Research characterising the gut microbiota in different populations and diseases has mushroomed since the advent of next-generation sequencing techniques. However, there has been less emphasis on the impact of dietary fibres and other dietary components that influence gut microbial metabolic activities. Dietary fibres are the main energy source for gut bacteria. However, fibres differ in their physicochemical properties, their effects on the gut and their fermentation characteristics. The diversity of carbohydrates and associated molecules in fibre-rich foods can have a major influence on microbiota composition and production of bioactive molecules, for example SCFAs and phenolic acids. Several of these microbial metabolites may influence the functions of body systems including the gut, liver, adipose tissues and brain. Dietary fibre intake recommendations have recently been increased (to 30 g daily) in response to growing obesity and other health concerns. Increasing intakes of specific fibre and plant food sources may differentially influence the bacteria and their metabolism. However, in vitro studies show great individual variability in the response of the gut microbiota to different fibres and fibre combinations, making it difficult to predict which foods or food components will have the greatest impact on levels of bioactive molecules produced in the colon of individuals. Greater understanding of individual responses to manipulation of the diet, in relation to microbiome composition and production of metabolites with proven beneficial impact on body systems, would allow the personalised approach needed to best promote good health.

Certain purified indigestible carbohydrates such as inulin have been shown to stimulate gut-derived hormones involved in glycaemic regulation and appetite regulation, and to counteract systemic inflammation through a gut microbiota-mediated mechanism. Less is known about the properties of indigestible carbohydrates intrinsic to food. The aim of this study was to investigate the possibility to affect release of endogenous gut hormones and ameliorate appetite control and glycaemic control by ingestion of a whole-grain cereal food product rich in NSP and resistant starch in healthy humans. In all, twenty middle-aged subjects were provided with a barley kernel-based bread (BB) or a reference white wheat bread during 3 consecutive days, respectively, in a randomised cross-over design study. At a standardised breakfast the following day (day 4), blood was collected for the analysis of blood (b) glucose regulation, gastrointestinal hormones, markers of inflammation and markers of colonic fermentation; 3 d of intervention with BB increased gut hormones in plasma (p) the next morning at fasting (p-glucagon-like peptide-1; 56 %) and postprandially (p-glucagon-like peptide-2; 13 % and p-peptide YY; 18 %). Breath H2 excretion and fasting serum (s) SCFA concentrations were increased (363 and 18 %, respectively), and b-glucose (22 %) and s-insulin responses (17 %) were decreased after BB intervention. Insulin sensitivity index (ISIcomposite) was also improved (25 %) after BB. In conclusion, 3 d of intervention with BB increased systemic levels of gut hormones involved in appetite regulation, metabolic control and maintenance of gut barrier function, as well as improved markers of glucose homoeostasis in middle-aged subjects, altogether relevant for the prevention of obesity and the metabolic syndrome.

In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2- or FFAR3-deficient animal models suggest that SCFA-mediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.

Wheat bran extract (WBE), containing arabinoxylan-oligosaccharides that are potential prebiotic substrates, has been shown to modify bacterial colonic fermentation in human subjects and to beneficially affect the development of colorectal cancer (CRC) in rats. However, it is unclear whether these changes in fermentation are able to reduce the risk of developing CRC in humans. The aim of the present study was to evaluate the effects of WBE on the markers of CRC risk in healthy volunteers, and to correlate these effects with colonic fermentation. A total of twenty healthy subjects were enrolled in a double-blind, cross-over, randomised, controlled trial in which the subjects ingested WBE (10 g/d) or placebo (maltodextrin, 10 g/d) for 3 weeks, separated by a 3-week washout period. At the end of each study period, colonic handling of NH3 was evaluated using the biomarker lactose[15N, 15N′]ureide, colonic fermentation was characterised through a metabolomics approach, and the predominant microbial composition was analysed using denaturing gradient gel electrophoresis. As markers of CRC risk, faecal water genotoxicity was determined using the comet assay and faecal water cytotoxicity using a colorimetric cell viability assay. Intake of WBE induced a shift from urinary to faecal 15N excretion, indicating a stimulation of colonic bacterial activity and/or growth. Microbial analysis revealed a selective stimulation of Bifidobacterium adolescentis. In addition, WBE altered the colonic fermentation pattern and significantly reduced colonic protein fermentation compared with the run-in period. However, faecal water cytotoxicity and genotoxicity were not affected. Although intake of WBE clearly affected colonic fermentation and changed the composition of the microbiota, these changes were not associated with the changes in the markers of CRC risk.

