• <tr id='mlg2dqhl'><strong id='mlg2dqhl'></strong><small id='mlg2dqhl'></small><button id='mlg2dqhl'></button><li id='mlg2dqhl'><noscript id='mlg2dqhl'><big id='mlg2dqhl'></big><dt id='mlg2dqhl'></dt></noscript></li></tr><ol id='mlg2dqhl'><option id='mlg2dqhl'><table id='mlg2dqhl'><blockquote id='mlg2dqhl'><tbody id='mlg2dqhl'></tbody></blockquote></table></option></ol><u id='mlg2dqhl'></u><kbd id='mlg2dqhl'><kbd id='mlg2dqhl'></kbd></kbd>

    <code id='mlg2dqhl'><strong id='mlg2dqhl'></strong></code>

    <fieldset id='mlg2dqhl'></fieldset>
          <span id='mlg2dqhl'></span>

              <ins id='mlg2dqhl'></ins>
              <acronym id='mlg2dqhl'><em id='mlg2dqhl'></em><td id='mlg2dqhl'><div id='mlg2dqhl'></div></td></acronym><address id='mlg2dqhl'><big id='mlg2dqhl'><big id='mlg2dqhl'></big><legend id='mlg2dqhl'></legend></big></address>

              <i id='mlg2dqhl'><div id='mlg2dqhl'><ins id='mlg2dqhl'></ins></div></i>
              <i id='mlg2dqhl'></i>
            1. <dl id='mlg2dqhl'></dl>
              1. Contact us Technology Information Products Group Introduction Home 笢恅唳 English
                     Location:Home> Science and Technology Information
                 

                                  Enzyme Technology

                   

                                  Nano Technology

                   

                                  Aquatic Technology

                   

                                  Animal Nutrition Technology

                   

                                  Feed Equation Technology

                   
                     
                 
                Effects of Mannanoligosaccharide on Growth Performance, the Development of Gut Microflora, and Gut Function of Broiler Chickens Raised on New Litter

                *School of Rural Science and Agriculture, and ‡Australian Poultry Science Cooperative

                Research Centre, University of New England, Armidale NSW 2351, Australia;

                and †Alltech Biotechnology P/L, Dandenong South, VIC 3175, Australia

                SUMMARY

                In search of substances to replace antibiotics as growth promoters for farm animals,

                mannanoligosaccharides (MOS) have been proposed as a possible alternative. In the present experiment, the influence of MOS on growth performance and bacteriological, morphological, and functional aspects of small intestine was investigated in broiler chickens at different ages. Three dietary treatments were used: a negative control without MOS or antibiotic, a positive control (Zn bacitracin), and 2 g of MOS/kg of diet. The MOS supplement tended to improve BW gain compared with the negative control in early life (P = 0.07). The counts of total anaerobic bacteria, lactic acid bacteria, and Clostridium perfringens were not affected by the supplementation of MOS. The counts of coliform bacteria were increased in young birds treated with MOS. No significant differences in the gut morphology and function were noticed between the MOS treatment and the negative or the positive control at d 14, but birds in the positive control group had significantly higher jejunal villi and mucosal alkaline phosphatase activities than MOS-supplemented birds at d 35. In the current study conducted under hygienic experimental conditions, the addition of MOS did not show a clear positive effect on performance or intestinal morphology and function.

                Key words: mannanoligosaccharide, gut microflora, gut morphology, brush-border enzymes, small intestinal digestibility of fat

                2007 J. Appl. Poult. Res. 16:280每288

                DESCRIPTION OF PROBLEM

                The addition of specific mannanoligosaccharides(MOS), derived from the outer cell wall of Saccharomyces cerevisiae, to a broiler chicken diet has been reported to improve their growth performance [1, 2]. It appears that the response in growth performance to MOS is more pronounced in early life [3, 4, 5]. Decreased improvement in the growth performance of broiler chickens associated with age may be related to a less-balanced gut microflora in younger than older birds. During the growth of the birds, the gut microflora changes; for example, it takes about 2wk for lactobacilli to become the predominant bacteria [6].

                It is well established that bacteria with type 1 fimbriae will bind to mannose-based receptors in the intestine. Furthermore, it has been demonstrated that MOS can act as a receptor analogue to prevent harmful bacteria possessing type-1 fimbriae from attaching to the gut wall, thereby helping birds to reach and maintain a healthy gut [7]. More recently, it has been reported that the actual form of MOSwill define their function and efficacy [8]. However, only a few studies have looked at the effects of MOS on the development of a normal gut microflora of birds [9].

