The effects of physical activity during pregnancy and lactation on the fetal outcome and the growth of pups was studied in Wistar rats (n 144). Rats were trained to swim for 2 h every day, 6 dsweek through pre-pregnancy, pregnancy and lactation. Maternal exercise during pregnancy, despite the dams having ad lib. access to food, resulted in low-birth-weight pups (5·6 (SD 0·7) g; n 178 in exercised dams v. 6·2(SD 0·8)g; n 238 in sedentary dams). Maternal exercise continued through lactation exaggerated further the growth retardation of these pups (30·0 (SD 4·7) g; n 78 in exercised dams v. 36·0 (SD 6·9) g; n 126 in sedentary dams). The effects of maternal exercise during pregnancy and lactation studied over two successive generations revealed a reduction in the growth rates of the second generation progeny of both exercised (5·3 (SD 0·9) g; n 125 at birth and 25·1 (SD 6·8) g; n 54 at weaning) and sedentary rats (6·0 (SD 0·2) g; n 110 at birth and 31·3 (SD 4·3) g at weaning) born to first-generation exercised rats. While slower growth in the former indicates a cumulative effect of exercise stress over two generations, that of the latter indicates that the generational effects are manifest even though the dams of the F1 generation were not exposed to exercise stress during pregnancy and lactation. These findings suggest that the adverse effect of maternal exercise during pregnancy and lactation on fetal outcome in one generation is transferred to the subsequent generation.

Dietary intakes of starch and non-starch polysaccharides (NSP) have been estimated for a rural West African community. These people eat directly from shared bowls of cooked food, and so measurement of any individual's food intake is not possible. Recently developed methodology for estimating food intake under these circumstances and the analysis of samples for dietary polysaccharides are combined to yield estimates of intakes of about 375 g starch and 25 g NSP/d for adult males, with lower intakes for women and children, related to their smaller body weights. These intakes are not direct measurements but are extremely plausible when compared with values obtained for other societies where the complication of the shared food bowl does not impinge upon the measurements.

The effects of either low (25 μmol/min) or high (235 μmol/min) infusion of NH4Cl into the mesenteric vein for 5 d were determined on O2 consumption plus urea and amino acid transfers across the portal-drained viscera (PDV) and liver of young sheep. Kinetic transfers were followed by use of 15NH4Cl for 10 h on the fifth day with simultaneous infusion of [1-13C]lleucine to monitor amino acid oxidation. Neither PDV nor liver blood flow were affected by the additional NH3 loading, although at the higher rate there was a trend for increased liver O2 consumption. NH3-N extraction by the liver accounted for 64–70% of urea-N synthesis and at the lower infusion rate the additional N required could be more than accounted for by hepatic removal of free amino acids. At the higher rate of NH3 administration additional sources of N were apparently required to account fully for urea synthesis. Protein synthesis rates in the PDV and liver were unaffected by NH3 infusion but both whole-body (P < 0·05) and splanchnic tissue leucine oxidation were elevated at the higher rate of administration. Substantial synthesis of [15N]glutamine occurred across the liver, particularly with the greater NH3 supply, and enrichments exceeded considerably those of glutamate. The [15N]urea synthesized was predominantly as the single labelled, i.e. [14N15N], species. These various kinetic data are compatible with the action of ovine hepatic glutamate dehydrogenase (EC 1.4.1.2) in periportal hepatocytes in the direction favouring glutamate deamination. Glutamate synthesis and uptake is probably confined to the perivenous cells which do not synthesize urea. The implications of NH3 detoxification to the energy and N metabolism of the ruminant are discussed.

