Diversion of the faecal stream is associated with diversion colitis (DC). Preliminary studies indicate that microbiome dysbiosis contributes to its development and potentially treatment. This review aims to characterise these changes in the context of faecal diversion and identify their clinical impact. A systematic search was conducted using MEDLINE, EMBASE and CENTRAL databases using a predefined search strategy identifying studies investigating changes in microbiome following diversion. Findings reported according to PRISMA guidelines. Of 743 results, 6 met inclusion criteria. Five reported significantly decreased microbiome diversity in the diverted colon. At phylum level, decreases in Bacillota with a concomitant increase in Pseudomonadota were observed, consistent with dysbiosis. At genus level, studies reported decreases in beneficial lactic acid bacteria which produce short-chain fatty acid (SCFA), which inversely correlated with disease severity. Significant losses in commensals were also noted. These changes were seen to be partially reversible with restoration of bowel continuity. Changes within the microbiome were reflected by histopathological findings suggestive of intestinal dysfunction. Faecal diversion is associated with dysbiosis in the diverted colon which may have clinical implications. This is reflected in loss of microbiome diversity, increases in potentially pathogenic-associated phyla and reduction in SCFA-producing and commensal bacteria.

Colonic fermentation of organic matter to short-chain fatty acids has been implicated in the improvement in insulin sensitivity achieved by feeding diets rich in complex carbohydrates. The present study assessed the potential role of the colon in determining postprandial glucose kinetics. Metabolic responses to a complex-carbohydrate test meal were determined in conjunction with a primed continuous infusion of D-[6,6-2H]glucose in a group of ileostomists and sex-matched controls. Glucose disposal (GD) was computed using non-steady-state kinetics on a single compartment model. Insulin sensitivity was derived using cumulative GD as the dependent variable, and time and the integrated insulin concentration as independent variables. The ileostomist group had a significantly higher postprandial plasma insulin concentration (P=0·034) compared with the control group, but no difference in the plasma glucose concentration. Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0·46 v. 0·13 mg glucose/min per pmol, P=0·015). The ileostomist group also showed a 50 % lower rate of glucose oxidation in the postprandial period (P=0·005), although the rate of non-oxidative GD was not significantly affected. The present study indicates that loss of the colon is associated with several characteristics of the insulin resistance syndrome, and favours a view that the colon has a role in the control of postprandial glucose.

This study investigated how readily achievable changes to the quantity and processing of starchy foods in a typical Western diet: (1) were reflected in levels of resistant starch (RS) and NSP excreted from the small intestine; and (2) more favourable profiles of butyrate, NH3 and phenol production. Two diets, a low-starch diet (LSD) and a high-starch, low-fat diet (HSLFD) were compared. The LSD with 20 % total energy (%E) from starch was based on a ‘typical’ Australian diet, while the HSLFD (40 %E as starch) was the same Australian diet modified by an increased content of legumes, starchy foods and coarsely-ground cereals and by a reduced fat content. Four subjects with iliostomies consumed each diet for 2 d, with ileal effluent collection on the second day. On the HSLFD compared with the LSD, RS in ileal effluent increased from from 0·49 to 1·7 g/MJ per d (P < 0·005) while ileal NSP excretion increased from 2·0 to 3·3 g/MJ per d (P < 0·05). Ileal effluents obtained after each diet were incubated for 24 h in vitro with a human faecal innoculum. After fermentation, ileal effluent from the HSLFD produced more butyrate relative to other short-chain fatty acids (17·5 v. 15·8 molar %, P < 0·005) and less phenol (2·3 v. 5·7 mg/l, P < 0·05) and NH3 (20·3 v. 23·1 mmol/l, P < 0·005) than the LSD diet. The HSLFD also generated a lower pH (6·15 v. 6·27, P < 0·05). On a wt/wt basis, RS was 2·3-fold higher in the HSLFD effluent while NSP did not increase, suggesting that the change in RS largely contributed to the fermentation effects. Changes in in vitro variables when the HSLFD ileal effluent was ground before fermentation indicated the importance of physical structure in determining ileal excretion of RS. We conclude that: (1) readily achievable modifications to the amount and processing of starchy foods in an Australian diet would produce potential benefits for in vitro fermentation variables; and (2) the physical structure of grains and cereals is important in determining access by colonic bacteria to a carbohydrate substrate.