                The present experiment was designed to test the hypothesis that the addition of an optimum dosage level of MOS [5] to broiler chicken diets could lead to less pathogens in the intestinal microflora and an improved gut function, allowing for more consistent production responses in the absence of prophylactic antibiotics.

                MATERIALS AND METHODS

                Birds and Diets

                Three hundred eighty-four one-day-old male Cobb [10] broiler chickens were included in the feeding experiment. The dietary treatments were a negative control without MOS or antibiotic, a positive control [Zn bacitracin (ZnB), 50 ppm and 30 ppm in the first and last 3 wk, respectively), and 2 g of MOS/kg of diet [11]. Each treatment consisted of 4 replicate pens (each 2.01.5 m) of 32 chickens each. Fresh sawdust was used as litter. The stocking density after excluding the area occupied by feeders (1.2 0.7 m) was approximately 15 birds/m2. The composition of the basal diet is shown in Table 1. Titanium dioxide, 5 g/kg, was incorporated in the basal diet as a marker for the calculation of digestibility coefficients.

                Table 1. Composition (g/kg) and nutritive value of basal diet

                 

                1Supplied the following per kilogram of diet (mg): vitamin A (as all-trans retinol), 12,000 IU; cholecalciferol, 3,500 IU; vitamin E (as D--tocopherol), 44.7 IU; vitamin K3, 2 mg; thiamine, 2 mg; riboflavin, 6 mg; pyridoxine hydrochloride, 5 mg; vitamin B12, 0.2 mg; biotin, 0.1 mg; niacin, 50 mg; D-Ca pantothenate, 12 mg; folic acid, 2 mg; Mn, 80 mg; Fe, 60 mg; Cu, 8 mg; I, 1 mg; Co, 0.3 mg; and Mo, 1 mg.

                2Allzyme PT, Alltech Pty Ltd., Victoria, Australia.

                Experimental Protocol

                The experiment was complied with the guidelines of the University of New England with respect to animal experimentation and care of chickens under study.

                Feed was offered ad libitum, and water was freely available at all times during the 42-d trial period. Feed intake was recorded on a pen basis at the end of wk 3 and 6. Mortality was recorded as it occurred, and feed per gain values were corrected for mortality. The birds were individually banded and weighed at 1, 21, and 42 d of age. Flock uniformity was calculated from the CV of their individual BW as described by Jackson et al. [12]. Because it was not convenient to collect feces from birds that were kept on litter, at 20 d of age, 3 birds from each pen were moved into individual AME cages, which gave 12 birds per treatment, for AME evaluation. Birds were given 4 d to adapt to their new environment. During the following 4 d, total collection of excreta was carried out for the determination of AME [13].

                At the end of 2 and 5 wk, 5 birds per pen were randomly chosen and killed by cervical dislocation, and the gastrointestinal tract was excised. The small intestine was divided into 3 segments: duodenum (from gizzard outlet to the end of the pancreatic loop), jejunum (from the pancreatic loop to Meckel*s diverticulum), and ileum (from Meckel*s diverticulum to the cecal junction). Approximately 2-cm lengths of the proximal jejunum and proximal ileum were removed for gut morphological measurements. The gut samples were flushed with ice-cold buffered PBS at pH 7.4 and immediately placed in 10% formalin solution. Another section, about 2 cm, from the proximal part of jejunum was cut and rinsed with PBS to remove the digesta. The section was wrapped in aluminum foil, snap-frozen in liquid N, and kept frozen until the analysis of brush-border enzymes. The contents of the duodenum, jejunum, ileum, and ceca were collected. Fresh digesta samples, about 1 g, from duodenum, ileum, and ceca were taken for bacterial analyses. The contents of the jejunum and ileum were freeze-dried and milled (0.5-mm screen) for the analysis of fat content. The cecal contents were stored at -20C until volatile fatty acid (VFA) analysis was performed.

