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The large intestine was found to reveal an obvious activity of various aminopeptidases and genuine dipeptidases in dogs and in humans. A dipeptidase was found specific by its independence of the C-terminal configuration of the peptide. This peptidase in an intrinsic membrane protein. Physiological significance of these enzymes is discussed.
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The surface pH of rat distal colonic mucosa and human rectal mucosa was measured in vitro using first a small pH electrode with a flattened tip. In buffer with pH 7.56 the mean rat colonic surface pH was 6.72. Lowering the buffer pH in steps resulted in a small fall in surface pH, the values being buffer pH 7.06 surface pH 6.64, buffer pH 6.58 surface pH 6.61 and finally buffer pH 6.09 surface pH 6.39. Similar results were obtained with a buffer where butyrate, 30 mmol/l replaced chloride and when a CO2/bicarbonate buffer was used. During the time taken for the study transmural potential difference only changed by 1-2 mV. Serosal surface pH changed with buffer pH, suggesting that the maintained surface pH is a property of the mucosal surface only. The surface pH of human rectal mucosa was similar to that of rat distal colonic mucosa. As buffer pH fell from pH 7.51 to 5.96 mucosal surface pH only fell from pH 6.80 to 6.26. The values obtained in ulcerative proctitis did not differ from normal mucosa. Secondly pH microelectrodes were used to measure the juxta mucosal pH and the pH-microclimate thickness when luminal pH was controlled. The microclimate had a pH 6.63 adjacent to the mucosa with a thickness of 840 micron. The importance of mucus in maintaining the microclimate was shown by n-acetyl cysteine thinning and prostaglandin E2 thickening the layer. These results describe a surface microclimate in the large intestine of appreciable thickness and a constant juxta mucosal pH. Luminal pH changes produce only a small change in microclimate pH.
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In the experiment on 80 rats, the intraoperative lavage of the colon (IL) in its perforation and acute obstructive ileus was performed. Lavage was performed before wound closure and placing the anastomosis. In using IL with hyperoxigenated solution, the favourable course of the postoperative period, increase in number of the animals survived, decrease in incidence of complications were noted. The wound and intestinal anastomosis healed by first intention. The method is recommended for the use in clinical practice.
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OBJECTIVE: The large intestine has been reported to have a capacity for iron absorption and expresses genes for iron absorption normally found in the duodenum. The importance and function of these genes in the large intestine are not understood. We therefore investigated the cellular localization and regulation of expression of these genes in mouse caecum and colon. MATERIAL AND METHODS: Gene expression was measured by real-time PCR using RNA extracted from iron-deficient and hypoxic mouse large intestine, compared to controls. Protein localization and regulation were measured by immunohistochemistry using frozen sections of the large intestine from the same mice. RESULTS: Dcytb (duodenal ferric reductase) was expressed at very low levels in the large intestine, compared to the duodenum, while Ireg1 and DMT1 were expressed at significant levels in the large intestine and were increased in iron-deficient caecum, proximal and distal colon, with the most significant increases seen in the distal colon. Hypoxia increased Ireg1 expression in the proximal colon. Immunohistochemistry detected significant levels of only IREG1, which was localized to the basolateral membrane of colonic epithelial cells. CONCLUSIONS: Iron absorption genes were expressed at lower levels in mouse caecum and colon than in the duodenum. They are regulated by body iron requirements. Colonic epithelial cells express basolateral IREG1in the same fashion as in the duodenum and this protein could regulate colonic epithelial cell iron levels.
