Whole bowel transit time is generally between 24 and 36 hours in healthy individuals, but values ranging from 0.4 to 5 days have been reported in the literature38 39. Transit through the large bowel is highly influenced by the pattern of daily activity. The highest calorie intake in the western world occurs in the evening and colonic motility decreases at night.
Dietary fibre in the form of bran and wholemeal bread, fruit and vegetables, increases faecal weight by acting as a substrate for colonic bacterial metabolism. This increased faecal bulk is associated with a reduced colonic transit time, although the mechanism is uncertain. In the healthy colon, an additional 20 g per day of bran increases faecal weight by 127% and decreases the mean transit time from 73±24 h to 43±7 h40. Not all fibres produce an equal effect on the colon, since the same quantity of fibre as cabbage, carrot or apple produced a smaller effect. The disparate effect of fibre provided as either rice bran or wheat bran was also demonstrated by a two-fold increase in faecal mass and stool frequency with rice bran over wheat bran, despite a similar accelerating effect on transit time with both types of fibre41. These differences almost certainly depend upon differing metabolism of the fibre by colonic bacteria.
Dietary fibre is either soluble and viscous, i.e. resistant starch, gums, mucilages and pectins, which amounts to approximately 30% of ingested fibre, or insoluble fibre such as cellulose. The relationship between bacterial degradation of fibre and the effect on faecal mass and whole gut transit time is complex. Three viscous polysaccharides, guar gum, ispaghula and xanthan gum varied in their responses to bacterial degradation in vitro41. Guar gum was rapidly fermented in vitro by faecal bacteria with concomitant loss of viscosity and reduction in pH; ispaghula maintained its viscosity during incubation, but the pH fell significantly, and xanthan gum incubations showed considerable individual variation. Faecal mass was increased only by ispaghula. Whole-gut transit time was reduced by gum feeding to a significantly greater extent in those subjects whose faecal bacteria reduced the viscosity of that gum, than in those subjects where the viscosity was maintained. The rate of proximal colonic transit is directly influenced by the presence and the metabolism of polysaccharides43. Using a lactulose-induced catharsis model of accelerated proximal colonic transit in healthy volunteers, ispaghula husk was found to significantly delay proximal colonic transit, whilst guar gum, being more rapidly degraded by bacterial metabolism, caused an accelerated proximal colonic transit (Figure 7.4).
The diet of an individual is closely linked with the proliferation of the colonic mucosa. Food deprivation and "elemental diets' can result in intestinal atrophy and decreased cell production44 45. Refeeding of starved rats with a fibre-free elemental diet supplemented with fermentable fibre stimulates colonic and small intestinal epithelial cell proliferation, whilst the addition of inert bulk to the elemental diet has no such effect46. This proliferative effect of fermentable fibre on the gut epithelium was not observed in germ free rats, suggesting that epithelial proliferation is effected by the products of bacterial fermentation rather than the presence of fermentable fibre.
Colonic intraluminal pressure decreases after eating either wheatbran or cellulose47, however, the physical characteristics of the dietary fibre may be important since coarse bran ingestion decreases colonic motility whereas ingestion of fine bran increases intracolonic pressure48.
Normal constituents of the colonic lumen include some unmetabolised carbohydrate, protein and bile salts, but very little fat. A considerable amount of starch enters the colon to contribute further substrate for bacterial fermentation. Fermentation produces short-chain fatty acids (SCFA's), notably acetate, propionate and butyrate. SCFA's, whilst being normal constituents of the colon, are not found in the terminal ileum except under conditions of colo-ileal reflux. The effect of SCFA's on the ileum is to stimulate propulsive motility, causing the ileum to be emptied49 and subsequent return of the SCFA's to the right colon where they aid water absorption. This reflux may be important in preventing bacterial overgrowth in the terminal ileum. Accumulation of SCFAs causes the pH to fall50.
Long-chain fatty acids (LCFA's) should not normally reach of the colonic lumen and generally are only found in patients with fat malabsorption. LCFA's are cathartic, a fact which may further contribute to the lack of fat metabolism, and have been shown to stimulate unusual motor patterns; an emulsion of oleic acid infused into the ascending colon accelerated colonic transit by induction of high amplitude, prolonged, propagating pressure waves originating near the ileocaecal junction12. This was associated with a narrowing of the ascending colon with a reduced reservoir function and may be the mechanism by which diarrhoea is produced in patients with fat malabsorption.
Coffee produced an increase in the motility of distal colon within four minutes of ingestion of both regular and decaffeinated coffee in 8 responders, but not in 6 non-responders51. The increase in rectosigmoid motility lasted at least 30 minutes.
Although constipation is associated with a slow transit through the left colon in most patients, right colon transit is essentially normal. By contrast, accelerated proximal colonic transit is a common feature of many diseases and treatment is often designed to reduce the transit rate to allow sufficient absorption of nutrients and electrolytes. An increased intestinal transit time is associated with a decreased stool weight and bacterial mass52.
Codeine phosphate or loperamide are commonly employed to produce a reduction in stool volume and correction of accelerated colonic transit in patients with diarrhoea53. These drugs exert their antidiarrhoeal effect through a change in the gastrointestinal motor function, leading to an increased capacitance of the proximal gut, and a delay in the passage of fluid through the gastrointestinal tract54 55.
Morphine delays transit in the caecum and ascending colon, increases colonic capacitance and reduces bowel movements in man56 57. The potency of opiates may be due to their action to modulate the normal neural controls via the enkephalinergic neurones in the colon. The possible role of endogenous opioids has been explored using naloxone, an opiate receptor antagonist. This has been shown to cause an accelerated transit through the colon in cats and in man, but without increasing the number of bowel movements56 58.
Loxiglumide is a specific and highly potent CCK-receptor antagonist which inhibits postprandial gall bladder contraction and causes an accelerated gastric emptying59-61. The effect of CCK-receptor antagonists on the colon is uncertain since loxiglumide shortens colonic transit time in healthy controls61, but prolongs colonic transit time in patients with accelerated colonic transit.
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