Intestinal Secretory Mechanisms in Irritable Bowel Syndrome–Diarrhea

Abstract

Although diarrhea is the predominant bowel dysfunction in as many as one-third of patients with irritable bowel syndrome (IBS), it is unclear whether there is a specific disorder of intestinal fluid or electrolyte secretion in IBS. Diarrhea is generally considered secondary to accelerated colonic transit in patients with IBS. Although a primary secretory diathesis has not been well documented in patients with IBS with diarrhea (IBS-D), several mechanisms that could potentially contribute to intestinal secretion have been reported. Some of these mechanisms also influence motor and secretory dysfunctions that contribute to the pathophysiology of IBS-D. We review the evidence supporting secretion in IBS-D caused by peptides and amines produced by enteroendocrine cells or submucosal neurons, enterocyte secretory processes, and intraluminal factors (bile acids and short-chain fatty acids). Understanding these mechanisms and developing clinical methods for their identification could improve management of patients with IBS-D.

Irritable bowel syndrome: an integrated explanatory model for clinical practice

“…Altered peripheral regulation of gut function is caused by changes in local neurotransmitter signaling, gut inflammation, and changes in microbiota, and provides a hypothesis to explain IBS and the differences between IBS‐D and IBS‐C (Fig. ) . Susceptibility to altered peripheral gut regulation may be increased by underlying gene mutations, polymorphisms and changes in mRNA expression .…”

Pathophysiology, Evaluation, and Management of Chronic Watery Diarrhea

“…46,47 Table 1 summarizes enteroendocrine mediators that cause net fluid flux towards the lumen, either by inducing intestinal secretion or by inhibiting absorption, or both (reviewed in detail in ref. 48). In addition, Table 1 summarizes information that supports the potential role of intestinal secretion in development of IBS and the neuroendocrine tumors that result in diarrhea.…”

Mucosal pathobiology and molecular signature of epithelial barrier dysfunction in the small intestine in irritable bowel syndrome

“…Notably, regulatory peptides, neurotransmitters, taste and odor receptors, and extrinsic innervation of the gut wall, all involved in the modulation of digestion, absorption, motility, and sensation along the gut, may also account for anatomical differences in barrier function. For instance, peptides like cholecystokinin and somatostatin are mainly secreted in the duodenum and motilin and the glucose‐dependent insulinotropic peptide in the duodenum and the jejunum; the peptide YY is mainly localized in the ileum and the colon, while vasoactive intestinal peptide and substance P are found throughout the gastrointestinal tract …”