Wheat bran and pectin (100 g/kg) were added to a basal diet and fed to rats. An in vitro dialysis technique was used to measure the distribution of caecal and faecal water between the bound, i.e. that held by bacteria and undigested macromolecules, and free water. Bran increased wet (67%) and dry (74%) faecal weight. Pectin increased wet faecal weight (59 %), but did not influence dry weight. In faeces both bran and pectin increased the amount of total and bound water, but only pectin increased total and bound water when expressed on a dry weight basis. Caecal wet (90%) and dry (67%) weights increased with pectin but not with bran. Bran did not change total water but increased bound water whereas pectin increased both. This suggests that water contributed more to the increase in stool bulk in the pectin- supplemented animals due to free and bound water associated with both increased numbers of bacteria and residual pectin. Pectin altered the distribution of water in faeces. Bran has no effect on water distribution and is only partly fermented. The residual water-holding capacity leads to an increased wet and dry stool output.

Intraperitoneal glucose tolerance tests were performed at 4-week intervals in groups of weanling rats before and after feeding with maize- or cassava-based diets with and without adequate protein and sublethal cyanide supplementation. Weaning weights were doubled (increase of about 50 g) after 4 weeks on control (maize-based with adequate protein) and protein-replete diets. Weight gain on the protein-deficient diets was much less (22 g or 50%), a pattern maintained by the rats on these diets until the age of 12 weeks. Plasma thiocyanate levels were identical at weaning and after 8 weeks of the control diet but increased by 200–300% after 4 weeks intake of the cassava or cyanide-supplemented feeds. Levels returned to normal in all groups after a further 4 weeks feeding with the control diet. Glucose tolerance (as assessed by the area under the 2 h glucose ν. time curve) was impaired to a varying extent in the rats after 4 weeks on the various diets: protein-replete cassava and protein-deficient maize diets by 50%, protein-deficient cassava diet by 300%, and cyanide-supplemented protein-deficient maize diet by 150%. The derangement in the rats on the protein-replete cassava diet was unaffected by a further 4 weeks intake of the control diet, unlike in the other groups where there was significant improvement in the glucose tolerance indices at the same time. It is concluded that in growing rats: (1) cassava intake and protein malnutrition may have independent and additive effects on the genesis of glucose intolerance, (2) cyanide supplementation of a cassava-free protein-replete diet has no effect on glucose tolerance.

Studies were carried out to determine the effects of the toxic principle linamarin, a cyanogenic glucoside, in a diet containing cassava (Manihot esculenta Crantz) in the form of gari fed to growing dogs for 14 weeks. There were three groups of dogs, each comprising six animals. One group was fed on a control diet with rice as the carbohydrate source, the second group was fed on cassava (gari) as the carbohydrate source and which was expected to release 10.8 mg HCN/kg cooked food, the third group was fed on the control diet to which enough NaCN was added at feeding time to release 10.8 mg HCN/kg cooked food in order to monitor the effects of the HCN released from gari. All diets contained 130 g erude protein (N × 6.25)/kg and were supplemented with vitamins and minerals. Each animal was given approximately 100 g diet/kg body weight for the duration of the experifnent. The biochemical variables investigated were plasma electrolytes, serum proteins, plasma-free amino acids, plasma enzymes and urine protein, and the histology of some metabolically active tissues, namely liver, kidney, myocardium, testis and adrenal gland, was studied. The gari diet caused an elevated plasma thiocyanate concentration (P < 0.01), elevated 24 h urinary thiocyanate excretion and elevated urinary protein excretion (P < 0.01), lowered serum albumin (P < 0.05), a plasma-free amino acid profile which resembled that found in kwashiorkor, lowered plasma K and Ca (P < 0.05). The rice + cyanide diet caused an elevated plasma thiocyanate (P < 0.01) and a 24 h urinary thiocyanate excretion that was significantly higher (P < 0.01) than that of the dogs fed on gari, but caused a urinary protein excretion that was significantly lower than that of the dogs fed on gari (P < 0.01), lowered serum albumin (P < 0.05), a plasma-free amino acid profile that indicated that the amino acids were not being utilized to the same extent as in the control (rice) group but were accumulating. Neither diet had an effect on plasma γ-glutamyltransferase (EC 2.3.2.2), alanine aminotransferase (EC2.6.1.2) or isocitrate dehydrogenase (EC 1.1.1.42) activities, plasma Na, Mg, and P concentrations. The gari diet caused generalized congestion and haemorrhage, periportal vacuolation of the liver, swelling, vacuolation and rupture of the epithelial cells of the proximal convoluted tubules of the kidney, myocardial degeneration and adrenal gland degeneration. In the testes there were occasional abnormal germ cells in the seminiferous tubules, and occasional seminiferous tubules denuded to basement membrane of germ cells but with remnants of Sertoli cells. Spermatogenesis, however, appeared to be normal since the percentage of round tubules in stage 8 of the spermatogenic cycle was not significantly different from that of the control dogs. The rice + cyanide diet caused nephrosis and a significantly reduced relative frequency of testicular tubules in stage 8 of the spermatogenic cycle (P < 0.01). There was also marked testicular germ cell sloughing and degeneration. There was adrenal gland hyperplasia and hypertrophy. It was concluded that the observed changes which occurred when the gari diet was consumed were not entirely due to cyanide.

