IBS Is Linked to Bowel Defects

Serotonin plays a critical role in the regulation of gastrointestinal(GI) motility, secretion, and sensation. Irritable bowel syndrome(IBS) is associated with clinical symptoms that include alterations innormal patterns of motility, secretion, and sensation. The role ofserotonin in the pathophysiology of IBS, however, remains unclear.

In the June 2004 issue of Gastroenterology, researchersreported the results of a study aimed at testing whether entericserotonin signaling is defective in patients with IBS and in patientswith ulcerative colitis (UC). Key elements of serotonin signaling,including measures of serotonin content, release, and reuptake,were analyzed in rectal biopsy samples from patients with UC(n = 22), patients with IBS with diarrhea (IBS-D; n = 15), patientswith IBS with constipation (IBS-C; n = 16), and controls (n = 34).

Results showed that mucosal serotonin, tryptophan hydroxylase1 messenger RNA (mRNA), serotonin transporter mRNA,and serotonin transporter immunoreactivity were all significantlyreduced in patients with UC, IBS-D, and IBS-C. The enterochromaffincell population was reduced in samples from patients withsevere UC but was unchanged in samples from patients withIBS. No changes were detected in any of the disease samplesrelative to the control samples when serotonin release wasinvestigated under basal and mechanical stimulation conditions.The authors concluded that both UC and IBS are associated withmolecular changes in serotonergic signaling mechanisms andthat these data support the assertion that disordered GI functionin IBS involves changes intrinsic to the bowel.