The present study was undertaken to provide detailed information on the effect of dietary fibre (DF) level on body composition, visceral organ weight, nutrient digestibility and on energy and protein metabolism of rats housed in cold (16°), warm (24°) or hot (32°) thermal environments. High- or low-fibre diets (257 v. 56 g DF/kg dry matter (DM)) were studied in a 6-week balance experiment (initial body weight about 100 g). Heat production was measured using open-air circuit respiration chambers. Pea fibre and pectin were used to adjust the DF level in the high-fibre diet. The ranking order of daily gain of rats kept in different environments was: 24°>16°>32°, while the ranking order for carcass protein was: 16°>24°>32°. Rats on the high-DF diet had a lower daily gain than those on the low DF diet, and more protein in DM of empty body weight (EBW) and less fat. The relative weights (g/kg EBW) of liver, heart and kidney decreased when increasing the environmental temperature. The relative weight of the heart was highest in rats on the high DF level, while liver and kidney weights were unaffected by DF. Per kg EBW, the stomach, small intestine, caecum and colon and the length of colon were significantly greater in rats consuming the high-fibre diet compared with those on the low-fibre diet. Rats kept at low temperature had a significantly heavier gastrointestinal (GI) tract than those kept at the highest temperature. Digestibility of protein, DM and energy was lowest for rats fed on the high-fibre diet. Heat production (HP) of fed rats as well as fasting HP decreased significantly as environmental temperature increased. HP as a proportion of metabolizable energy (ME) was significantly lower for rats at 24° compared with the other environmental temperatures. The proportion of energy retained as protein was slightly higher in rats fed on the high-fibre than on the low-fibre diet. Based on the results of the present study the authors measured a net energy value of 5·4 kJ/g DF fermented; approximately 50% of the DF came from peas. Possible implications of the present findings are discussed.

The effect of a probiotic composed of Bacillus, Lactobacillus, Streptococcus, Saccharomyces and Candida species (each at 107–8 colony-forming units (cfu)/g rice bran), given at a level of 150 g/kg diet for 6 weeks, on lipid metabolism was examined in the faeces, serum and liver of male rats. Liver weight decreased 35% in the rats fed on a high-fat, high-cholesterol diet containing the probiotic. Total cholesterol concentration in the serum was significantly lower in the probiotic group than in the control group throughout the experimental period in rats fed on the high-fat, high-cholesterol diet, and HDL-cholesterol concentration was significantly higher (P < 0·05) in the probiotic group than in the control group which was fed for the 6 week experimental period on a basal diet. The serum VLDL + IDL + LDL cholesterol concentrations in the probiotic groups were reduced compared with those of the corresponding control groups. The probiotic groups fed on the high-fat, high-cholesterol diet and the basal diet had lower hepatic cholesterol concentrations than did the corresponding control groups (P < 0·05). Hydroxymethylglutaryl coenzyme A reductase (NADPH) (EC. 1.1.1.34) activity in the liver was lower in rats fed on the high-fat, high-cholesterol diet with the probiotic. The neutral and acidic steroid concentrations in faeces were higher in the probiotic group than in the control group fed on the high-fat, high-cholesterol diet. Escherichia coli decreased and Bifidobacterium and Eubacterium increased in the faecal microflora of rats fed on the dietary probiotic. Lactobacillus in the probiotic groups was higher than that in the control groups. The present study shows that the probiotic promotes Bifidobacterium and Eubacterium in the faecal microflora, and reduces cholesterol levels in the serum and liver of rats.

The body weight and feed intake of rats fed on a Zn-deficient diet for 28 d were reduced compared with those of control rats. The feed intakes of the Zn-deficient and control groups during the period were 10·2 (SE 0·3) and 15·7 (SE 0·2) g/d respectively. Cyclic variations in feed intake and body-weight changes were found in analysis not only of all the data for five rats but also that in each individual rat. Cosinor analysis revealed that the cyclical period of both the feed intake and body-weight change in the Zn-deficient rats was 3·5 (SE 0·1) d. The mesor and amplitude value of the feed intake in the Zn-deficient rats was 10 1 (SE 0·4) g/d and 3·5 (SE 0·5) g/d respectively, and that of body-weight change was 1·4 (SE 0·1) g/d and 7·9 (SE 1·3) gObihiro d respectively. Among pyrimidine-catabolizing enzymes, dihydropyrimidinase (EC3.5.2.2) activity showed significantretardation in the Zn-deficient rat liver with decrease of the enzyme protein. The ratio of apo-form to holo-form dihydropyrimidinase in the liver was not affected by the Zn-deficient diet.

