The study evaluated the influence of dietary factors on some physiological aspects of digestion in chickens. The effects of dietary carbohydrates, inulin and sucrose, were tested in relation to the bacterial fermentation in the gastrointestinal tract of broiler chickens. Supplementation of inulin (1%) did not modify the acetate, lactate, ammonia and pH in the upper digestive tract, while sucrose decreased the lactate concentration in the crop and gizzard digesta.
Inulin was found to be butyrogenic in the caecal contents without affecting total production of short chain fatty acids. Inulin also changed the pattern of biogenic amine production in the jejunal and caecal digesta resulting in an elevated concentration of putrescine.
However, jejunal and caecal microbial composition was not changed following inulin supplementation according to denaturing gradient gel electrophoresis. Inulin induced morphometric changes in the intestinal mucosal architecture that were characterized by longer jejunal villi and deeper crypts wihout affecting villus:crypt depth ratio. Inulin decreased the transmural tissue resistance when jejunal segments from inulin-fed broilers were mounted in Ussing chamber. However, sodium-dependent glucose and sodium-dependent glutamine transport was not affected by the dietary treatment with inulin except higher transmural tissue resistance. Unlikely, in vitro addition of inulin (0.1%) in the Ussing chamber with tissues from laying hens did not affect the short circuit current (Isc) or transmural tissue resistance. Mucosal exposure of jejunal tissue sheets from laying hens to alpha toxin did not alter Isc. However, changes in the transmural tissue conductance ([Delta]Gt) tended (p = 0.18) to be higher after 90 minutes exposure to the toxin. The percentage increase in the [Delta]Gt became statistically significant in toxin-treated tissues at this time interval. Application of a mucolytic agent (N-acetyl-L-cysteine) did not modify the influence of alpha toxin on transmural conductivity. The effect of alpha toxin on [Delta]Gt became statistically significant (p 0.05) after 120 minutes of incubation. The addition of purified alpha toxin to the serosal side of the gut epithelium induced a biphasic increase in Isc. The magnitude of the increase of Isc of both peaks was similar, but the second phase response lasted longer. Adding D-glucose on the mucosal side of the jejunum increased (p< 0.05) Isc from a baseline value of 42 ± 28 µA/cm2 to a maximal value of 103 ± 27 µA/cm2.
Pre-incubation with alpha toxin almost fully inhibited this stimulation of Isc by D-glucose. Mucosal application of inulin (0.1%) did not modify the electrophysiological changes induced by alpha toxin.
In conclusion, inulin influenced the metabolic activities of the intestinal bacteria without affecting composition. Nutrient transport activity remained unaltered following inulin feeding in spite of longer jejunal villi and deeper crypts. The higher transmural conductivity with a concomitant decreased sodium-dependent glucose absorption in the alpha toxin incubated jejunal tissues partly explain the pathogenicity of disease caused by alpha toxin.