Bacterial Β-glucuronidase Activity Research Articles

Вивчення активності бета-глюкуронідази як маркера ефективності комплексної корекції симптомного аденоміозу

Disruption of the intestinal microflora and, in particular, an increase in the activity of bacterial β-glucuronidase, which is involved in estrogen metabolism and immune inflammation, is one of the probable factors in the development of adenomyosis. Aim - to investigate the activity of fecal β-glucuronidase in patients with symptomatic adenomyosis and determine its significance as a laboratory marker of the effectiveness of complex correction of this pathology Materials and methods. 150 women were examined - 120 patients with symptomatic adenomyosis who received standard treatment or an elimination diet depending on the detected type of food intolerance (study groups), and 30 healthy individuals without clinical and laboratory signs of inflammatory processes in the body and intestinal diseases (comparison group). The activity of β-glucuronidase in feces was determined for all of them using phenolphthalein glucuronide as a substrate. Statistical data processing was carried out using the SPSS 21 program. Results. Our results indicate that the activity of fecal β-glucuronidase in patients of the study groups was 1.5 times higher than in healthy women of the comparison group. Minimizing the consumption of disruptor products in combination with nutritional correction made it possible to reduce the frequency of complaints from the gastrointestinal tract. A significant decrease in β-glucuronidase activity was established in the study groups. Conclusions. Determination of fecal β-glucuronidase activity can probably be an objective marker of the effectiveness of complex correction of symptomatic adenomyosis, which requires further research. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors.

Reduced estrogen signaling contributes to bone loss and cardiac dysfunction in interleukin-10 knockout mice.

Characterization of the interleukin (IL)-10 knockout (KO) mouse with chronic gut inflammation, cardiovascular dysfunction, and bone loss suggests a critical role for this cytokine in interorgan communication within the gut, bone, and cardiovascular axis. We sought to understand the role of IL-10 in the cross-talk between these systems. Six-week-old IL-10 KO mice and their wild type (WT) counterparts were maintained on a standard rodent diet for 3 or 6 months. Gene expression of proinflammatory markers and Fgf23, serum 17β-estradiol (E2), and cardiac protein expression were assessed. Ileal Il17a and Tnf mRNA increased while Il6 mRNA increased in the bone and heart by at least 2-fold in IL-10 KO mice. Bone Dmp1 and Phex mRNA were repressed at 6 months in IL-10 KO mice, resulting in increased Fgf23 mRNA (~4-fold) that contributed to increased fibrosis. In the IL-10 KO mice, gut bacterial β-glucuronidase activity and ovarian Cyp19a1 mRNA were lower (p < 0.05), consistent with reduced serum E2 and reduced cardiac pNOS3 (Ser1119 ) in these mice. Treatment of ileal lymphocytes with E2 reduced gut inflammation in WT but not IL-10 KO mice. In conclusion, our data suggest that diminished estrogen and defective bone mineralization increased FGF23 which contributed to cardiac fibrosis in the IL-10 KO mouse.

The effect of raw, hydrobarothermally treated and fermented rapeseed cake on plasma biochemical parameters, total tract digestibility and gut function in laying hens

Abstract This study evaluated the effects of inclusion of raw, hydrobarothermally treated and fermented rapeseed cake (RRC, HRC and FRC, respectively) in diets fed to laying hens. Hydrobarothermal treatment decreased the hydroxyglucobrassicin and neoglucobrassicin content of rapeseed cake (RC), whereas fermentation significantly reduced the content of all glucosinolates (GLS) and phytate phosphorus (PP) concentration. Both HRC and FRC increased the serum concentrations of total protein (TP) and globulin (GLB), compared with group C. Group HRC hens had desirably lowest blood triacylglycerol (TAG) levels and aspartate aminotransferase (AST) activity. Group FRC hens were characterized by the lowest alkaline phosphatase (ALP) activity, and the highest concentrations of phosphorus (P) and triiodothyronine (T3). Regardless of its form, RC improved ether extract (EE) digestibility, and decreased dry matter (DM) digestibility and calcium (Ca) retention. In comparison with group C, RRC, HRC and FRC decreased cecal digesta weight and enhanced the activity of bacterial α-galactosidase and ß-galactosidase; HRC also increased ammonia concentration in the ceca and reduced β-xylosidase activity. The activity of α-glucosidase and α-arabinopiranosidase was highest, and the activity of bacterial β-glucuronidase was lowest in the ceca of group FRC hens. The cecal concentrations of acetic acid, propionic acid, and total short-chain fatty acids (SCFA s) were highest in birds fed a diet containing RRC and lowest in group HRC. In conclusion, RC fermentation considerably reduces the concentrations of GLS and PP. A diet containing 20% FRC is more recommended than diets containing RRC and HRC because it exerted a beneficial effect on metabolic parameters and intestinal function in laying hens.