Lipid-Zn interaction in the testes of mice was studied by feeding them low-fat (30 g maize oil/kg; group LFZD) and high-fat (90 g maize oil/kg; group HFZD) Zn-deficient diets for 6 weeks. The results were compared with those of corresponding Zn-supplemented-diet-fed controls (groups LFZS and HFZS). The integument-related Zn-deficiency symptoms appeared in group HFZD and not in group LFZD mice despite lack of Zn in their ration and an equal level of Zn in their blood serum. The feed intake, gain in body weight and testes weight of the LFZD group were comparable with those of the LFZS and HFZS groups (P < 0·05) but were higher than those of the group HFZD (P <·05). The testes of group HFZD displayed necrotic changes marked by the presence of giant cells, lower RNA, DNA and protein concentrations and higher phospholipid and cholesterol levels than those of mice in the LFZD group. The concentrations of these fractions were not significantly different between LFZD and HFZS. The results do not support the hypothesis that Zn is essential either for testicular function or for nucleic acid and protein synthesis in animals fed on a low-fat diet; however, it appears to be essential for animals fed on a high-fat diet. The changes observed in the testes of the HFZD animais suggest the excess intake of fat as their cause in Zn-deficient animals.

We questioned whether a dietary fibre supplement known to lower fasting plasma cholesterol concentrations can also lower the postprandial plasma cholesterol, glucose and insulin concentrations when it is administered just before a meal. Two studies were conducted in healthy middle-aged volunteers of both sexes in whom the fasting plasma total cholesterol concentrations were above normal. In the first study the dietary fibre treatments (2.2 g) were psyllium and a psyllium-citrus pectin mixture to which the subjects (four males, eight females) had no prior exposure. Controls received no supplement. The meals were high-fat breakfasts and lunches. In the second study the dietary fibre (6 g) was from sugar-beet root and the reference control was α-cellulose (2 g); the meal was of glucose. The volunteers (eight males, eight females) had prior exposure to the fibre supplements three times daily for 3 weeks. After adjustments for fasting values and changes in haemodilution, the psyllium and psyllium-citrus pectin mixture in the first experiment had no significant effects on the postprandial measurements of plasma glucose, insulin: glucose ratio, total-, LDL- and HDL-cholesterol, and triacylglycerol. By contrast, the sugar-beet fibre in the second study significantly decreased the area under the glucose response curve by 6·9%, the area under the insulin response curve was lower by 9·6%, although not significantly, and the post-glucose meal HDL-cholesterol concentration was significantly (12%) higher. Additionally, the 3-week treatment with sugar-beet fibre significantly lowered the fasting total- and LDL-cholesterol concentrations, by 8·5% and 9·6% respectively. We conclude that low doses of psyllium and citrus pectin at breakfast and lunch have no effects on the postprandial plasma measurements, but that sugar-beet fibre taken daily for 3 weeks affects both fasting and postprandial plasma metabolites favourably in these individuals with mildly increased risk of ischaemic heart disease. Further, we observed that small changes in haemodilution occur after meals, as indicated by plasma albumin concentration and packed cell volume. Underemphasis of the dietary fibre effects may occur when postprandial haemodilution is not taken into account.

The capacity of intestinal lactase (EC 3.2.1.23) of piglets to hydrolyse lactose in vivo was investigated by measuring the response of blood galactose to doses of lactose, galactose plus glucose and both whole and skimmed milk. Following the administration of oral doses of lactose dissolved in water to piglets from 2 to 18 d of age the adjusted galactose area under the curve (AUC) was between 1·12 and 1·36 arbitrary units, while following a dose of galactose plus glucose dissolved in water it was between 1·56 and 1·98 arbitrary units. Whereas these results suggest that the rate of digestion of lactose appeared to limit the amount of galactose reaching the peripheral blood after a dose of lactose dissolved in water, there was no significant correlation between the capacity of piglets to hydrolyse physiological amounts of lactose and the age of the piglets (2- to 18-d-old piglets; r 0·11). Following oral doses of sow's milk containing either lactose, or galactose plus glucose, the adjusted galactose AUC values were 0·94 and 1·00 arbitrary units respectively, in 10-d-old piglets. Thus, the limitation to the digestion of lactose observed when it was present in water was not evident for lactose in sow's milk. Since there was no significant difference between the adjusted galactose AUC following a dose of whole milk (0·95 arbitrary units) and that following a dose of skimmed milk (1·03 arbitrary units), the presence of fat in sow's milk did not appear to affect the utilization of lactose by the sucking piglets.