                Analytical Methods

                Intestinal content from each segment was mixed in a 10-mL prereduced salt medium [14] and then prepared and serially diluted according to the procedure described by Engberg et al. [15]. Anaerobic bacteria were determined using anaerobic roll tubes containing Wilkins-Chalgren anaerobe agar [16] incubated at 37C for 7 d. Lactic acid bacteria were enumerated on deMan, Rogosa, and Sharpe agar [17] incubated in an anaerobic condition at 37C for 48 h. Coliform and lactose-negative enterobacteria were counted on MacConkey agar [18] incubated aerobically at 37C for 24 h as red and colorless colonies, respectively. The population of Clostridium perfringens was determined on perfringens agar [19] incubated anaerobically at 37C for 24 h.

                Gross energy of the feed and digesta was determined using a bomb calorimeter [20] standardized with benzoic acid. The contents of DM and fat in the feed and digesta were determined using standardized procedures [21]. Titanium dioxide in the feed and digesta was determined by the method of Short et al. [22] and the digestibility coefficients were calculated [23]. The concentrations of cecal volatile fatty acids were determined as described by Kocher [24]. Briefly, approximately 2 to 3 g of thawed digesta was suspended in 3 mL of 0.1 M sulfuric acid and centrifuged (15 min at 12,000 g) at 4. Caproic acid, 0.1mL, was added to 1 mL of the supernatant. After the sample was frozen in liquid N and air was eliminated, it was bathed in liquid N in a thermo flask overnight. Subsequently, the sublimated sample was thawed for analysis by gas chromatography [25].

                The intestinal segments fixed with formalin solution were prepared for paraplast embedding, sectioned at 7-m thickness, and stained with hematoxylin-eosin. About 15 villi and 15 crypts were measured in each type of tissue from each chicken.

                The mucosal homogenate and brush-border membrane vesicles (BBMV) were prepared as described by Shirazi-Beechey et al. [26], with minor modifications by Iji [27]. The activities of BBMV enzymes, maltase (EC. 3.2.1.20), sucrase (EC. 3.2.1.26), and alkaline phosphatase (AP; EC. 3.1.3.1) were analyzed in line with methods described previously in research with mammalian tissues [28, 29, 30]. An enrichment factor was derived to ascertain the purity of BBMV, because the specific activity of membrane-bound enzymes should be higher in BBMV than in the crude homogenate under an ideal condition. The enrichment factor was determined by analyzing and comparing the specific activities of maltase and AP in the mucosal homogenate with activities in the BBMV. The specific activities of maltase and AP were enriched 2.5 and 3 times higher in the BBMV relative to those in the homogenate at d 14, respectively, and 9 and 6 times at d 35, respectively. The morphology and enzyme data of a replicate were obtained by averaging the relevant data of 2 birds in the replicate (pen).

                Statistical Analysis

                All the data were statistically analyzed by ANOVA of SPSS [31]. Significance level was set at P < 0.05.

                RESULTS AND DISCUSSION

                Growth Performance and AME

                The effects of dietary treatments on the growth performance and AME are summarized in Table 2. In general, birds were in a very healthy condition. Mortality rate was very low (2%, data not shown), and flock uniformity was high (around 90%, data not shown), which is a clear sign of generally good health conditions of birds. There were no significant differences in BW gain among treatments, although the addition of MOS or ZnB showed a tendency (P = 0.07) for improved BW gain during wk 1 to 3. The average BW of 21-d-old birds was 4% more than the value given in the Cobb broiler nutrition guide [32]. This superior performance would have made it difficult for a further response to the supplements.

                 

                Table 2. Apparent ME of diet, feed intake (FI), BW gain (BWG), and feed conversion ratio (FCR) of birds on the different diets1

                 

                1Values are means of 4 replicates of 22 birds each for 1 to 21 d and 19 birds each for 22 to 42 d. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                2Values are means of 12 replicates.

                 

                Mannanoligosaccharides did not affect AME value of the diet, which is in agreement with the reports by Hughes [13] and the results found in our earlier work [5]. In contrast, Ferket et al. [33] reported significantly higher AME values in 12-wk-old turkey poults when MOS was added at 2 g/kg to the diet. The results from our own work [34] suggest that MOS at 2 g/kg has a tendency to improve the net energy value of a sorghumwheat- based diet. These inconsistencies may be due to differences in species, diets, and rearing conditions.

