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The effects of live yeast (LY) and mannan-oligosaccharide (MOS) supplementation on intestinal disruption induced by Escherichia coli in broilers were investigated. The experimental design was a 3×2 factorial arrangement with three dietary treatments (control, 0·5 g/kg LY (Saccharomyces cerevisiae, 1·0×1010 colony-forming units/g), 0·5 g/kg MOS) and two immune treatments (with or without E. coli challenge from 7 to 11 d of age). Samples were collected at 14 d of age. The results showed that E. coli challenge impaired (P<0·05) growth performance during the grower period (1-21 d) and the overall period (1-35 d) of broilers, increased (P<0·05) serum endotoxin and diamine oxidase levels coupled with ileal myeloperoxidase and lysozyme activities, whereas reduced (P<0·05) maltase activity, and compromised the morphological structure of the ileum. Besides, it increased (P<0·05) the mRNA expressions of several inflammatory genes and reduced occludin expression in the ileum. Dietary treatment with both LY and MOS reduced (P<0·05) serum diamine oxidase and ileal myeloperoxidase levels, but elevated villus height (P<0·10) and the ratio of villus height:crypt depth (P<0·05) of the ileum. It also alleviated (P<0·05) E. coli-induced increases (P<0·05) in ileal Toll-like receptor 4, NF-κ B and IL-1 β expressions. Moreover, LY supplementation reduced (P<0·05) feed conversion ratio of birds during the grower period and enhanced (P<0·05) the community diversity (Shannon and Simpson indices) of ileal microbiota, whereas MOS addition counteracted (P<0·05) the decreased ileal IL-10 and occludin expressions in challenged birds. In conclusion, both LY and MOS supplementation could attenuate E. coli-induced intestinal disruption by alleviating intestinal inflammation and barrier dysfunction in broilers. Moreover, LY addition could improve intestinal microbial community structure and feed efficiency of broilers.

The inhibition of the attachment of bacteria to the intestine by receptor analogues could be a novel approach to prevent enterotoxigenic Escherichia coli (ETEC) K88-induced diarrhoea in piglets. The objective of the present study was to screen the ability of different feed ingredients (FI) to bind to ETEC K88 (adhesion test, AT) and to block its attachment to the porcine intestinal mucus (blocking test, BT) using in vitro microtitration-based models. In the AT, wheat bran (WB), casein glycomacropeptide (CGMP) and exopolysaccharides exhibited the highest adhesion to ETEC K88 (P< 0·001). In the BT, WB, CGMP and locust bean (LB) reduced the number of ETEC K88 attached to the intestinal mucus (P< 0·001). For WB and LB, fractionation based on their carbohydrate components was subsequently carried out, and each fraction was evaluated individually. None of the WB fractions reduced the adhesion of ETEC K88 to the mucus as did the original extract, suggesting that a protein or glycoprotein could be involved in the recognition process. With regard to the LB fractions, the water-extractable material reduced the adhesion of ETEC K88 (P< 0·001) to the mucus similar to the original extract (P< 0·001), indicating, in this case, that galactomannans or phenolic compounds could be responsible for the recognition process. In conclusion, among the FI screened, the soluble extracts obtained from WB, LB and CGMP exhibited the highest anti-adhesive properties against ETEC K88 in the BT. These results suggest that they may be good candidates to be included in diets of weaned piglets for the prevention of ETEC K88-induced diarrhoea.

