fried chicken fillet, raisins, bigarreaus (sweet cherries) and curry sauce with carbohydrate: fat ratios of either 0·77 or 2·04, and polysaccharide: (mono+di)saccharide ratios (P: MD) varying between 5·3 and 0·95. Before and at various time intervals after the start of the meal, blood samples were analysed for glucose, insulin, triacylglycerol (TG), free glycerol (FG), free fatty acids (FFA) and cholesterol. Elevated postprandial glucose and insulin peaks were induced by the meals containing a larger amount of carbohydrate. The type of carbohydrate in the meal appeared to have little or no effect on the peak maximum. A small second glucose peak was seen at 2 h after the meals with P: MD > 3·1. The TG concentration in the blood showed a similar and rapid rise. After the meal containing the largest amount of simple sugars, the TG curve levelled off 1 h after the start of the meal and then remained at a nearly constant level (1·5 mM). In contrast, a larger amount of complex carbohydrates induced a TG concentration which rapidly rose to a maximum of 1·75 mM, and subsequently decreased slowly to somewhat below that of the simple sugar-rich meal at 4 h. The postprandial curves after the fat-rich meals showed a continuous rise of TG up to a maximum of about 2 mM at 2 h, and a subsequent slow decrease. FG and FFA all showed a rapid drop immediately after the start of the consumption of the meals, followed by a rebound at 1 h. The postprandial curves of total cholesterol, as well as the areas below the curve of both total cholesterol and free, unesterified cholesterol were lower after the carbohydrate-rich meals than after the fat-rich meals. This is attributed to the larger amount of cholesterol in the fat-rich meals.

The thermogenic, cardiovascular and metabolic responses to a 30 kJ/kg body-weight test meal were studied in eight normal-weight, healthy female subjects after a 6 or 48 h fast. There was no significant change in metabolic rate following the 48 h fast, but plasma glucose, insulin, noradrenaline and respiratory exchange ratio were all reduced, and plasma β-hydroxybutyrate was increased. Forearm blood flow was increased, with reduction in diastolic blood pressure. After the 48 h fast, there was a reduction in the metabolic rate response 40–90 min after food (control+0·54 (se 0·05), 48 h fast + 0·27 (se 0·12) kJ/min, I < 0·01), and in forearm blood flow and diastolic blood pressure responses, but increases in heart rate, blood glucose and plasma insulin responses to the ingestion of the test meal. There was no significant relationship between plasma catecholamine concentration and food ingestion or metabolic rate. Fasting induced considerable adaptation in these subjects and altered some of the physiological responses to food ingestion.

Basolateral and brush-border membranes were prepared from the intestines and kidneys of spontaneously hypertensive (SHR) and normotensive (WKY) rats fed on a calcium-adequate diet and assayed for their enzyme activities. In intestinal basolateral membranes the activities of Na+ K+-ATPase (EC 3.6.1.37) Ca2+-ATPase (EC 3.6.1.38) and alkaline phosphatase (EC 3.1.3.1) were lower in SHR rats when compared with WKY rats, whilst 5'-nucleotidase (EC3.1.3.5) (a marker for basolateral membranes) was unaffected. In kidney basolateral membranes all enzymes were similar in activity in SHR and WKY rats. In intestinal brush-border membranes the activities of Ca2+-ATPase and alkaline phosphatase were lower in SHR rats when compared with WKY rats, whilst microvillus aminopeptidase (EC 3.4.11.2) (a marker for brush-border membranes) was unaffected. In kidney brush-border membranes all enzymes were similar in activity in SHR and WKY rats. The blood pressures of the SHR rats were considerably higher than those of the WKY rats. When SHR rats were fed on a Ca-deficient diet the activities of Na+K+-ATPase, Ca2+-ATPase and alkaline phosphatase in basolateral membranes and Ca2+-ATPase and alkaline phosphatase in brush-border membranes were all increased in the intestine when compared with SHR rats fed on a Ca-adequate diet. The equivalent enzymes in the kidneys of SHR rats, and the intestines and kidneys of WKY rats, were not affected by altering the Ca in the diet. The blood pressures of SHR rats fed on a Ca-deficient diet were higher than in those fed on a Ca-adequate diet. Blood pressures of WKY rats were not affected by altering the diet in this way. The results indicate that the absorption of Ca by active mechanisms may be reduced in SHR rats compared with WKY rats. Changing the level of Ca in the diet modified both blood pressure and the activities of enzymes which catalyse active Ca transport. The implications of these results to the aetiology, and possible nutritional treatment, of essential hypertension are discussed.

