Gut microbiota have been shown to play a critical role in the maintenance of host health. Probiotics, which regulate gut microbiota balance, could serve as an effective alternative to antibiotic growth promoters. Since changes in the gastrointestinal tract, caused by a variety of different strains, groups and amounts of microorganisms, may be reflected in its histological structure, the aim of the present study was to examine the effects of rising doses of a mixed probiotic preparation on the structure and development of the small intestine of female turkeys. Eighty, three-day-old, healthy, female turkeys (Big-6 breed) were used in the current (16-week) study. The turkeys were randomly allocated to four weight-matched (59.70 ± 0.83 g) groups (n = 20), according to probiotic treatment dose (0, 107 cfu•g−1, 108 cfu•g−1 or 109 cfu•g−1, in 500 g•1000 kg−1) (cfu – a colony-forming unit). Three, non-genetically modified strains of probiotic cultures obtained from poultry, four bacterial and one yeast culture, were used. Histomorphometric analysis of the structure of the small intestinal wall of the duodenum and jejunum was performed. All probiotic doses used in the current study exerted a beneficial effect on the histological structure of the small intestine; however, the observed effect was dose and region dependent. Significant increases in villi height, crypt depth, villi and crypt width, mucosa thickness, epithelial height, enterocyte number, absorption surface and intestinal ganglia geometric indices were observed, specifically in the duodenum of birds receiving an intermediate dose of probiotic (108 cfu•g−1). The probiotic doses used in the current study differed significantly in their effect on the small intestine (P < 0.01), with the intermediate dose (108 cfu•g−1) significantly improving 58% of the parameters assessed, compared to the control. The duodenum was more susceptible to the favourable effects of the probiotic than the jejunum (56% v. 31% improvement in the parameters assessed) (P < 0.01). The weakest favourable effect was observed in the group that received the highest dose of probiotic.

Protein deficiency impairs local and systemic immune responses to Heligmosomoides bakeri infection but little is known about their individual and interactive impacts on tissue architecture of maternal lymphoid (thymus, spleen) and visceral (small intestine, kidney, liver, pancreas) organs during the demanding period of lactation. Using a 2×2 factorial design, pregnant CD1 mice were fed a 24% protein sufficient (PS) or a 6% protein deficient (PD) isoenergetic diet beginning on day 14 of pregnancy and were infected with 100 H. bakeri larvae four times or exposed to four sham infections. On day 20 of lactation, maternal organs were examined histologically and serum analytes were assayed as indicators of organ function. The absence of villus atrophy in response to infection was associated with increased crypt depth and infiltration of mast cells and eosinophils but only in lactating dams fed adequate protein. Infection-induced lobular liver inflammation was reduced in PD dams, however, abnormalities in the kidney caused by protein deficiency were absent in infected dams. Bilirubin and creatinine were highest in PD infected mice. Infection-induced splenomegaly was not due to an increase in the lymphoid compartment of the spleen. During lactation, infection and protein deficiency have interactive effects on extra-intestinal pathologies.

An experiment was carried out to examine the effect of increasing the proportion of Wimmera ryegrass hay in a lucerne hay-based diet on net transfer of nutrients to the intestine, and on the disappearance of n-alkanes in the reticulo-rumen and the hindgut of sheep. Following a latin square design, four adult ewes were fed 1:0, 0·33:0·67, 0·67:0·33 and 0:1 proportions of legume and grass. Increasing the proportion of ryegrass in the diet linearly decreased the intake of DM (P= 0·017), organic matter (P= 0·021) and N (P= 0·001). However, neutral-detergent fibre intake was not affected (P= 0·148), nor was its digestibility coefficient (P>0·10). Diet had no effect on duodenal flows of nutrients (P>0·10), although the proportion of N intake (NI) recovered at the duodenum as non-NH3 N (NAN) increased linearly with Lolium rigidum in the diet (P= 0·002). Full recovery of NI as NAN was achieved at NH3 concentrations in the rumen below 110 g/l. Microbial N contribution to NAN varied in a quadratic manner (P< 0·05) with the proportion of grass in the diet, although efficiency of microbial synthesis was not affected (P>0·10). Duodenal recovery of consumed n-alkanes was not affected by diet and was complete for those present in higher concentrations in the forages. Isolated rumen bacteria contained significant amounts of n-alkanes, contributing to the duodenal flow of these hydrocarbons in variable proportions depending on the diet consumed.