Lactose malabsorption is associated with rapid production of high levels of osmotic compounds, such as organic acids and SCFA in the colon, suspected to contribute to the onset of lactose intolerance. Adult rats are lactase deficient and the present study was conducted to evaluate in vivo the metabolic consequences of acute lactose ingestion, including host–microbiota interactions. Rats received diets of 25 % sucrose (S25 control group) or 25 % lactose (L25 experimental group). SCFA and lactic acid were quantified in intestinal contents and portal blood. Expression of SCFA transporter genes was quantified in the colonic mucosa. Carbohydrate oxidation (Cox) and lipid oxidation (Lox) were computed by indirect calorimetry. Measurements were performed over a maximum of 13 h. Time, diet and time × diet variables had significant effects on SCFA concentration in the caecum (P< 0·001, P= 0·004 and P= 0·007, respectively) and the portal blood (P< 0·001, P= 0·04 and P< 0·001, respectively). Concomitantly, expression of sodium monocarboxylate significantly increased in the colonic mucosa of the L25 group (P= 0·003 at t= 6 h and P< 0·05 at t= 8 h). During 5 h after the meal, the L25 group's changes in metabolic parameters (Cox, Lox) were significantly lower than those of the S25 group (P= 0·02). However, after 5 h, L25 Cox became greater than S25 (P= 0·004). Thus, enhanced production and absorption of SCFA support the metabolic changes observed in calorimetry. These results underline the consequences of acute lactose malabsorption and measured compensations occurring in the host's metabolism, presumably through the microbiota fermentations and microbiota–host interactions.

High cereal fibre intake is associated with reduced risk for type 2 diabetes, but wheat fibre had little or no effect on glycaemic control or oral glucose tolerance in clinical trials lasting 4–12 weeks. To explain this discrepancy, we hypothesised that colonic adaptation to increased wheat fibre intake takes many months but eventually results in increased SCFA production and glucagon-like peptide-1 (GLP-1) secretion. Thus, the primary objective was to determine the time-course of the effects of increased wheat fibre intake on plasma acetate, butyrate and GLP-1 concentrations in hyperinsulinaemic human subjects over 1 year. Subjects with fasting plasma insulin ≥ 40 pmol/l were randomly assigned by computer to receive either a high-wheat fibre cereal (fibre group; 24 g fibre/d; twenty assigned; six dropped out, fourteen included) or a low-fibre cereal (control group; twenty assigned; six dropped-out, fourteen included) daily for 1 year. Acetate, butyrate and GLP-1 were measured during 8 h metabolic profiles performed every 3 months. There were no differences in body weight in the fibre group compared with the control group. After 9 months baseline-adjusted mean 8 h acetate and butyrate concentrations were higher on the high-fibre than the control cereal (P < 0·05). After 12 months on the high-fibre cereal, baseline-adjusted mean plasma GLP-1 was 1·3 (95 % CI 0·4, 2·2) pmol/l (P < 0·05) higher than at baseline (about 25 % increase) and 1·4 (95 % CI 0·1, 2·7) pmol/l (P < 0·05) higher than after 12 months on control. It is concluded that wheat fibre increased SCFA production and GLP-1 secretion in hyperinsulinaemic humans, but these effects took 9–12 months to develop. Since GLP-1 may increase insulin sensitivity and secretion, these results may provide a mechanism for the epidemiological association between high cereal fibre intake and reduced risk for diabetes.

The fermentation of starch in vitro produces a higher proportion of butyrate than the fermentation of most other substrates. The α-glucosidase inhibitor acarbose increases the amount of starch entering the colon, and has been shown to increase faecal butyrate in humans. It is generally considered that colonic butyrate is quantitatively removed by the colonic mucosa and liver and does not appear in peripheral blood. However, studies in animals suggest that a small proportion of colonic butyrate reaches peripheral blood. Thus, we hypothesised that an increase in colonic butyrate production would result in a rise in serum butyrate in human subjects. To test this, subjects with impaired glucose tolerance were randomly treated in a double-blind fashion with placebo (n 11) or acarbose (n 11) (100 mg three times per day). Serum short-chain fatty acid concentrations were measured twelve times over 12 h with subjects eating a standard diet before randomization and after 4 months of therapy. At baseline, 12 h mean serum butyrate concentrations were similar in the placebo and acarbose groups (2·8 (SE 0·7) AND 3·3 (se 0·6) μm, respectively). After 4 months on placebo, mean serum butyrate (2·6 (se 0·5) μm) was no different from baseline. However, after 4 months on acarbose, serum butyrate had increased to 4·2 (se 1·0) μm, a value which differed significantly from both the baseline value in the acarbose group and the treatment value in the placebo group. We conclude that acarbose increased serum butyrate in subjects with impaired glucose tolerance. These results support the hypothesis that increased colonic butyrate production in human subjects can be detected by an increase in serum butyrate.