Stomach contents of mice fed on a standard rodent breeding diet contained 29–733 pM-soluble non-haem-iron. A very variable percentage (3–100, mean 49·3 (se 4·7), n 37) of this Fe was rapidly (half-life < 1–2 s) available for chelation by the strong Fe(II) chelator ferrozine, with little or no further Fe being available on addition of ascorbate. Ferrozine-available Fe could be detected in the duodenal lumen at concentrations up to 60 μM in vivo and after in vitro neutralization of stomach contents. No significant changes in quantity of stomach ferrozine-available Fe or soluble non-haem-Fe occurred in mice with adaptive enhancement of Fe absorption induced by chronic hypoxia. Electron paramagnetic resonance (e.p.r.) spectroscopy of the soluble portion of mouse stomach contents demonstrated a g = 4·3 signal (rhombic Fe(III)) equivalent to up to 20 % of soluble non-haem-Fe. The signal was unaffected by addition of excess ferrozine and increased on subsequent neutralization, suggesting redistribution of Fe from other e.p.r.-silent species. Solutions of Fe-nitrilotriacetate (NTA) (a synthetic Fe chelate used as a bioavailable, model Fe solution) were found to contain both rapidly and slowly ferrozine-available Fe (after addition of ascorbate) depending on pH, NTA:Fe ratio and the presence of Ca(II) ions. Fe-ascorbate mixtures (a model solution for Fe absorption studies) also contained ferrozine-available Fe. These results suggest the presence of Fe(II), rhombic Fe(III) and other e.p.r.-silent Fe species in the soluble fraction of mouse stomach contents. The ferrozine-available (Fe(II)) fraction is not limited by the reducing power in the diet, but by binding to ligands. Neutralization with bicarbonate leads to a loss of ferrozine-available Fe and increase in rhombic Fe(III) at the expense of both ferrozine-available and other e.p.r.-silent Fe species. The ferrozine-available Fe in mouse stomach and duodenal lumen can be related to Fe species present in model solutions used for in vitro studies of mucosal uptake mechanisms.

Breast-fed infants in Bangladeshi villages were weighed at 1, 2, 6, 9 and 12 months. The concentrations of zinc and copper in the breast milk were measured and the daily intake of these elements calculated. Breast milk Zn concentration decreased over the year but was comparable with that found in developed countries. The calculated daily intake decreased from 17·7 to 8·0 μmol (10–30% of recommended dietary allowances (RDA); National Academy of Sciences, 1980). Breast milk Cu concentration also fell over the year and was lower than that reported from developed countries. Calculated daily Cu intake was 1·95–2·63 μmol (RDA 7·81–15·63 μmol). Deficiencies of trace elements may therefore be a problem in poorly nourished communities where breast feeding is continued for several years with only small amounts of additional food. Breast milk may not be adequate as the only source of infant nutrition after the first few months of life in Bangladesh.

Metallothionein contains about 30% cysteine and is a major protein in newborn rat liver. This protein and glutathione constitute two major intracellular cysteine pools in newborn rat liver. When pregnant rats were fed on a soya-bean-protein diet, low in sulphur amino acids, the hepatic glutathione levels of the dams were decreased. However, this did not affect the levels of glutathione or metallothionein in the pups. The activity of the glutathione-degrading enzyme γ-glutamyltransferase (EC 2.3.2.2) in the livers of pups was maximum at birth and gradually decreased with age when the hepatic glutathione was transported to the kidney. In the pups born from dams fed on soya-bean-protein diet the decline in the hepatic enzyme activity was delayed, suggesting a continued degradation of glutathione in the liver. These results suggest that even with a maternal nutritional deficiency of sulphur amino acids, the transfer of cysteine to the fetus is not impaired. However, the hepatic intra-organ degradation of glutathione is continued in these pups for a prolonged period after birth compared with pups born from control mothers. The increased degradation of glutathione in the liver may be essential to meet the requirement of cysteine in pups born from dams fed on the soya-bean-protein diet.

