Rectal instillation of butyrate provides a novel clinically relevant model of noninflammatory colonic hypersensitivity in rats.
Level 5 - mechanism / opinion, no new human data
Preclinical animal experiment without human subjects
PubMed 15940632 · doi:10.1053/j.gastro.2005.03.082
What was done
Rats received rectal instillations of butyrate solution (8–1000 mmol/L) twice daily for 3 days to establish a model of noninflammatory colonic hypersensitivity. Colonic hypersensitivity was evaluated with colorectal distention tests and referred cutaneous lumbar hyperalgesia with von Frey hairs. Colonic mucosa was assessed macroscopically and histologically. Pharmacological responses were tested using morphine, U50488H (a kappa opioid agonist), trimebutine, neonatal capsaicin pretreatment, a calcitonin gene-related peptide (CGRP) receptor antagonist, and a neurokinin 1 receptor antagonist.
What was found
Butyrate enemas induced concentration-dependent, sustained colonic hypersensitivity and referred mechanical hyperalgesia (most pronounced in female rats) without macroscopic or histological mucosal damage. Pain parameters were alleviated by morphine, U50488H, trimebutine, capsaicin pretreatment, and the CGRP receptor antagonist, but not the neurokinin 1 receptor antagonist. The abstract reported no specific numerical values, sample sizes, or effect estimates.
Why it matters
This establishes a noninflammatory rat model reflecting key visceral pain features of irritable bowel syndrome and highlights CGRP receptor antagonism as a possible therapeutic mechanism.
Limits
Findings are limited to a rodent model and cannot capture the complex clinical and psychosocial presentation of human irritable bowel syndrome. The abstract does not report animal numbers, exact measurements, or statistical values.
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- context Short-chain fatty acids like butyrate improve the body's capacity to sense and respond to stool in the rectum.