An evaluation of endo-beta-D-mannanase (Hemicell) effects on broiler performance and energy use in diets varying in beta-mannan content.

Two experiments were conducted to evaluate the effects of a commercial endo-beta-D-mannanase (Hemicell) on overall performance, MEn, net energy for gain, and some serum parameters of broilers fed diets varying in beta-mannan level (experiment 1) and to evaluate effects of enzyme level on the same variables in broilers fed diet high in beta-mannan (experiment 2). As a semipurified beta-mannan source, guar gum was used to alter the dietary beta-mannan level. In experiment 1, guar gum was added at 0, 0.5, 1, and 2% in a corn-soy-based starter diet with (0.05%) and without endo-beta-D-mannanase supplementation in a 4 x 2 factorial design. Enzyme supplementation improved (P < 0.01) feed efficiency at control and each guar gum inclusion level, whereas 2% guar gum supplementation reduced (P < 0.01) BW and increased (P < 0.01) 14-d feed:gain ratio. Enzyme supplementation also increased dietary MEn and net energy gain. In experiment 2, endo-beta-D-mannanase was added at 0, 0.5, 1, and 1.5% in a corn-soy-based starter diet containing 1% guar gum. Increasing endo-beta-D-mannanase supplementation did not affect (P > 0.10) final BW but improved 14-d feed:gain ratio at all inclusion levels. As in the first experiment, ME improved (P < 0.05) with increasing enzyme inclusion. Dietary endo-beta-D-mannanase inclusion significantly reduced water:feed ratio and total dry fecal output (P < 0.01). Taken together, the results of these 2 experiments indicate that endo-beta-D-mannanase supplementation may improve the utilization of nutrients in diets containing beta-mannan.

Beneficial effect of beta-mannanase feed enzyme on performance of chicks challenged with Eimerla sp. and Clostridium perfringens.

Two experiments were conducted to determine the effect of a beta-mannanase feed enzyme on the performance of broiler chicks subject to a necrotic enteritis disease challenge model involving oral inoculation of Eimeria sp. and Clostridium pefringens. Beta-mannanase is known to improve productive performance when added to poultry and swine diets. In both experiments, disease challenge in the absence of feed additives demonstrated significant reductions in performance as measured by weight gain, feed conversion, and the incidence of coccidial lesion scores. Significant mortality was also observed in challenged groups in Experiment 1. The disease challenge model was therefore judged as highly effective. Additions of a commonly used antibiotic, bacitracin methylene disalicilate (BMD), and coccidiostat, salinomycin, were highly effective in partially counteracting negative effects of the disease challenge. In both experiments, addition of beta-mannanase significantly improved performance and reduced lesion scores in disease-challenged groups. The degree of improvement was somewhat less than that afforded by a combination of BMD and salinomycin in Experiment 1 but was not different from that afforded by BMD alone in Experiment 2. We conclude that the beta-mannanase enzyme can play a role in circumstances where the use of antibiotics is not desired.

Effects of beta-mannanase in corn-soybean meal diets on laying hen performance.

Recently, a patented enzyme product (beta-Mannanase, Hemicell) has been shown to improve feed conversion in corn-soybean diets fed to broilers and swine. The mechanism of beta-Mannanase is to degrade beta-mannan, which is an antinutritional factor existing in many legumes, including soybean and canola meals. The objective of this study was to determine whether or not performance can be improved by including beta-Mannanase in diets of commercial laying hens, 18 through 66 wk of age. A 2 x 2 x 2 factorial arrangement of treatments was employed. There were two energy sequences of 2,926-2,907-2,885 and 2,827-2,808-2,786 kcal ME/kg, which changed at 33 and 43 wk of age respectively; two dietary enzyme levels (0 and 110 units/g); and two Hy-Line strains (W36 and W77). Hen-day production, hen-housed production, BW, feed intake, mortality, egg weight, and specific gravity data were collected biweekly. Data were analyzed in four cycles (each with six 2-wk periods) and also for the whole experiment. beta-Mannanase increased egg weight from 51.4 to 51.7 g/egg (P < 0.05) in the first 12-wk cycle. This effect was consistent across energy levels. beta-Mannanase significantly improved hen-day and hen-housed production after the first cycle. Hen-day production of the beta-Mannanase group was 0.70, 1.07, and 1.5% greater than the control for cycles two, three, and four, respectively (P < 0.01). After 30 wk of age, average hen-day production of hens fed the low-energy diets with beta-Mannanase was similar or superior to that of hens fed the high-energy diets without the enzyme. The study indicates that beta-Mannanase is capable of increasing egg weight in commercial layers at early stages of production, and increasing egg production, particularly delaying the postpeak decline in productivity.

Stimulation of lactic acid production in chick embryo fibroblasts by serum and high pH in the absence of external glucose.

Lactic acid production by chick embryo fibroblasts occurs in the absence of exogenous glucose. Fifteen to 50-fold less lactic acid is formed in the absence of glucose than in its presence. Nevertheless, serum and pH stimulation enhances this residual lactic acid production to the same relative extent as when glucose is present. The amount of lactic acid formed cannot be accounted for by the catabolism of residual glucose in the medium since its concentration is less than one-tenth that of the lactic acid eventually produced. Moreover, the residual glucose concentration remains constant or increases during the course of the experiment. To a large extent lactic acid accumulation in the absence of external glucose is dependent on the presence of amino acids in the medium, but amino acid transport is not affected by the stimulatory agents used in this study. The results suggest that treatments which stimulate cell multiplication also activate those enzymatic pathways which convert amino acids to pyruvic and thence to lactic acid.

Glucose utilization, pH reduction and density dependent inhibition in cultures of chick embryo fibroblasts.

The multiplication rate of sparse cultures of chick embryo cells is only slightly lower at pH 6.9 than at pH 7.4. There is, however, a marked reduction in the multiplication rate of the pH 6.9 cultures before they reach confluency. Cultures at pH 7.4 continue to multiply beyond confluency with only a slight decrease in the multiplication rate. Eighty to ninety percent of the glucose taken up by the cells growing at each pH is converted to lactic acid which is released into the medium. Metabolic reduction in pH of the medium is almost entirely accounted for by the amount of lactic acid produced by the cells. Neither the intracellular nor extracellular accumulation of lactic acid nor the accompanying reduction in pH is sufficient to explain density dependent inhibition of the rate of multiplication of chick cells. The rate of lactic acid production and the multiplication rate of chick cells are independent of glucose concentration in the range of 2--16 mM. In view of the kinetic parameters for the uptake of glucose, this shows that glycolysis is not limited by the rate of glucose uptake and that depletion of glucose from the medium cannot account for the onset of density dependent inhibition of multiplication. However, when cells reach very high population densities, conventional glucose concentrations of 5 mM can be depleted overnight by chick cells. Since the multiplication rate of cells is dependent on glucose concentration when it falls below 2 mM, depletion of glucose may cause some growth inhibition in crowded cultures supplied with conventional medium.