                Microbial Composition and Activity

                The effects of dietary treatments on the intestinal microbial composition of birds at d 14 are shown in Table 3. No significant differences were observed in the intestinal microbial composition of birds at d 35 (data not shown). The populations of total anaerobic bacteria and lactic acid bacteria in the small intestine were not affected by dietarytreatments. Similarly, Ceylan et al. [35] found no significant differences in the populations of the cecal microflora in birds fed a range of additives including probiotics, organic acids, MOS, and antibiotics. No significant differences between MOS treatment and both controls were observed in the counts of C. perfringens, and the values were very close to the detection limit (around 103 bacteria/g of digesta) due to the inclusion of coccidiostat in the basal diet.

                 

                Table 3. Effects of dietary treatments on the counts (log cfu/g of digesta) of selected bacteria in the digestive tractof chicken at d 141

                a,bMeans within a row not sharing a common superscript letter are significantly different (P < 0.05).

                1Values are means of 4 replicates. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                 

                However, coliform counts in the duodenum and ileum were significantly higher (P < 0.05) in 14-d-old birds fed a MOS-supplemented diet compared with both control diets in the present study. This contrasts with the reports that have shown that MOS addition significantly decreased the number of Escherichia coli in the small intestine or feces of chickens [36, 37].

                As a receptor analogue, it is suggested that MOS can act as a decoy for those pathogenic or potentially pathogenic bacteria possessing type-1 fimbriae (mannose-sensitive lectins) and prevent them from attaching to the gut mucosa, thus reducing the chance of them to colonize the gut and cause disease. It is reported that around 68% tested E. coli isolated from poultry possess type 1 fimbriae [38]. Therefore, it was expected that the number of coliform in the small intestine of birds would be reduced by the addition of MOS. However, the opposite trend was observed in the present experiment. An increase in the intestinal coliform population was noticed in some early antibiotic studies with a positive growth response taking place simultaneously [39].

                One possibility for the increase in the count of coliform bacteria in young birds might be because MOS may not only bind but also displace those type 1 fimbriae bacteria attached to the gut wall. In vitro studies examining E. coli attached to epithelial cells suggest that the bacteria could be displaced from these epithelial cells within 30 min when exposed to a mannan derivative [40]. Similar results have been found with the same commercial MOS product [41].

                Recently, Brzoska et al. [42] reported that birds receiving MOS had more E. coli compared with the antibiotic treatment, and a similar trend was found with birds receiving lactic acid bacteria and organic acids. Hence, another possibility may be that when MOS increases the number of coliform in the gut, the profile of coliform bacteria, particularly E. coli species, might be changed to a population of coliform bacteria potentially beneficial to growth performance. Some species of E. coli can improve growth in the absence of antibiotics [43]. Escherichia coli-derived phytase has been reported to help nutrient utilization of chickens [44].

                Although diet had no effect on the concentrations of the individual VFA and the total VFA in the ceca of birds (Table 4),MOS supplementation increased (P < 0.05) the molar ratio of acetic acid compared with the negative control at d 14. A similar trend was observed with the birds fed the ZnB-supplemented diet. Ao [45] reported that the cecal propionic acid level was increased by the addition of MOS when birds were given a sorghum-based diet at 35 d of age. These results indicate that the gut microflora and its activity were altered by MOS.

                 

                Table 4. Effects of dietary treatments on cecal volatile fatty acid (VFA) concentrations and molar ratios1

                a,bMeans within a row not sharing a common superscript letter are significantly different (P < 0.05).

                1Values are means of 4 replicates. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                Intestinal Morphology, BBMV Enzymes,and Small Intestinal

                Digestibility of Fat

                In general, our trial did not show significant effects of MOS on the development of gut structure and function in birds. However, bird response to in-feed additives depends on the experimental conditions. The extent of bird response might not be evident when it is under good hygiene experimental conditions, as was the case in the present experiment.

                The MOS supplement numerically increased the villus height and the specific activity of maltase in the jejunum compared with the negative control at d 14 (Tables 5 and 6). Similar results were noticed on ZnB treatment. However, at the same age, a significant increase (P < 0.05) in the ileal digestibility of fat was observed in the birds supplemented with ZnB but not in the birds supplemented with MOS compared with the negative control (Table 7). Engberg et al. [46] suggested that fat digestibility might be improved by the addition of ZnB as an inhibition of lactobacilli, which means the degree of bile acid deconjugation is reduced and in return fat absorption is improved. However, the populations of lactobacilli were not determined in the current trial.

