Non-infectious diseases such as CHD and certain cancers have become major causes of death and disability in affluent countries. Probiotics (principally lactic acid bacteria; LAB) may assist in lowering the risk of these diseases. Experimental studies with probiotics have given generally inconclusive outcomes for infectious disease and for biomarkers for non-infectious disease. In part this situation may reflect their inability to colonise the adult human gut effectively. Prebiotics can assist in promoting colonisation, and resistant starch (RS), as a high-amylose starch, is a prebiotic and synbiotic. This starch exerts its synbiotic action through adhesion of the bacteria to the granule surface. Consumption of RS assists in recovery from infectious diarrhoea in man and animals. A rice porridge, high in RS, appears to modify the autochthonous porcine large-bowel microflora favourably through lowering Escherichia coli and coliform numbers. Many of the beneficial effects of RS on large-bowel function appear to beexerted through short-chain fatty acids (SCFA) formed by bacterial fermentation. In man LAB are found in relatively highest numbers in milk-fed infants where theprofile of fermentation products differs quite markedly from that in adults. It appearsunlikely that ingestion of current probiotics will alter either total SCFA or the proportions of the major acids. More emphasis needs to be given to the investigation of the effects of complex carbohydrates, including RS, on the autochthonous microflora of the human large bowel.

Maize starch was acylated with acetic, propionic or butyric anhydride to produce the corresponding acylated starch. In the first experiment, butyrylated starch at a degree of substitution (DS) of 0.25 (i.e., 1 acyl unit per 4 glucosyl units) was fed to rats for 3 d. Cecal and distal colonic SCFA concentrations were 170 and 78% higher, respectively, in rats fed the butyrylated starch. However, the greatest increase was in butyrate with corresponding increases of 460 and 212%. Subsequently, acetylated, propionylated or butyrylated starches with DS of ∼0.18 were prepared on a larger scale. Body weight gain did not differ between rats fed these acylated starches or a control starch for 14 d. Large bowel pH was significantly lower and digesta mass significantly higher throughout the large bowel in rats fed the acylated starches. Cecal + distal colonic starch averaged 12 mg in rats fed the control starch and 103, 134 and 135 (pooled SEM = 6) mg in rats fed acetylated, propionylated or butyrylated starch, respectively. Large bowel SCFA concentrations and pools were significantly higher in rats fed the three acylated starches and were disproportionately greater in the SCFA that had been esterified to the starch. In the cecum, acetate, propionate and butyrate pools were 280, 690 and 1060% higher, respectively, in rats fed the corresponding acylated starch than in those fed the control diet. In the distal colon, the corresponding increases were 320, 940 and 1370%. These data indicate that acylated starches are resistant starch (RS) and raise large bowel SCFA, apparently through bacterial release of the esterified fatty acid and fermentation of the residual starch.

Propolis has abundant polyphenolic constituents and is used widely as a health/functional food. Here, we investigated the effects of polyphenol-rich propolis extracts (PPE) on intestinal barrier function in human intestinal epithelial Caco-2 cells, as well as in rats. In Caco-2 cells, PPE increased transepithelial electrical resistance and decreased lucifer yellow flux. PPE-treated cells showed increased expression of the tight junction (TJ) loci occludin and zona occludens (ZO)-1. Confocal microscopy showed organized expressions in proteins related to TJ assembly, i.e., occludin and ZO-1, in response to PPE. Furthermore, PPE led to the activation of AMPK, ERK1/2, p38, and Akt. Using selective inhibitors, we found that the positive effects of PPE on barrier function were abolished in cells in which AMPK and ERK1/2 signaling were inhibited. Moreover, rats fed a diet supplemented with PPE (0.3% in the diet) exhibited increased colonic epithelium ZO-1 expression. Overall, these data suggest that PPE strengthens intestinal barrier function by activating AMPK and ERK signaling and provide novel insights into the potential application of propolis for human gut health.

Resistant starch (RS), fed as high amylose maize starch (HAMS) or butyrylated HAMS (HAMSB), opposes dietary protein-induced colonocyte DNA damage in

Propolis is an important hive product and considered beneficial to health. However, evidence of its potential for improving gut health is still lacking. Here we use rats to examine whether dietary supplementation with propolis could be used as a therapy for ulcerative colitis. Rats were fed with a Western style diet alone (controls) or supplemented with different amounts of Chinese propolis (0.1%, 0.2%, and 0.3%) to examine effects on acute colitis induced by 3% dextran sulphate sodium (DSS) in drinking water. Propolis at 0.3%, but not lower levels, significantly improved colitis symptoms compared with the control group, with a less pronounced disease activity index (DAI) (p < 0.001), a significant increase in colon length/weight ratio (p < 0.05) and an improved distal colon tissue structure as assessed by histology. Although short chain fatty acid levels in digesta were not altered by propolis supplementation, 16S rRNA phylogenetic sequencing revealed a significant increase in gut microbial diversity after 21 days of 0.3% propolis supplementation compared with controls including a significant increase in bacteria belonging to the Proteobacteria and Acidobacteria phyla. This is the first study to demonstrate that propolis can attenuate DSS-induced colitis and provides new insight into diet-microbiota interactions during inflammatory bowel disease.