The digestibility of D-tagatose, its effect on the digestibility of macronutrients and the metabolic response of the microbiota of the gastrointestinal tract to the ingestion of this carbohydrate were studied in pigs. Eight pigs were fed a low fiber diet comprising 15% sucrose (control group). Another eight pigs were fed a similar diet except that 100 g sucrose per kg diet was replaced by D-tagatose (test group). After 18 d, the pigs were killed and the gastrointestinal contents removed for analysis. The digestibility of D-tagatose was 25.8 +/- 5.6% in the distal third of the small intestine. The small intestinal digestibilities of dry matter (86.9 +/- 1.3 vs. 92.9 +/- 0.9%), gross energy (74.4 +/- 1.6 vs. 80.7 +/- 1.8%) and sucrose (90.4 +/- 2.5 vs. 98.0 +/- 0.5%) were lower (P < 0. 05) in the pigs fed D-tagatose. Digestibilities of starch, protein and fat did not differ between groups. D-Tagatose, sucrose and starch were fully digested in the large intestine. The fecal digestibilities of energy, dry matter and fat did not differ between the two groups, whereas D-tagatose reduced the fecal digestibility of protein (91.1 +/- 0.6 vs. 93.5 +/- 0.7%, P < 0.05). D-Tagatose served as a substrate for the microbiota in the cecum and proximal colon as indicated by a reduced pH, and a greater ATP concentration, adenylate energy charge (AEC) ratio and concentration of short-chain fatty acids. In particular, the increase in the concentrations of propionate, butyrate and valerate suggests possible health benefits of this monosaccharide.
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The experiments were carried out on 3 bulls (body weight: 172, 229 and 193 kg), equipped with ileo-caecal cannulas and with catheters in the jugular veins on both sides. The offered pelleted ration consisted of straw 73%, molasses 12%, cereals 10%, ammonium hydrogen carbonate 3% and urea 2%. Feed intake amounted to about 3 kg per animal and day. During a preliminary period of 5 days 50% of ileal digesta were collected for 12 hours daily, deep-freezed and stored. In the main experiment 15N-urea was infused intravenously for 24 hours. During this period and during the following 6 hours ileal digesta were collected and replaced by precollected, unlabelled digesta. The urea metabolism was estimated by the 15N-labelling of blood urea, by the 15N-excretion via faeces and urea, by the appearance of 15N in ileal digesta and by the 15N-labelling of faecal NAN, NH3 and bacterial fraction. The time course of the 15N-labelling of plasma urea during infusion can be described by an exponential function. The urea flux rate was estimated from the calculated plateau value. The flux rate for the 3 animals was 28.8, 30.7 and 34.8 mumol per minute per kg0.75, respectively. During the infusion of 15N-urea 1.0-2.4% of the infused amount of 15N' appeared in ileal digesta, half of it in the TCA precipitable fraction. At the same time the 15N-labelling of faecal NH3 increased sharply, however, the 15N-labelling of the faecal bacterial fraction was smaller by one order of magnitude. Deficiency of fermentable substrates and problems of inhomogenity of the NH3 pool are supposed as reasons for this result. 30 to 50% of the urea flux entered the digestive tract, the direct entry of urea into the large intestine seems to be only very low.
The experiment was carried out on 3 bulls with body weights of 201, 168 and 190 kg, respectively. The animals were equipped with a ileo caecal re-entrant cannula and with catheters in the jugular veins on both sides. The pelleted ration was composed of straw 70-72%, cereals 10%, molasses 12-41%, ammoniumhydrogencarbonate 3%, urea 2% and mineral mixture 1%. During a preliminary period ileal digesta were collected, deep-freezed and stored. During the main experiment 15N-urea was infused intravenously for 24 hours. In this period and during the following 6 hours outflowing ideal digesta were collected quantitatively. At the same time precollected, unlabelled digesta together with a supplement of partly hydrolysed straw meal were reintroduced into the caecal part of the cannula. Plasma urea-N, urinary-N as well as several N-fractions of faeces and digesta were analysed for 15N abundance. A urea flux rate of 27.9 +/- 3.4 mumol per minute per kg 0.75 was estimated. It was calculated that 52% of this amount of urea was transferred into the digestive tract. In both, digesta and faeces NH3-N was highest 15N-labelled indicating a direct urea entry and degradation in both segments of the digestive tract. The amounts of 15N-excess found during the period of digesta replacement were in faeces 0.25 and in ileal digesta 4.02% of the infused amount of 15N. Although the microbial utilization of endogenous urea-N was generally low in the large intestine there was a clear stimulation of this process due to the additional supply of the large intestine with a fermentable source.
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