In order to understand better the molecular mechanisms involved in the pathogenesis of anaemia of inflammation, we carried out a time-course study on the effects of turpentine-induced acute and chronic inflammation on duodenal proteins involved in Fe absorption in mice. Expression levels of these proteins and hepatic hepcidin and serum Fe levels were determined in inflamed mice. In acutely inflamed mice, significantly increased expression of ferritin was the earliest change observed, followed by decreased divalent metal transporter 1 expression in the duodenum and increased hepcidin expression in the liver. Ferroportin expression increased subsequently, despite high levels of hepcidin. Hypoferraemia, which developed at early time periods studied, was followed by increased serum Fe levels at later points. The present results thus show that acute inflammation induced several changes in the expression of proteins involved in duodenal Fe absorption, contributing to the development of hypoferraemia. Resolution of inflammation caused attenuation of many of these effects. Effects in chronically inflamed mice were less consistent. The present results also suggest that inflammation-induced increases in ferritin appeared to override the effects of hepcidin on the expression levels of ferroportin in enterocytes.

The stomach and small intestine manifest a myoelectric activity pattern called the migrating myoelectric complex (MMC), which is controlled by both environmental and intrinsic factors. The daily MMC pattern has been little investigated, therefore the purpose of the present study was to study it, in weaned pigs given food twice a day. A wireless telemetric recording system was used for 24-h electromyography of the antrum and duodenum. The activity of the antrum showed little change if any, whereas the myoelectric activity of the duodenum significantly changed with respect to the time of day and feeding in conscious pigs. Namely, there were more frequent and regular MMC cycles occurring in the duodenum at night as compared with that during daytime. This change was due to the shortening of phase II of the MMC cycles that were registered at night. Phase I of the MMC showed transient variability in relation to feeding with no impact on the day/night differences. Phase III of the duodenal MMC cycle as well as the ‘feeding pattern’ did not change along with the time of day and feeding regime. In conclusion, daily variation in the duodenum may provide different conditions for digestive processes in the day and night.

Duodenal Fe2+ uptake is essential to body Fe2+ homeostasis, but the interaction of metals with the uptake process remains unclear. The present study compared the effects of four essential trace metals (Mn2+, Zn2+, Co2+ and Ni2+) with two toxic metals (Pb2+ and Cd2+) on Fe2+ uptake across the brush border membrane of villus-attached duodenal enterocytes. Everted rat duodenum was exposed to buffer containing 0·2 mM-59FE2+–ASCORBATE WITH OR WITHOUT THE COMPETING METAL (2 Mm) and the tissue was then processed for autoradiography allowing Fe2+ uptake to be determined at specific crypt–villus regions. The quantification method ensured that uptake by cells, rather than Fe2+ binding to the tissue surface, was measured. Fe2+ uptake was significantly inhibited by Cd2+ in upper villus enterocytes only and Pb2+ was without effect on Fe2+ uptake. The inhibition by Cd2+ was not due to general cell damage as judged by the release of lactate dehydrogenase from tissue into incubation fluid. Essential divalent trace metals reduced uptake significantly along the whole length of the crypt–villus axis. Cd2+ uptake, measured separately, took place at all regions of the villus–crypt axis, highest uptake being into crypt enterocytes. The very different uptake profiles for Cd2+ and Fe2+ suggests that the divalent metal transporter 1 is not the principal transporter of Cd2+. The addition of Fe2+ to incubation buffer inhibited Cd2+ uptake by both crypt and villus enterocytes. The possibility that the inhibitory actions of Fe2+ and Cd2+ on the uptakes of Cd2+ and Fe2+ respectively can be explained by a non-competitive action or the involvement of an additional metal transporter is discussed.

The aim of this present study was to identify the earliest point at which riboflavin deficiency affects post-weaning bowel development in rats. After weaning, eighty Wistar rats were weight-matched as pairs, one animal being fed a normal synthetic diet and the other being fed the same diet but deficient in riboflavin. Body weight, feeding and rates of growth were monitored and eight pairs of animals were taken for analysis at 45, 69, 93, 117 and 141 h. Riboflavin status was monitored by determining the erythrocyte glutathione reductase activation coefficient (EGRAC), and hepatic flavins were measured by a fluorescence assay. Changes to the number and dimensions of villi and crypts in the duodenum were determined, as well as crypt division (bifurcation) and the DNA synthesis index of the crypt epithelium by bromodeoxyuridine (BrdU) labelling. Riboflavin deficiency was established in the experimental rats, as demonstrated by a significant increase in EGRAC after 45 h (P<0·001) and decreased liver flavins after 96 h (P<0·001). After 96 h a significant increase in the size and cellularity of the crypts (P<0·001 in both cases) was seen in these riboflavin-deficient animals, with a decreased incidence of bifurcating crypts and of BrdU-labelled cells. No changes to villus number or size were observed. The present study has demonstrated that developmental changes to the duodenal crypt arise shortly after circulating riboflavin measurements show evidence of deficiency. These changes primarily affect cell proliferation and crypt bifurcation, and precede long-term changes such as the reduction of villus number.