Nutrients not absorbed in the small bowel will form substrates for microbial growth in the colon which may have implications for the development of colon cancer. The aim of the present study was to investigate whether fibre-rich oat and barley diets increase the excretion of energy-supplying nutrients from the small bowel compared with a low-fibre wheat diet, and whether a possible. increase could be related to the β-glucan content. Nine ileastomy subjects were served four types of bread together with a low-fibre basal diet (12 g dietary fibre/d). The breads were based on either wheat flour (W diet, 7 g dietary fibre/d), oat bran (OB diet, 29 g dietary fibre/d), the same amount of oat bran with addition of β-glucanase (EC 3.2.1.4) (OBE diet, 19 g dietary fibre/d) or a fibre-rich barley fraction (B diet, 35 g dietary fibre/d). An increased ileal excretion of starch was observed with the barley diet but no effect of the oat β-glucan on starch recovery was found. The NSP + Klason lignin in the ileostomy effluents accounted only for 24, 31, 24 and 35% of the gross energy excretion in the W, OB, OBE and B diet periods respectively. A large part of the dry weight and energy (30, 21, 28 and 27%, in the W, OB, OBE and B diets respectively) in the effluents could not be identified as fat, protein, total starch or NSP + Klason lignin. This unidentified part was probably made up of oligosaccbarides, endogenous losses and nutrient complexes. Methods for identifying and analysing these components should be developed and their role as substrates for colonic fermentation and colon cancer development ought to be investigated.

The recovery of inulin, a naturally occurring β(2→l)-fructan isolated from Jerusalem artichoke (Helianthus tuberosus L.), in the small intestine of man was studied in ileostomy subjects. The ileostomists were given a low-dietary-fibre diet based on white wheat bread and virtually free of inulin, and the same diet with the addition of 10 g and 30 g inulin product respectively, and the recovery and mean transit time (MTT) of inulin were estimated by tracking inulin in ileal effluent. The recovery of inulin was approximately 87% at both ingestion levels. MTT was 4·9 (SE 0·6) h at an intake of 10 g inulin product decreasing to 3·4 (SE 0·3) h at an intake of 30 g Inulin product. A significant change in the fructose: glucose ratio of inulin from ingestion (4·1) to recovery in ileal effluent (4·5–4·7) and a lower recovery of the glucose residue than of the fructose residue of inulin indicate that the low-molecular-weight inulins are more sensitive to hydrolysis than the high-molecular-weight fragments. The loss of inulin during passage through the small intestine is presumably due to hydrolysis by either acids or enzymes and to microbial degradation by the microfiora permanently colonizing the distal small intestine. The concentrations of lactic acid (LA) and short-chain fatty acids (SCFA) in frequently collected ileal effluents on the control day were approximately 6 mmol/l and approximately 55 mmol/l respectively. During periods with inulin ingestion the concentration of LA increased to 18–26 mmol/l (P < 0·052), while the concentration of SCFA ran converse and decreased to 18–32 mmol/l (P < 0·023). The osmotic loads (68 and 204 mosmol/l) associated with the ingestion of inulin product caused minor malabsorption of low-molecular-weight sugars.

The effect of addition of sugar-beet fibre to the diet on sterol excretion from the small intestine was studied in nine ileostomy subjects. A constant low-fibre diet was given in two 3 d periods with and without 32 g sugar-beet fibre/d in random order. Care was taken to minimize bacterial alteration of the ileostomy contents. The addition of sugar-beet fibre increased net cholesterol excretion by 52 (SE 9)%(P < 0·01), from 294 (SE 99) to 451 (SE 124) mg/d, and decreased bile acid excretion by 26 (SE 15)% (P < 0·01), from 764 (SE 118) to 567 (SE 96) mg/d. The increased cholesterol and decreased bile acid excretion found with sugar-beet fibre addition is different from the pattern associated with fibre sources such as pectin and oat fibre. The interaction between dietary fibre and sterol metabolism may be mediated, therefore, by different mechanisms depending on the fibre source.

Dietary nitrate and nitrite may affect colonic pathophysiology. These anions influence fermentation, and nitrite has been shown to augment sodium absorption by the colon and participate in the formation of N-nitroso compounds. There is, however, no general agreement as to how much dietary nitrate and nitrite reaches the colon. To help resolve this question, balance studies were performed on six healthy ileostomy subjects who were given diets that varied in nitrate content from 0.83 to 5.20 mmol/d. Nitrate and nitrite excretion in ileal effluent and urine were measured by anion-exchange chromatography with conductivity detection. There was no significant nitrite in the diets, urine, or ideal effluent. Dietary nitrate was largely excreted in urine (1.31–4.25 mmol/d). The urinary excretion findings indicated net synthesis of nitrate at low dietary intakes and net catabolism of nitrate at high intakes. Nitrate losses in ileal effluent were very low (0.03–0.05 mmol/d, 0.03–0.06 mmol/kg) and unrelated to intake for all the diets. It is concluded that dietary nitrate and nitrite do not enter the colon from the small intestine in amounts that would affect fermentation and mucosal metabolism in man. The possibility of significant amounts of nitrate reaching the colon via blood in normal subjects has not been excluded.