                Alkaline phosphatase has been used as an indicator of intestinal maturation [47]. In contrast with the report of Iji et al. [48], the specific activity of AP in the current study was not improved as a result of dietary supplementation with MOS compared with the negative control (Table 6). However, a significant increase in the specific activity of AP was noticed in the birds supplemented with ZnB compared with MOS treatment at d 35. At the same age, birds fed the ZnBsupplemented diet had higher (P < 0.05) villus height:crypt depth ratio than those in the MOS group (Table 5). In general, measurements of villus height and crypt depth give an indication of the likely maturity and functional capacity of enterocytes [49]. A higher ratio indicates shallower crypts, in relation to villus height or longer villi in relation to the crypt. Longer villi would partly result in increased surface area for digestion and absorption, and although the latter was not measured in the current study, the results would suggest greater surface area in the ZnB group. Additionally, the differences in the specific activity of AP and gut morphology may suggest that birds in the ZnB group have a relatively high proportion of mature enterocytes, which would be expected to improve the capacity for digestion and absorption of nutrients from the small intestine. However, no significant differences were observed in fat digestibility between ZnB treatment and MOS treatment at d 35.

                 

                Table 5. Effects of dietary treatments on villus height, crypt depth, and villus height:crypt depth ratio of small intestine of birds on the different diets1

                a,bMeans within a row not sharing a common superscript letter are significantly different (P < 0.05).

                1Values are means of 4 replicates. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                2Ratio of villus height:crypt depth.

                Table 6. Effects of dietary treatments on jejunal protein content (mg/g of tissue) and specific activities (米mol of product/mg of protein per min) of membrane-bound digestive enzymes1

                a,bMeans within a row not sharing a common superscript letter are significantly different (P < 0.05).

                1Values are means of 4 replicates. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                2Protein content in the mucosal homogenate.

                3Protein content in the brush-border membrane vesicle (BBMV).

                 

                Table 7. Effects of dietary treatments on the intestinal digestibility of fat by broiler chickens on the different diets1

                a,bMeans within a row not sharing a common superscript letter are significantly different (P < 0.05).

                1Values are means of 4 replicates. NC = negative control; MOS = 2 g of Bio-Mos/kg of feed; ZnB = Zn bacitracin, 50 ppm during 1 to 21 d and 30 ppm during 22 to 42 d.

                CONCLUSIONS AND APPLICATIONS

                1. Dietary supplementation of MOS did not significantly improve the growth performance of birds.

                2. Some aspects of gut microflora and gut activity were different in young birds when MOS was included in the feed.

                3. The inclusion of MOS did not show a clear positive effect on the intestinal digestibility of nutrients, morphology, or the mucosal enzyme activities.

                REFERENCES AND NOTES

                1.Hooge, D. M. 2004. Meta-analysis of broiler chicken pen trials-evaluating dietary mannan oligosaccharide, 1993每2003. Int. J. Poult. Sci. 3:163每174.

                2. Rosen, G. D. 2007. Holo-analysis of the efficacy of Bio-Mosin broiler nutrition. Br. Poult. Sci. 48:21每26.

                3. Tucker, L. A., E. Esteve-Garcia, and A. Connolly. 2003. Dose response of commercial mannan oligosaccharides in broiler chickens. Poster presented at WPSA 14th Eur. Symp. Poult. Nutr., Lillehammer, Norway. World*s Poult. Sci. Assoc., Norwegian Branch, Lillehammer.

                4. Jamroz, D., A. Wiliczkiewicz, J. Orda, T. Wertelecki, and J. Skorupinska. 2003. Effect of a feed antibiotic or mannan oligosaccharides in broiler chickens. Poster in Alltech*s 20th Annu. Symp. Nutr. Biotechnol. Feed Food Ind., Lexington, KY. Nottingham Univ. Press, UK.

                5. Yang, Y., M. Choct, and P. A. Iji. 2005. Effect of dietary mannanoligosaccharide level on performance and gross morphology of digestive tract segments of broiler. Pages 72每75 in Proc. 17th Annu. Aust. Poult. Sci. Symp., Sydney, NSW, Australia. Poult. Res. Found., Univ. Sydney, Australia.

                6. Barnes, E. M., G. C. Mead, and D. A. Barnum. 1972. The intestinal flora of the chicken in the period 2 to 6 weeks of age, with particular reference to the anaerobic bacteria. Br. J. Nutr. 13:311每326.