A diet rich in fibre seems to protect against the metabolic syndrome (MetS), but there is scarce information about the role of fibre intake in patients with the MetS and diabetes. The aim of the present study was to evaluate the effects of soluble fibre from partially hydrolysed guar gum (PHGG) on the MetS and cardiovascular risk factors in patients with type 2 diabetes. In the present randomised controlled clinical trial, forty-four patients with type 2 diabetes (males 38·6 %, age 62 (SD 9) years, diabetes duration 14·2 (SD 9·6) years) and the MetS underwent clinical, laboratory and dietary evaluations at baseline, 4 and 6 weeks. All patients followed their usual diet and the intervention group (n 23) received an additional 10 g/d of PHGG. In the intervention group, waist circumference (WC), glycated Hb (HbA1c), 24 h urinary albumin excretion (UAE) and serum trans-fatty acids (FA) were reduced in comparison with baseline after 4 and 6 weeks: WC 103·5 (SD 9·5) to 102·1 (SD 10) to 102·3 (SD 9·7) cm; HbA1c 6·88 (SD 0·99) to 6·64 (SD 0·94) to 6·57 (SD 0·84) %; 24 h UAE 6·8 (interquartile range 3·0-17·5) to 4·5 (interquartile range 3·0-10·5) to 6·2 (interquartile range 3·0-9·5) mg; trans-FA 71 (interquartile range 46-137) to 67 (interquartile range 48-98) to 57 (interquartile range 30-110) mg/l (P< 0·05 for all). The only change in the control group was weight reduction: 77·0 (SD 13·5) to 76·2 (SD 13·3) to 76·1 (SD 13·4) kg (P= 0·005). Other MetS components (blood pressure, TAG, HDL-cholesterol, fasting plasma glucose), total and LDL-cholesterol, C-reactive protein and endothelin-1 did not change in either group. In patients with type 2 diabetes and the MetS, the addition of PHGG to the usual diet improved cardiovascular and metabolic profiles by reducing WC, HbA1c, UAE and trans-FA.

Konjac glucomannan (KGM) has been shown to increase human colon microbial ecology and reduce faecal toxicity in mice. The main goal of the present study was to assess the effects of a KGM supplement into a low-fibre diet on precancerous markers of colon cancer in a double-blind, placebo- and diet-controlled study. Adult volunteers consumed defined diets supplemented with konjac (4·5 g/d) or placebo (maize starch) for 4 weeks. Stools collected before and at the end of the supplementation were analysed for β-glucosidase, β-galactosidase and β-glucuronidase activities, microflora and bile acids. Faecal water was co-incubated with Caco-2 cells, a model of human colonocytes, to determine the cytotoxicity and DNA-damaging effect as assessed by the comet assay. The results indicated that the KGM supplement significantly decreased faecal β-glucuronidase activity by 25·6 (se 7·8) % and faecal secondary bile acid level by 42·4 (se 11·8) %. In contrast, consuming the defined diet supplemented with placebo for 4 weeks did not improve these determinants. The KGM-supplemented diet, but not the placebo diet, significantly increased the survival rate (%) of Caco-2 cells co-incubated with faecal water for 1 and 3 h, respectively. In addition, KGM significantly reduced the DNA damage induced by the faecal water alone or in combination with H2O2. The faecal bifidobacteria and lactobacilli levels increased only with the KGM-supplemented diet. Therefore, we conclude that supplementation of KGM into a low-fibre diet improved the faecal microbial ecology and metabolites, which may contribute to the reduced toxicity of faecal water and precancerous risk factors of human colon cancer.

The effect of a high-fibre bread mixed with guar-gum (75 g/kg flour) on serum glucose, connecting peptide (C-peptide), haemoglobin A1 (HbA1), high-density-lipoprotein-cholesterol (HDL-cholesterol) and triglycerides was examined in fourteen elderly patients with diabetes mellitus type II. The mean daily consumption of guar gum was 8.1 g. Gastrointestinal disorders were not observed. Consumption of guar-gum bread resulted in a significant decrease in C-peptide values on the 1st day and blood glucose values after 3 weeks (both measured 90 min after breakfast). C-peptide values remained low, while an unaccountable 'rebound' phenomenon was seen in the blood glucose values 90 min after breakfast at the end of the study. No significant change was seen in respect to HDL-cholesterol and triglycerides. However, a small significant increase in HbA1 was noted.

The effect of a palatable granulated guar-gum preparation (10 g twice daily) was studied in obese subjects. The acute effect of a single dose of guar gum to reduce the peak postprandial whole blood glucose levels (about 10%) was verified. Following long-term treatment, a further reduction was seen in the obese subjects with the highest postprandial glucose levels. Since the postprandial plasma insulin levels were essentially unchanged, this finding suggested an increased responsiveness to insulin. Total serum cholesterol levels were significantly reduced following long-term treatment but serum alpha-cholesterol levels, representing the high-density-lipoprotein fraction, was unchanged. Body-weight was significantly reduced during guar-gum treatment even though the patients were asked to maintain their normal dietary habits. Daily hunger ratings recorded for up to 10 weeks showed that guar gum reduced hunger significantly better than commercially available bran taken in the same way. Thus, guar gum seemed to influence carbohydrate and lipid metabolism in a beneficial way in obese subjects. The reduction in hunger would offer an additional benefit to these patients.