Comparative Effects of Cellulose and Soluble Fibers (Pectin, Konjac Glucomannan, Inulin) on Fecal Water Toxicity toward Caco-2 Cells, Fecal Bacteria Enzymes, Bile Acid, and Short-Chain Fatty Acids

Abstract

The aim of this study was to compare the effects of cellulose and three soluble dietary fibers, pectin, konjac glucomannan (KGM), and inulin, on the cytotoxicity and DNA damage of fecal water-treated Caco-2 cells, a human colon adenocarcinoma cell line, and to investigate the fecal components that potentially modulate the fecal toxicity, that is, bacterial enzymes, bile acids, and short-chain fatty acids. Six-week-old BALB/cJ mice were randomly allocated to consume an AIN-93 diet that contained no dietary fiber (fiber-free) or 5% (w/w) cellulose, pectin, KGM, and inulin for 3 weeks. Feces were collected during days 18-21. Fecal waters were co-incubated with Caco-2 cells to determine the cytotoxicity and DNA damage. In addition, the fecal bacterial enzymes, bile acids, and short-chain fatty acids were determined. Results indicated that all fiber diets similarly increased the survival rate (%) of fecal water-treated Caco-2 cells as compared with the fiber-free diet. The inhibition of fecal water-induced DNA damage in Caco-2 cells was greater for the pectin and inulin diets than for the cellulose and KGM diets. In contrast, cellulose exerted the greatest inhibitory effect on the fecal β-glucuronidase activity. Cellulose and all soluble dietary fibers reduced the secondary bile acid concentrations in the fecal water, but only soluble fibers increased the fecal concentrations of short-chain fatty acids, as compared with no fiber. Therefore, this study suggests that all dietary fibers substantially reduced the fecal water toxicity, which is associated with decreased secondary bile acid levels by all fibers, reduced fecal β-glucuronidase activity by cellulose, and increased short-chain fatty acid levels by soluble dietary fibers.

Konjac glucomannan polysaccharide and inulin oligosaccharide enhance the colonic mucosal barrier function and modulate gut-associated lymphoid tissue immunity in C57BL/6J mice

“…Butyrate, which is the major fuel for colonocytes and stimulates colonocyte differentiation and normal proliferation (25,26) , could play an important role. The present study and previous studies (2,14,27) did indicate that KGM and inulin oligosaccharide significantly increased the faecal butyrate concentration, which could in turn increase the mucosal layer thickness.…”

“…Faecal SCFA Aliquots (0•5 g) of faecal composites were analysed for acetate, propionate and n-butyrate with 4-methyl-n valeric acid as an internal standard by the method described previously (14) . The SCFA extracted using ether from faecal samples were injected onto a GC (GC-2014; Shimadzu) fitted with a glass capillary column (0•25 mm, 30 m Stabilwax-DA; Restek Corp.) and a flame ionisation detector.…”

“…The fraction of inulin with the degree of polymerisation lower than 10, namely, inulin oligosaccharide, is widely used as a supplement in functional food. Both KGM and inulin oligosaccharide have been shown to increase the production of SCFA and stimulate the growth of bifidobacteria and lactobacilli in animal/human studies (13)(14)(15) . However, the effects of these soluble fibres on the mucosal barrier function have not been determined, which need to be determined in animal models, so that the histology of mucosal layer could be clearly observed.…”

Beneficial health characteristics of native and hydrolysed konjac (Amorphophallus konjac) glucomannan

“…There are limited reports comparing the microbial fermentation of konjac glucomannan with other dietary fibres. These reports do, however, include in vitro , animal and human trials.…”

An investigation of the relationship between dietary fiber, fecal bacterial composition, and colon cancer

“…Butyric acid is the primary fuel used by normal colonocytes. It appears to play an important role in gene expression, cell cycle and apoptosis in colon epithelial cells (Wang et al 2006;Chen et al 2010). It's protective role in human colon cancer is thought to be through an inhibition o f histone deacetylase and a promotion o f apoptosis (Lupton 2004).…”