254 (PB-078) Poster - Bacterial β-glucuronidase activity in postmenopausal breast cancer patients: a pilot study

Background: Long lifetime exposure to elevated estrogen levels is associated with a higher risk for developing estrogen receptor-positive (ER+) breast cancer in postmenopausal women. A factor that can influence estrogen levels is the intestinal bacterial enzyme β-glucuronidase (GUS), which can de-conjugate estrogens, leading to their reabsorption into the circulation. In this pilot study, we aimed to investigate if there was a significant difference in fecal GUS activity between postmenopausal ER+ breast cancer patients and postmenopausal controls.

Gut microbiota profiles and fecal beta-glucuronidase activity in kidney transplant recipients with and without post-transplant diarrhea.

Post-transplant diarrhea is a common complication after solid organ transplantation and is frequently attributed to the widely prescribed immunosuppressant mycophenolate mofetil (MMF). Given recent work identifying the relationship between MMF toxicity and gut bacterial β-glucuronidase activity, we evaluated the relationship between gut microbiota composition, fecal β-glucuronidase activity, and post-transplant diarrhea. We recruited 97 kidney transplant recipients and profiled the gut microbiota in 273 fecal specimens using 16S rRNA gene sequencing. We further characterized fecal β-glucuronidase activity in a subset of this cohort. Kidney transplant recipients with post-transplant diarrhea had decreased gut microbial diversity and decreased relative gut abundances of 12 genera when compared to those without post-transplant diarrhea (adjusted p value<.15, Wilcoxon rank sum test). Among the kidney transplant recipients with post-transplant diarrhea, those with higher fecal β-glucuronidase activity had a more prolonged course of diarrhea (≥7days) compared to patients with lower fecal β-glucuronidase activity (91% vs 40%, p=.02, Fisher's exact test). Our data reveal post-transplant diarrhea as a complex phenomenon with decreased gut microbial diversity and commensal gut organisms. This study further links commensal bacterial metabolism with an important clinical outcome measure, suggesting fecal β-glucuronidase activity could be a novel biomarker for gastrointestinal-related MMF toxicity.

Targeted inhibition of gut bacterial β-glucuronidase activity enhances anticancer drug efficacy

Irinotecan treats a range of solid tumors, but its effectiveness is severely limited by gastrointestinal (GI) tract toxicity caused by gut bacterial β-glucuronidase (GUS) enzymes. Targeted bacterial GUS inhibitors have been shown to partially alleviate irinotecan-induced GI tract damage and resultant diarrhea in mice. Here, we unravel the mechanistic basis for GI protection by gut microbial GUS inhibitors using in vivo models. We use in vitro, in fimo, and in vivo models to determine whether GUS inhibition alters the anticancer efficacy of irinotecan. We demonstrate that a single dose of irinotecan increases GI bacterial GUS activity in 1 d and reduces intestinal epithelial cell proliferation in 5 d, both blocked by a single dose of a GUS inhibitor. In a tumor xenograft model, GUS inhibition prevents intestinal toxicity and maintains the antitumor efficacy of irinotecan. Remarkably, GUS inhibitor also effectively blocks the striking irinotecan-induced bloom of Enterobacteriaceae in immune-deficient mice. In a genetically engineered mouse model of cancer, GUS inhibition alleviates gut damage, improves survival, and does not alter gut microbial composition; however, by allowing dose intensification, it dramatically improves irinotecan's effectiveness, reducing tumors to a fraction of that achieved by irinotecan alone, while simultaneously promoting epithelial regeneration. These results indicate that targeted gut microbial enzyme inhibitors can improve cancer chemotherapeutic outcomes by protecting the gut epithelium from microbial dysbiosis and proliferative crypt damage.