                7. Spring, P., C. Dawson, and K. E. Newman. 2000. The effects of dietary mannanoligosaccharides on cecal parameters and the concentrations of enteric bacteria in the ceca of salmonella-challenged broiler chicks. Poult. Sci. 79:205每211.

                8. Newman, K. 2006. Quantifying the efficacy of MOS. Feed Mix. 14:2每4.

                9. Kocher, A., S. A. Denev, I. Dinev, I. Nikiforov, and C. Scheidemann. 2005. Effects of mannanoligosaccharides on composition of the cecal microflora and performance of broiler chickens. Pages 216每220 in Proc. 4 BOKU-Symp. Tiererna“hr., Tiererna“hr. ohne antibiotische Leistingsfo“rderer. Univ. Bodenkunde Wien., Vienna, Austria.

                10. Baiada Hatchery, Kootingal NSW, Australia.

                11. MOS, Bio-Mos, Alltech Inc., Nicholasville, KY.

                12. Jackson, M. E., K. Geronian, A. Knox, J. McNab, and E. McCartney. 2004. A dose-response study with the feed enzyme -mannase in broilers provided with corn-soybean meal based diets in the absence of antibiotic growth promoters. Poult. Sci. 83:1992每1996.

                13. Hughes, R. J. 2003. Variation in the digestion of energy by broiler chickens. PhD Diss. Univ. Adelaide, Australia.

                14. Holdeman, L. V., E. P. Cato, and E. C. Moore. 1977. Anaerobic Laboratory Manual. Virginia Tech, Blacksburg.

                15. Engberg, R. M., M. S. Hedemann, S. Steenfeldt, and B. B. Jensen. 2004. Influence of whole wheat and xylanase on broiler performance and microbial composition and activity in the digestive tract. Poult. Sci. 83:925每938.

                16. CM0619, Oxoid, Basingstoke, Hampshire, UK.

                17. CM0361, Oxoid.

                18. CM0007, Oxoid.

                19. CM0543 OPSP, Oxoid.

                20. Calorimeter C7000, Protech Group, Coolum, Australia.

                21. AOAC. 1994. Official Methods of Analysis. 15th ed. Assoc. Offic. Anal. Chem. Washington, DC.

                22. Short, F. J., P. Gorton, J. Wiseman, and K. N. Boorman. 1996. Determination of titanium dioxide added as an inert marker in chicken digestibility studies. Anim. Feed Sci. Technol. 59:215每221.

                23. DC = 1 − {[digesta nutrient (g/kg)/digesta TiO2 (g/kg)]/[diet nutrient (g/kg)/diet TiO2 (g/kg)]}.

                24. Kocher, A. 2000. Enzymatic degradation of non-starch polysaccharides in vegetable protein in poultry diets. PhD Diss., Univ. New England, Armidale, Australia.

                25. The gas chromatography was equipped with a flame ionization detector and a polyethylene glycol packed column (1.5 m long, 5.6 mm inside diameter). The column was operated at 100 to 150 with high-purity He, at 20 mL/min, as the carrier gas.

                26. Shirazi-Beechey, S. P., B. A. Hirayama, Y. Wang, D. Scott, M. W. Smith, and E. M. Wright. 1991. Ontogenic development of lamb intestinal sodium-glucose co-transporter is regulated by diet. J. Physiol. 437:691每698.

                27. Iji, P. A. 1998. Natural development and dietary regulation of body and intestinal growths in broiler chickens. PhD Diss., Univ. Adelaide, Australia.

                28. Dahlqvist, A. 1964. Method for assay of intestinal disaccharidases. Anal. Biochem. 7:18每25.

                29. Forstner, G. G., S. M. Sabesin, and K. J. Isselbacher. 1968. Rat intestinal microvillus membranes. Purification and biochemical characterization. Biochem. J. 106:381每390.

                30. Holdsworth, E. S. 1970. The effect of vitamin D on enzyme activities in the mucosal cells of the chick small intestine. J. Membr. Biol. 3:43每53.

                31. SPSS Version 12, SPSS Inc., Chicago, IL. Data were analyzed by ANOVA. The differences between mean values were identified by the least significant difference.