The voluntary intake (VI) of separated leaf and stem fractions of a grass and legume (Panicum maximum and Lablab purpureus respectively) was determined using Hereford steers fistulated at the rumen and oesophagus. VI of leaf fractions was higher than that of the stem fraction (8·23 ν. 3·67 kg/d, P < 0·001) while that for the legume diets was higher than for the grass diets (6·65 ν. 5·22 kg/d, P < 0·05). The total number of eating chews per day was higher on the leaf than stem fraction (1·6 × 104 ν. 9·8 × 103, P < 0·05). The mean number of rumination chews (2·4 × 104) was similar (P > 0·05) for all four diets. The mean resistance of large particles (LP, i.e. retained on a 1·18 mm sieve during wet sieving) to breakdown (chews per g LP breakdown) during eating was lower for leaf than stem fractions (8–4 ν 23·7) and lower for the grass than legume diets (10–5 ν 21·6). The mean resistance to breakdown of LP by rumination (chews per g LP breakdown) was lower in leaf than in stem fractions (8·2 ν. 13·2, P < 0·01) and higher in grass than in legume (12·5 ν 9·0, P < 0·05). The resistance of LP to breakdown during rumination was higher than during eating for the grass diets, but was lower for the legume. Fractional passage rates (FPR) of small particles (i.e. passing through a 1·18 mm sieve during wet sieving) from the reticulo-rumen were negatively related to dimensions of particles, with greater ease of outflow for legume than for grass particles of the same length or diameter. When corrected for content of cellulase-indigestible fibre, FPR of small particles of leaf was greater than for small stem particles. It was concluded that VI of tropical forages was associated with the resistance of LP to breakdown by chewing during both eating and rumination and that the patterns of escape of small particles from the reticulo-rumen were only partially explicable in terms of particle dimensions, and that other properties of the particles may be of importance.

The endogenous urinary excretion of the purine derivatives allantoin, uric acid and xanthine plus hypoxanthine were measured in twenty-nine lambs, ten cattle (six steers, one cow and three preruminant calves) and four pigs. The sheep and mature cattle were nourished by intragastric infusion and the calves were given a milk-substitute. The pigs were fed on a purine-free diet. The excretion of total purine derivatives was substantially greater by the cattle, being 514 (se 20.6) μmol/kg live weight (W)0·75 per d compared with 168 (se 5·0) μmol/kg W0·75 per d by the sheep and 166 (se 2·6) μmol/kg W0·75 per d by the pigs. Plasma from normally fed sheep, cows and pigs was incubated with either xanthine or uric acid. Sheep and pig plasma had no xanthine oxidase (ec 1. 2. 3. 2) activity whereas plasma from cattle did. Uricase (ec 1. 7. 3. 3) was not present in plasma of cattle and pigs and appeared to be present in trace amounts only in sheep plasma. It is suggested that the species differences in endogenous purine derivative excretion were probably due to the different profiles of xanthine oxidase activity in tissues and particularly in the blood. This is because a high xanthine oxidase activity in tissues and particularly in the blood. This is because a high xanthine oxidase activity would reduce the chance to recycle purines, by increasing the probability of degradation to compounds which could not be salvaged.

The present study examined the relationship between the supply of exogenous nucleic acid (NA) purines and their recovery as the derivatives hypoxanthine, xanthine, uric acid and allantoin in urine. Six lambs, totally nourished by intragastric infusions of volatile fatty acids (VFA) and casein (i.e. no rumen fermentation), were given by abomasal infusion a microbial NA concentrate at six levels (from zero to 24·5 mmol purines/d). The true digestibility between the abomasum and terminal ileum of the NA purines was measured in a separate experiment using three lambs. The relative proportion of urinary allantoin increased, and that of other derivatives decreased, as the amount of NA infused was increased. The relationship between total excretion of purine derivatives (Y; mmol/d) and exogenous purines absorbed (X; mmol/d) was Y = 0·84 X + 0.150W0·75e-0.25X, where W is body-weight (kg). This implies that the endogenous contribution to the total excretion of derivative decreased as the supply of exogenous purines increased, with an associated progressive replacement of de novo synthesis by exogenous purines. The model also implies that 0·16 of the purines were eliminated through routes other than derivative excretion in urine. Once excretion exceeded 0·6 mmol/kg W0·75 per d, endogenous excretion was effectively zero and thus Y = 0·84 X. In normally fed sheep, derivative excretion should therefore relate to the microbial purines and, hence, microbial protein absorbed according to these models. The changing proportions of allantoin and other derivatives in urine were probably due to changes in the relative importance of endogenous and exogenous purines as precursors.