Vancomycin relieves mycophenolate mofetil-induced gastrointestinal toxicity by eliminating gut bacterial β-glucuronidase activity.

Mycophenolate mofetil (MMF) is commonly prescribed and has proven advantages over other immunosuppressive drugs. However, frequent gastrointestinal side effects through an unknown mechanism limit its use. We have found that consumption of MMF alters the composition of the gut microbiota, selecting for bacteria expressing the enzyme β-glucuronidase (GUS) and leading to an up-regulation of GUS activity in the gut of mice and symptomatic humans. In the mouse, vancomycin eliminated GUS-expressing bacteria and prevented MMF-induced weight loss and colonic inflammation. Our work provides a mechanism for the toxicity associated with MMF and a future direction for the development of therapeutics.

Ethylacetate fractional extract of Mentha spicata attenuates irinotecan‐induced mucositis in mice

Irinotecan induced‐mucositis is an inflammatory event of intestine that has negative impact on patient health and affect treatment efficacy. Irinotecan first metabolized in the liver by a carboxylesterase (CES) to the active cytotoxic metabolite (SN‐38), which subsequently glucuronidated by hepatic enzymes to the inactive metabolite SN38G. The SN‐38G undergo deconjugation in the intestine liberating the active SN‐38 via β‐glucuronidase produced by the intestinal bacterial flora. Consequently, SN‐38 triggers inflammation events characterized by delayed intestinal mucositis and diarrhea. This study aims to ameliorate irinotecan‐induced mucositis and diarrhea in mice model using ethylacetate fractional extraction of Mentha spicata(EAEMS), an edible widley consumed plant. Mice model of irinotecan‐induced mucositis and diarrhea produced by I.P injection of irinotecan (75mg/Kg/day) for 4 days. EAEMS administered orally (160mg/kg) twice daily for 7 days starting one day before irinite can dose. Diarrhae scores and mice body weight variation measured to assess the severity of mucositis and diarrhea. Jejunal IL‐1β and MPO measured as markers of intestinal inflammation. β‐glucuronidase activity in fecal pelletes were measured also. Compared to model control mice, results revealed that animals received EAEMS presented with significantly lower diarrhea scores and body weight loss. Furthermore, jejunal IL‐1β and MPO significantly reduced and associated with significant inhibition of fecal β‐glucuronidase activity in animals received EAEMS compared to model control mice. In conclusion, we showed for the first time that EAEMS has a protective effect against irinotecan‐induced mucositis and diarrhea, an effect suggested to be mediated by inhibition of bacterial β‐glucuronidase activity. This promising result might have a therapeutic application in cancer patients suffering from delayed‐onset diarrhea due to irinotecan treatment.Support or Funding InformationUniversity of Baghdad, College of PharmacyThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Intestinal bacterial β-glucuronidase as a possible predictive biomarker of irinotecan-induced diarrhea severity.

Irinotecan is an anticancer drug with a broad spectrum of activity, characterized by multistep and complex pharmacology. Regardless of its schedule of administration, neutropenia and delayed-type diarrhea are the most common side effects. The latter was the dose-limiting toxicity in phase I trials, and its prediction by pharmacogenetic (UGT1A1*28/*28) testing remains sub-optimal. Recent studies have highlighted the important role of the intestinal bacterial β-glucuronidase (BGUS) in the onset of irinotecan-induced diarrhea. Intestinal BGUS hydrolyses glucuronidated metabolites to their toxic form in intestines, resulting in intestinal damage. BGUS selective inhibitors that are currently in development may alleviate irinotecan-induced diarrhea, and may help to reduce its morbidity and enhance its activity. The discussion and description of irinotecan pharmacology may generate ideas that form the basis of clinical trials focusing on a personalized approach to treatment. In addition, we hypothesize that using BGUS activity as a predictive biomarker of irinotecan-induced diarrhea severity will help to select cancer patients for treatment with irinotecan chemotherapy (whether at full or adapted dose).