                32. Teeter, R., and C. Wiernuz. 2003. Cobb Broiler Nutrition Guide. Cobb-Vantress Inc., Siloam Springs, AR.

                33. Ferket, P. R., C. W. Parks, and J. L. Grimes. 2002. Mannan oligosaccharides versus antibiotics for turkeys. Pages 43每63 in Proc. Alltech 18th Annu. Symp., Lexington, KY. Nottingham Univ. Press, UK.

                34. Yang, Y., M. Choct, and P. A. Iji. 2006. University of New England, Armidale NSW, Australia. Personal communication.

                35. Ceylan, N., Y´ . C¸ yftcy, and Z. Y´ lhan. 2003. The effects of some alternative feed additives for antibiotic growth promoters on the performance and gut micro flora of broiler chicks. Turk. J. Vet. Anim. Sci. 27:727每733.

                36. Stanley, V. G., H. Chukwu, C. Gray, and D. Thompson. 1996. Effects of lactose and Bio-MOS in dietary application on growth and total coliform bacteria reduction in broiler chicks. Abstr. South. Poult. Sci. Soc. 17th Annu. Meet., Louisville, KY. South. Poult. Sci. Soc., Atlanta, GA.

                37. Song, J. Y., and W. Li. 2001. The preparation of mannanoligosaccharide from Saccharomyces cerevisiae and its effect on intestinal microflora in chicken. J. Zhejiang Univ. (Agric. and Life Sci.) 27:447每450.

                38. Finucane, M. C., K. A. Dawson, P. Spring, and K. E. Newman. 1999. Effects of mannanoligosaccharide on composition of the gut microflora of turkey poults. Poult. Sci. 78(Suppl. 1):77. (Abstr.)

                39. Lindgren, N. O. 1954. Studies in the growth promoting action of antibiotics in poultry nutrition. Nord. Vet. Med. 6:701每706.

                40. Ofek, I., and E. H. Beachey. 1978. Mannose binding and epithelial cell adherence of Escherichia coli. Infect. Immunol. 22:247每254.

                41. Peuranen, S., A. Kocher, and K. A. Dawson. 2006. Yeast cell preparations prevent the attachment of enteropathogenic Escherichia coli on broiler gut mucus. Reprod. Nutr. Dev. 46:S111(Abstr.)

                42. Brzoska, F., S. B. Buluchevskij, B. Sliwinski, and K. Stecka. 2005. Preliminary study of the microbial spectrum of the digestive tract in broilers fed diets with and without antibiotic supplementation. J. Anim. Feed Sci. 14(Suppl. 1):431每434.

                43. Jukes, T. H. 1955. Antibiotics in Nutrition. Med. Encyclopedia Inc., New York, NY.

                44. Ravindran, V., P. C. Morel, G. G. Partridge, M. Hruby, and J. S. Sands. 2006. Influence of an Escherichia coli-derived phytase on nutrient utilization in broiler starters fed diets containing varying concentrations of phytic acid. Poult. Sci. 85:82每89.

                45. Ao, Z. 2004. Diet and early nutrition: Their effects on immunity and gut development in broiler chickens. PhD Diss. Univ. New England, Armidale, Australia.

                46. Engberg, R. M., M. S. Hedemann, T. D. Leser, and B. B. Jensen. 2000. Effect of zinc bacitracin and salinomycin on intestinal microflora and performance of broilers. Poult. Sci. 79:1311每1319.

                47. Henning, S. J. 1987. Functional development of the gastrointestinal tract. Page 285 in Physiology of the Gastrointestinal Tract. 2nd ed. L. R. Johnson, ed. Raven Press, New York, NY.

                48. Iji, P. A., A. A. Saki, and D. R. Tivey. 2001. Intestinal structure and function of broiler chickens on diets supplemented with a mannan oligosaccharide. J. Sci. Food Agric. 81:1186每1192.

                49. Hampson, D. J. 1986. Alterations in piglet small intestinal structure at weaning. Res. Vet. Sci. 40:32每40.

                Acknowledgments

                The financial support offered by Alltech Pty Ltd. to the first author is greatly appreciated. We are also grateful for the help of the staff and students at the poultry science group: Mark Porter, Barbara Gorham, Shuyu Song, Monette Swanson, Janak Vidanarchchi, Yumin Bao, and Adam Sacranie.

                 

                All rights reserved @ 2010 Guangzhou BOSAR Group    E-mail:bosar-gz@163.com