Some data suggest that the colonic microflora may adapt to produce more butyrate if given time and the proper substrate. To test this hypothesis, we investigated the effect of prolonged feeding of resistant potato starch on butyrate production. Rats were fed on either a low-fibre diet (basal) or the same diet supplemented with 90 g resistant potato starch/kg (PoS) for 0·5, 2 and 6 months. Short-chain fatty acid (SCFA) concentrations were determined in caecal and colonic contents at the end of each ingestion period. Total SCFA concentration increased over time throughout the caecocolonic tract with PoS, but was not modified with the basal diet. While propionate concentration was unchanged, butyrate concentration was highly increased by PoS at each time period in both the caecum and colon. Moreover, the butyrogenic effect of PoS increased over time, and the amount of butyrate was increased 6-fold in the caecum and proximal colon and 3-fold in the distal colon after 6 months compared with 0·5 months. Accordingly, the ratio butyrate: - total SCFA increased over time throughout the caecocolonic tract (12·6 (SE 2·8) v. 28 (SE 1·8) % in the caecum, 10·5 (SE 1·4) v. 26·8 (SE 0·9) % in the proximal colon, and 7·3 (SE 2·4) v. 23·9 (SE 2·7) % in the distal colon at 0·5 v. 6 months respectively), while the proportion of acetate decreased. Neither the proportion nor the concentration of butyrate was modified over time with the basal diet. Butyrate production was thus promoted by long-term ingestion of PoS, from the caecum towards the distal colon, which suggests that a slow adaptive process occurs within the digestive tract in response to a chronic load of indigestible carbohydrates.

We studied the effects of a fermentable sugar-alcohol (lactitol) on the concentrations of enteroglucagon and gastrin in the blood of rats for 7·5 h after feeding. The control and treatment groups were fed on semi-purified diets containing either non-fermentable cellulose or lactitol respectively, at 100 g/kg. Compared with the cellulose-fed group, the animals fed with lactitol had higher levels of enteroglucagon (5−10 times higher than control; P < 0·05) and lower serum gastrin (70−80% of control; P< 0.·05) for several hours after the withdrawal of feed. In contrast, varying the level of dietary lipid (maize oil) over a range of 8−120 g/kg had no effect on the release of either peptide. These results suggest that poorly absorbed fermentable dietary carbohydrate stimulates postprandial plasma enteroglucagon and inhibits serum gastrin release in the rat. The mechanism is uncertain but an endocrine response by the colon to fermentation products seems probable.

Low- and intermediate-molecular-weight polyphenols are usually extracted by using different solvents (e.g. water, methanol, aqueous acetone). The aim of the present work was to study the possible effects of some extractable polyphenols (EPP) on fat and protein digestibilities and on the colonic microflora. Degradability of these compounds through the intestinal tract was also studied. Catechin and tannic acid (TA) were chosen as representatives of the most common basic structures of EPP (flavonoids and gallic acid respectively). Three groups of eight male Wistar rats were given either a control diet free of EPP, or diets containing 20 g/kg dry matter of catechin and TA. Body-weight and food intake were monitored during a 3-week experimental period. Faeces and urine were collected daily during the third experimental week. EPP and fat were determined in faeces, and N in both urine and faeces. Only 3.1 and 4.6% of the ingested catechin and TA respectively were excreted in faeces, indicating that absorption and/or degradation of these EPP had occurred. HPLC analysis of the poly phenolic content of faeces showed qualitative differences between groups. A significant increase of total faecal weight as well as water, fat and N excretion was produced by TA. Catechin only caused an increase in fat excretion. In vitro fermentation assays were also performed to study the effect of EPP on the colonic microflora. Both catechin and TA affected the yield of end-products of fermentation, and were also degraded during the fermentation process.

The effect of eating chocolate containing sugar alcohols as sweetening agents on colonic fermentation has been investigated by monitoring breath H2 levels. Levels were compared with those occurring after the consumption of normal, sugar-containing chocolate. Ten healthy volunteers aged 19 to 21 years ingested equal amounts of either sorbitol, isomalt or sucrose incorporated into standard chocolate bars. Breath H2 levels after consumption of chocolate containing either sorbitol or isomalt were significantly higher than those after consumption of chocolate containing sucrose (P < 0.001). After consumption of chocolate containing sorbitol, double the mean estimated volume of breath H2 was produced over 6 h compared with that produced after eating chocolate containing isomalt. Taken together with results relating to the incidence of intolerance symptoms, these findings demonstrate that sorbitol is associated with greater colonic fermentation compared with isomalt.