The effect ofPerilla frutescensleaf on 1, 2-dimethylhydrazine-induced initiation of colon carcinogenesis in rats

In this study, the chemopreventive properties of Perilla frutescens leaf extract (PLE) on rat colon carcinogenesis were investigated during initiation and postinitiation stages. Rats were fed orally by 50 and 500 mg/kg bw of PLE continuously from 1 week before subcutaneously injection of 1,2-dimethylhydrazine (DMH) until the end of experiment. PLE administration reduced the aberrant crypt foci (ACF) number in DMH-treated rats through the inhibition of hepatic cytochrome P4502E1 (CYP2E1) and bacterial β-glucuronidase activity in the colonic lumen. These events led to the reduction of DNA methylation in colonic epithelial cells. For the postinitiation model, rats were injected (s.c.) with DMH, followed by PLE administration until the end of experiment. PLE administration also reduced the ACF number in DMH-induced rats, resulting from apoptosis induction and reduction of proliferation in colon crypt cells. These studies demonstrated that perilla leaf could inhibit ACF formation and progression in DMH-initiated colon carcinogenesis in rats. Practical applications This study revealed the inhibitory effect of PLE on chemical-induced colon carcinogenesis in rats. Altogether, our data supported that PLE acts as a chemopreventive agent for colon cancer. Thus, PLE might be developed as food supplement or functional tea for colon cancer prevention.

Bidirectional interactions between indomethacin and the murine intestinal microbiota.

The vertebrate gut microbiota have been implicated in the metabolism of xenobiotic compounds, motivating studies of microbe-driven metabolism of clinically important drugs. Here, we studied interactions between the microbiota and indomethacin, a nonsteroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenases (COX) -1 and -2. Indomethacin was tested in both acute and chronic exposure models in mice at clinically relevant doses, which suppressed production of COX-1- and COX-2-derived prostaglandins and caused small intestinal (SI) damage. Deep sequencing analysis showed that indomethacin exposure was associated with alterations in the structure of the intestinal microbiota in both dosing models. Perturbation of the intestinal microbiome by antibiotic treatment altered indomethacin pharmacokinetics and pharmacodynamics, which is probably the result of reduced bacterial β-glucuronidase activity. Humans show considerable inter-individual differences in their microbiota and their responses to indomethacin - thus, the drug-microbe interactions described here provide candidate mediators of individualized drug responses.

Ellagitannins and Flavan-3-ols from Raspberry Pomace Modulate Caecal Fermentation Processes and Plasma Lipid Parameters in Rats.

Raspberry pomace is a source of polyphenols, which nutritional and health promoting properties are not sufficiently known. The aim of this 8-weeks study was to scrutinize if raspberry extracts (REs) with different ellagitannins to flavan-3-ols ratios might favorably affect the caecal fermentation processes and blood lipid profile in rats. Forty male Wistar rats were fed with a standard diet or its modification with two types of REs (E1 and E2) characterized by different ratios of ellagitannins to flavan-3-ols (7.7 and 3.1 for E1 and E2, respectively) and added to a diet at two dosages of polyphenolic compounds (0.15 and 0.30% of a diet; L and H treatments, respectively). Irrespective of polyphenols dietary level, both REs reduced the activity of bacterial β-glucuronidase, increased production of butyric acid in the caecum and reduced triacylglycerols in blood plasma. The E1 treatment at both dosages caused more effective reduction in the concentration of ammonia and elevated acetate level in the caecal digesta than E2. On the other hand, only the E2 treatment lowered value of the atherogenic index when compared with control group. When comparing dosages of REs, a higher one was more potent to reduce the activity of bacterial β-glucosidase, β-, α-galactosidase and lowered value of the HDL profile in plasma. To conclude, REs may favorably modulate the activity of the caecal microbiota and blood lipid profile in rats; however, the intensity of these effects may be related to the dosages of dietary polyphenols and to their profile, e.g., ellagitannins to flavan-3-ols ratio.