The hypocholesterolaemic properties of an ethanol extract from defatted fenugreek (Trigonella foenumgraecum) seeds were investigated. Purification of the crude extract by dialysis produced an isolated component with haemolytic properties. The dialysate was also found to contain saponins demonstrated by thin-layer chromatography. Experiments in vitro employing the everted-sac technique showed that the ethanol extract had the ability to inhibit taurocholate and deoxycholate absorption in a dose-dependent manner. In two separate feeding experiments, hypercholesterolaemic rats were fed on 30 or 50 g ethanol extract/kg for a 4-week period. Reductions in plasma cholesterol levels ranged from 18 to 26% and a tendency for lower concentrations of liver cholesterol was observed. These results indicate that the ethanol extract from fenugreek seeds contained hypocholesterolaemic components which appear to be saponins that interact with bile salts in the digestive tract.

The effect of dietary L-carnitine on the growth and growth efficiency of African catifish (Clarias gariepinus, Burchell 1822) fingerlings was investigated. Six dietary levels of L-carnitine, varying from the conrol level (about 125 mg/kg) to 3920 mg/kg, were each tested at two dietary lipid levels (96 and 155 g/kg). The diets were isonitrogenous and were fed to thirty-six experimental groups of 100 fish weighing 5 g at a feeding level of 25·2 g/kg live weight(w)0.8 per d, during 18 d. The average final weight varied from 19·1 to 28·0 g. At a dietary lipid level of 96 g/kg the metabolic growth increased from 30·8 to 36·5 g/kg w0.8 per d. At the higher dietary lipid level the metabolic growth increased from 30·9 to 35·4 g/kg w0.8 per d. To assess the dose–response relationship between dietary L-carnitine and growth performance in the African catfish a linear-plateau model was fitted to the experimental data. According to this model, metabolic growth was at a maximum at L-carnitine levels of 500 mg/kg and above at a lipid level of 96 g/kg and at L-carnitine levels of 684 mg/kg and above at a lipid level of 155 g/kg. The fitted maximum metabolic growth was higher at a dietary lipid level of 96 g/kg (35·9 g/kg w0.8 per d) than at 155 g/kg (34·7 g/kg w0.8 per d). Feed conversion improved significantly with increasing dietary levels of L-carnitine, reaching a fitted plateau at L-carnitine levels of 448·8 and 236·7 mg/kg respectively for the high and low dietary fat levels. Other growth efficiency variables, e.g. protein efficiency ratio, protein retention and energy retention improved accordingly. Taking into consideration that all fish received the same amount of feed, the results of the present study demonstrate that the positive effect of increased levels of dietary L-carnitine is the result of an improved feed utilization, probably because of a stimulated protein-sparing action.