This study investigated the effect of the change of diet and feeding regimen at weaning on myoelectrical activity of the intestine of piglets. For this purpose the electromyographic recordings of duodenal myoelectrical activity were carried out in relation to the different weaning status of piglets. Six piglets, in two experimental trials were surgically modified with two serosal, bipolar electrodes on the duodenum. The myoelectrical activity was recorded in the same piglets before weaning when they were sucking their sow and after weaning when the diet was changed to solid dry food (standard commercial concentrate for weaned pigs). In sucking piglets the intestinal myoelectrical activity pattern exhibited triple-phased migrating myoelectric complex (MMC), undisturbed by sow nursing. After weaning, feeding with solid food induced a long-term post-prandial pattern with higher frequency of electrical response activity (ERA) when compared with phase II of the MMC. The duration of the MMC cycles increased with time over the experiment by proportionately 0•11 and 0•14 in the periods before and after weaning. However, weaning significantly shortened MMC cycle duration by proportionately 0•21. The duration of phase II was significantly prolonged with time over the experiment by 0•07 to 0•10 and it was not affected by weaning. Phase III of MMC were of constant duration over the whole experimental period.

In summary, changes in the diet and feeding regimen have an influence on the characteristics of intestinal myoelectrical activity in piglets around weaning.

The rates of utilization and oxidation of glutamine and glucose by oesophageal and duodenal tissues have been investigated in both rats and human subjects. In the rat, glutamine utilization by oesophageal tissue was 2–3-fold lower than that in the duodenum, and this substrate contributed less than 10 % to the total oxidative metabolism of the tissue, even when glutamine was the only substrate provided. In contrast, rat duodenal tissue derived about 34 % of the total CO2 production from glutamine-C, and this contribution was not suppressed by the addition of either glucose or a mixture of the other substrates. Rates of glucose utilization and oxidation by the duodenum were lower than those for glutamine, and were significantly (P<0·001) suppressed by addition of glutamine. In both oesophageal and duodenal tissues, less than 10 % of the glutamine-C utilized was fully oxidized, approximately 60–70 % was converted to glutamate, and 30–40 % to alanine. Results obtained using human biopsy tissue samples were similar to those observed in the rat. Glutamine oxidation contributed 34 (sd 4) % of the total CO2 production by the duodenal tissue, but only 8 (sd 4) % to oesophageal tissue oxidation. The findings suggest that glutamine is not an important or preferred fuel for oesophageal tissue, whereas it is for duodenal tissue. Thus, these tissues can be expected to respond differently to glutamine administration.

Four preruminant calves with implanted electrodes in the duodenum and a catheter in the external jugular vein were used for investigation of plasma gut regulatory peptide profiles during different phases of migrating myoelectric complex (MMC) in the small intestine. The effects of different dietary proteins on the rhythmic activity of gut peptides and gastrointestinal motility were compared. In particular, the effects of skimmed-milk protein (retaining physiological patterns of abomasal clotting, and abomaso-intestinal digesta flow) v. fish protein (devoid of clotting activity and modifying the digesta flow) were studied. In calves fed on the milk diet, plasma concentrations of pancreatic polypeptide, motilin, secretin, cholecystokinin (CCK) and somatostatin, but not vasoactive intestinal polypeptide or gastrin, fluctuated in phase with the duodenal MMC in the preprandial period. Feeding transiently affected the intestinal MMC and abolished the peptide fluctuations in a specimen-specific manner. In contrast, calves fed on the fish-protein diet showed more profound changes in intestinal MMC. In these animals the MMC-related fluctuations were significant only for plasma CCK. In conclusion, the source of dietary protein has an impact on the physiological endocrine function of the small intestine. Observed fluctuations of plasma gut regulatory peptides seem to be secondary to duodenal motility cycles.

Daily secretion of pancreatic juice, including postprandial responses to food, was investigated in two groups of calves: preruminant (fed with liquid food) and ruminant (fed with solid food). Male Friesian calves (1 week old and 6 weeks old) were surgically fitted with a pancreatic duct catheter, duodenal cannula and two duodenal electrodes. Continuous 24 h collections of pancreatic juice and myoelectrical recordings were performed with minimal restraint and disturbance of animals. In both groups of calves clear periodic fluctuations in pancreatic juice secretion (volume, protein output and trypsin activity) coinciding with duodenal migrating myoelectric complexes (MMC) were recorded. Secretion of juice per cycle and per day was greater in ruminant calves, but the frequency and amplitude of cycles were lower in this group. There were no differences between day and night-time preprandial pancreatic cycles and duodenal MMC in preruminant calves, whilst in ruminant calves, evening MMC were longer than morning MMC. The pancreatic cephalic phase (increase of volume flow, protein output and trypsin activity during and just after food intake) was significant only in preruminant calves following morning feeding. Postprandial pancreatic cycles did not differ from preprandial cycles, except the pancreatic cycle (juice volume and trypsin activity) in which food was offered in preruminant calves. No gastric or intestinal phase was observed in either group of calves. In conclusion, biological cycles of the gastrointestinal tract are present in both preruminant and ruminant calves, and these cycles evolve along with the change from liquid to solid food.