Purple Rice Extract Supplemented Diet Reduces DMH-Induced Aberrant Crypt Foci in the Rat Colon by Inhibition of Bacterial β-Glucuronidase

Purple rice has become a natural product of interest which is widely used for health promotion. This study investigated the preventive effect of purple rice extract (PRE) mixed diet on DMH initiation of colon carcinogenesis. Rats were fed with PRE mixed diet one week before injection of DMH (40 mg/kg of body weight once a week for 2 weeks). They were killed 12 hrs after a second DMH injection to measure the level of O6-methylguanine and xenobiotic metabolizing enzyme activities. In rats that received PRE, guanine methylation was reduced in the colonic mucosa, but not in the liver, whereas PRE did not affect xenobiotic conjugation, with reference to glutathione-S-transferase or UDP-glucuronyl transferase. After 5 weeks, rats that received PRE with DMH injection had fewer ACF in the colon than those treated with DMH alone. Interestingly, a PRE mixed diet inhibited the activity of bacterial β-glucuronidase in rat feces, a critical enzyme for free methylazoxymethanol (MAM) release in the rat colon. These results indicated that purple rice extract inhibited β-glucuronidase activity in the colonic lumen, causing a reduction of MAM-induced colonic mucosa DNA methylation, leaded to decelerated formation of aberrant crypt foci in the rat colon. The supplemented purple rice extract might thus prevent colon carcinogenesis by the alteration of the colonic environment, and thus could be further developed for neutraceutical products for colon cancer prevention.

Effect of different dietary levels of low-glucosinolate rapeseed (canola) meal and non-starch polysaccharide-degrading enzymes on growth performance and gut physiology of growing turkeys

Zduńczyk, Z., Jankowski, J., Juśkiewicz, J., Mikulski, D. and Slominski, B. A. 2013. Effect of different dietary levels of low-glucosinolate rapeseed (canola) meal and non-starch polysaccharide-degrading enzymes on growth performance and gut physiology of growing turkeys. Can. J. Anim. Sci. 93: 353–362. One-day-old male turkey poults were randomly assigned to eight dietary treatments and were fed diets containing 0, 60, 120, or 180 g kg−1of low-glucosinolate rapeseed meal (RSM) from 1 to 56 d of age without or with a commercial non-starch polysaccharide-degrading enzyme product containing pectinase, cellulase, xylanase, glucanase, mannanase and galactanase activities. There were no significant differences (P&gt;0.05) in body weight and feed conversion ratio between the Control soybean meal-based diet and the diets containing RSM. Overall, the inclusion of up to 180 g kg−1of RSM did not affect the growth performance of turkeys. When compared with the Control treatment, the diet with the lowest RSM content increased the pH of the small intestinal contents and the amounts of cecal digesta. The moderate level of RSM also increased the pH of the small intestinal contents although no increase in the cecal digesta contents was noted. In comparison with other treatments, the highest RSM content increased the content of the small intestinal digesta considerably and decreased the pH of the small intestinal contents to that of the Control treatment. All three dietary levels of RSM significantly reduced the activity of bacterial β-glucuronidase in the ceca. Enzyme supplementation tended to reduce ileal viscosity (P=0.079), decreased ammonia concentration, increased the glycolytic activities of the intestinal microflora enzymes α-glucosidase, α-galactosidase, and β-galactosidase, decreased the activity of β-glucuronidase and increased the growth rate of turkeys.

Physiological effects of chicory root preparations with various levels of fructan and polyphenolic fractions in diets for rats