Three castrated male Holstein cattle (423 (SD 19) kg live weight) fitted with elevated carotid artery, portal, and mesenteric venous catheters, and abomasal and ileal cannulas were used to study small-intestinal starch digestion. The cattle were infused abomasally with water (275 ml/h), glucose (66 g/h), maize dextrin (66 g/h) or maize starch (66 g/h) in an incomplete Latin square design, with eight infusion periods. Infusion with carbohydrate resulted in higher arterial glucose concentrations and greater net portal glucose flux than when cattle were infused with water. Arterial glucose concentration and net portal glucose flux were highest when glucose was infused. In the small intestine, 85% of abomasally infused glucose, 78% of infused dextrin, and 66% of infused starch disappeared. Of the carbohydrate that disappeared in the small intestine, that which could be accounted for as net portal glucose flux was 73% for glucose, 60% for dextrin, and 57% for starch. Ileal digesta contained unpolymerized glucose, and short-chain soluble α-glucoside. Of the infused dextrin flowing past the ileum (14 g/h), 0·3 g/h was glucose, 6·2 g/h was soluble α-glucoside, and 7·5 g/h was insoluble α-glucoside. Of the infused starch flowing at the ileum (22·2 g/h), 0-9 g/h was glucose, 5·3 g/h was soluble α-glucoside, and 15·9 g/h was insoluble α-glucoside. The average chain lengths of the soluble α-glucosides in ileal digesta were 2·07 and 2·36 for dextrin and starch infusions respectively, indicating mostly di- and to a lesser extent trisaccharides. We conclude that (1) when 66 g raw starch is presented to the small intestine per h, about half of the intestinal disappearance appears as glucose in the portal vasculature, and (2) α-1,4 glucosidase (EC 3.2.1.20) activity at the brush border is the rate-limiting step to small-intestinal starch digestion in cattle.

The exact mechanisms by which non-starch polysaccharides increase stool output are unknown. In the present study the hypothesis that the site of fermentation and short-chain fatty acid (SCFA) accumulation is related to the action of non-starch polysaccharides (NSP) on stool output was tested. The basal diet (45 g NSP/kg) of forty-three male Wistar rats was supplemented with 50 g/kg of either guar, karaya, tragacanth, gellan, xanthan or ispaghula for 28 d. A further twenty-three rats were maintained on the basal diet for the same time period. Faeces were then collected over 2 d and caecal contents obtained post-mortem. Caecal and faecal wet and dry weights and SCFA were measured. Each supplement had a different effect on the caecal and faecal contents but they appeared to fall into three groups when compared with the basal diet. In group 1, guar gum affected only caecal SCFA. It had no effect on stool output or faecal SCFA. In group 2, karaya increased caecal SCFA and tragacanth, karaya and xanthan increased faecal SCFA and faecal water. In group 3, ispaghula and gellan had no consistent effect on caecal or faecal SCFA concentrations but increased Total faecal SCFA output and increased faecal wet and dry weight. Although the knowledge that SCFA are rapidly absorbed in the large intestine has led us to believe that they play no role in determining faecal output, these results suggest that in some cases where NSP are slowly fermented, and increase faecal SCFA, the role of the SCFA may need to be reassessed.

Urinary Mg is suggested to be an effective inhibitor of the formation and growth of calcium oxalate stones. In order to examine the influence of variations in dietary Mg on urinary Mg excretion, ten healthy male subjects were kept on two different standard diets for 5 d each. In the course of the test period, 24 h urine samples were collected. Diets 1 and 2 were calculated according to the dietary recommendations of the German Society of Nutrition (Deutsche Gesellschaft für Ernährung, 1986). Diet 1 was established as a model of a balanced mixed diet, whereas diet 2 represented an ovo-lacto-vegetarian meal plan. Diets 1 and 2 were isoenergetic with equal amounts of the main nutrients, estimated from food tables, and a constant fluid intake. In contrast to the content of Mg (336 mg) and dietary fibre (28 g) of diet 1, diet 2 was rich in Mg (553 mg) and dietary fibre (52 g). On the ingestion of diet 1, renal Mg excretion was 5·09 (SEM 0·35) mmol on the control day and increased slightly but not significantly to 5·40 (SEM 0·52) mmol on the corresponding day on diet 2. Urinary Mg excretion as a percentage of estimated dietary intake was about double on the balanced mixed diet (37%) than on the Mg-rich vegetarian diet (24%). As both diets contained equal amounts of most nutrients, these results indicate a lower excretion rate of Mg from the vegetarian diet than from the mixed diet. This would appear to be primarily due to the higher Mg and fibre contents and to the lower Mg utilization, that are important factors in decreasing Mg absorption and consequently urinary excretion rate.