The experiment was aimed at studying the effects of easily fermentable oligosaccharides and phenolic compounds from chicory root meal (CRM) on the fermentative processes in the caecum, the antioxidative status and the lipoprotein profile of rats. Five different diets were fed ad libitum to 40 Wistar rats (eight animals per group, individually housed): a control group (C); group PCM (10% processed CRM, deprived of polyphenolic fraction); group PCMO (8% processed CRM and 1.6% oligofructose); group UCM (10% unprocessed CRM); and group FP (8.3% fructan-polyphenol concentrate from CRM). Diets PCM, PCMO, UCM and FP induced favourable metabolic changes in the caecum, blood lipid profile and the antioxidative status of the body. In the caecum, the experimental diets increased the production of volatile fatty acids (VFA) and acidification of digesta as well as a decrease in the ammonia concentration and bacterial β-glucuronidase activity. In blood serum, the total cholesterol concentration was reduced and, simultaneously, the proportion of HDL in the total cholesterol concentration was increased. The presence of the polyphenolic fraction in the unprocessed meal (diets UCM and FP) evoked a significant increase in the total antioxidative status in blood serum. Dietary fibre and the polyphenolic fraction present in diet UCM and the FOS-polyphenol concentrate in diet FP did not exhibit an antagonistic activity regarding the physiological parameters analysed, except for in the intensity of caecal fermentation. The results of the experiment point to the benefits of dietary supplementation with chicory preparations containing both prebiotic saccharides and polyphenolic compounds, which enable us to take advantage of the physiological traits of both components.

Effect of the dietary polyphenolic fraction of chicory root, peel, seed and leaf extracts on caecal fermentation and blood parameters in rats fed diets containing prebiotic fructans.

The aim of this 28d experiment was to examine the physiological response of growing rats to a dietary combination of prebiotic chicory fructans, with polyphenols originating from different parts of the chicory plant, i.e. roots, root peels, seeds and leaves. A total of forty rats were assigned to groups fed the following diets characterised by a similar content of oligofructose and inulin: control, with 10% of a root extract (a low level of dietary polyphenols, 0·05%), with 6·5% of a root peel extract (a medium level of dietary polyphenols, 0·107%), with a combination of 8% of a peel extract and 0·8% of a seed extract (a high level of dietary polyphenols, 0·208%) and with 2·5% of a leaf extract (a medium level of dietary polyphenols, 0·106%, with chicoric acid constituting half of them). Chicory seeds are the richest source of polyphenols, especially abundant in dicaffeoylquinic acids. When applied as a dietary supplement, the mixture of monocaffeoylquinic and dicaffeoylquinic acids, from the extracts made of roots, root peels and seeds, elicited more favourable changes in parameters of the antioxidative status of the body and in the activity of bacterial β-glucuronidase in the faeces and caecal digesta. In turn, the extract from chicory leaves, containing considerable quantities of chicoric acid and polyphenolic glycosides, apart from chlorogenic acids, also triggered desirable changes in the lipid profile of the blood serum. The high concentration of polyphenols in the extracts examined enables their application as dietary supplements to be administered in low doses.

Effect of Lactobacillus casei 114001 Probiotic on Bioactivity of Rutin

Male Wistar rats were maintained for 2 weeks on a semisynthetic ration with 0.4% rutin or on the same ration with 0.4% rutin and Lactobacillus casei 11,4001 suspension in physiological saline in a dose of 2 x 10⁹ CFU per rat. Addition of Lactobacillus casei 114001 potentiated biological activity of rutin. Its antioxidant efficiency increased due to more pronounced increase in antioxidant capacity of the plasma, decrease in plasma content of LPO products, and more pronounced increase in reducing activity and antioxidant capacity of the cytosol of the liver and intestinal mucosa. The probiotic sharply increased the capacity of rutin to suppress pro carcinogenic activity of bacterial β-glucuronidase.

The effect of diets containing soybean meal, soybean protein concentrate, and soybean protein isolate of different oligosaccharide content on growth performance and gut function of young turkeys

An experiment was conducted to investigate the effects of diets containing soybean meal (SBM), soybean protein concentrate (SPC), and soybean protein isolate (SPI) on growth performance and gut function of the young turkey. A total of 812 one-day-old male turkey poults were randomly assigned to 4 dietary treatments, with 7 pens per treatment and 29 birds per pen. The 4 experimental diets contained SBM, SBM-SPC, SPC, and SPI and were fed throughout the two 4-wk experimental periods. In each period, the diets were isonitrogenous and isocaloric and contained similar amounts of total and water-soluble nonstarch polysaccharides. The content of oligosaccharides differed among the diets and averaged 2.4, 1.9, 0.9, and 0.1% for SBM, SBM-SPC, SPC, and SPI, respectively. When compared with SBM, birds consuming the SBM-SPC and SPC diets had higher (P < 0.05) final BW (4.32 vs. 4.45 and 4.46 kg, respectively). Incorporation of SPI as a substitute for SBM resulted in improved (P < 0.05) feed utilization (from 1.76 to 1.67) but did not affect the final BW. Significant changes in cecal concentrations of short-chain fatty acids were observed and averaged 130, 103, and 89 μmol/g of digesta for the SBM, SBM-SPC, and SPC diets, respectively. This coincided with the proportional decrease in dietary oligosaccharide content (from 2.4 to 0.9%) and was further substantiated by a significant decrease in ileum weights. Feeding the SPI diet resulted in the lowest ileal and cecal tissue weights as well as the lowest cecal short-chain fatty acids concentration. There was no effect of diet on digesta pH, viscosity, and mucosal sucrase and maltase activities. Bacterial β-glucuronidase activity was decreased (P = 0.08) in the cecum (from 0.98 to 0.60 U/g) with decreased dietary oligosaccharide content. In conclusion, partial or almost complete substitution of SBM with SPC suppressed the fermentation processes in the ceca but enhanced the growth rate. Substitution of SBM with SPI significantly improved feed utilization but decreased BW of 4-wk-old turkeys with no effect on growth rate of older 8-wk-old birds.

Lupin kernel fibre foods improve bowel function and beneficially modify some putative faecal risk factors for colon cancer in men

Consumption of some dietary fibres may benefit bowel health; however, the effect of Australian sweet lupin (Lupinus angustifolius) kernel fibre (LKFibre) is unknown. The present study examined the effect of a high-fibre diet containing LKFibre on bowel function and faecal putative risk factors for colon cancer compared to a control diet without LKFibre. Thirty-eight free-living, healthy men consumed an LKFibre and a control diet for 1 month each in a single-blind, randomized, crossover study. Depending on subject energy intake, the LKFibre diet was designed to provide 17-30 g/d fibre (in experimental foods) above that of the control diet. Bowel function self-perception, frequency of defecation, transit time, faecal output, pH and moisture, faecal levels of SCFA and ammonia, and faecal bacterial beta-glucuronidase activity were assessed. In comparison to the control diet, the LKFibre diet increased frequency of defecation by 0.13 events/d (P=0.047), increased faecal output by 21 % (P=0.020) and increased faecal moisture content by 1.6 % units (P=0.027), whilst decreasing transit time by 17 % (P=0.012) and decreasing faecal pH by 0.26 units (P<0.001). Faecal butyrate concentration was increased by 16 % (P=0.006), butyrate output was increased by 40 % (P=0.002) and beta-glucuronidase activity was lowered by 1.4 micromol/h per g wet faeces compared to the control diet (P<0.001). Addition of LKFibre to the diet incorporated into food products improved some markers of healthy bowel function and colon cancer risk in men.

Lactulose-induced diarrhoea in rats: effects on caecal development and activities of microbial enzymes

The intake of large amounts of lactulose and other non-digestible oligosaccharides can cause diarrhoea in rats and humans. The purpose of our study was to estimate tendency and scope of changes in caecum development, amount and composition of caecal digesta and activity of caecal microbial enzymes under the influence of lactulose-rich diet evoking or not evoking diarrhoea. Male Wistar rats were fed on 8%-lactulose diet for 4 weeks. Feeding with lactulose induced enlargement of the caecum (digesta and wall) compared to the control group. However, the hypertrophy of the caecal wall in rats with diarrhoea was less than in these without that ailment. Dry matter of caecal digesta was significantly decreased in rats with diarrhoea. Diarrhoea lowered concentrations of enzymatic protein and short-chain fatty acids in the caecum, and the activity of bacterial β-glucuronidase, α- and β-galactosidase, α- and β-glucosidase in caecal digesta, compared to rats without diarrhoea. The ammonia concentration in the caecum was enhanced by diarrhoea symptoms. Occurrence of diarrhoea significantly deteriorated functioning of the caecal ecosystem what in turn limited potential benefits of diet supplementation with lactulose.