The 4th Joint Session between JDDW-KDDW-TDDW1(JDDW)
Thu. November 5th   9:00 - 11:15   Room 9: Portopia Hotel Main Building Kairaku 3
JKT1-1
 TRP channel is associated with regulating colonic peristalsis and visceral hypersensitivity in lower gastrointestinal functional disorders.
Ken Inoue
Kyoto Prefectural University of Medicine
The patients with functional gastrointestinal disorders (FGIDs) have chronic unexplained gastrointestinal symptoms. FGIDs include the irritable bowel syndrome (IBS) and functional dyspepsia (FD), currently classified by Rome IV. The main symptom of IBS （irritable bowel syndrome：IBS）, which is a typical functional gastrointestinal disorder, chronic intermittent abdominal pain and associated diarrhea, constipation, or both. The pathology of IBS involves genome, cerebrointestinal peptides, gastrointestinal motility abnormalities, visceral hypersensitivity, gastrointestinal immunity, mucosal permeability, gut flora, psychosocial factors, etc.
The gastrointestinal tract has functions not only of digestion and absorption, but also of a sensor that senses various chemical and physical stimulation. The digestive tract has a system for regulating immune function, endocrine function, and nerve function. Multimodal sensors of the digestive tract include TRP (Transient Receptor Potential) channels. TRP channels respond to a wide variety of sensory stimuli, including temperature, nociceptive compounds, touch, osmolarity, and pheromones. It was reported that TRP channel expressed in the digestive tract. It has been reported that TRP channels may be involved in the pathophysiology of various diseases, and research is progressing as a new drug discovery target. Since the mechanism of rectal hypersensitivity and faecal urgency seems to involve increased TRPV1, drugs that target the mechanisms of this receptor should be assessed. TRPV2 may contribute to intestinal motility through NO production, and TRPV2 is a promising target for controlling intestinal movement. It was reported that mildly cool water and the cooling agent menthol activate same TRP channel, TRPM8. It was reported that TRPM8 agonist (menthol) suppressed gastrointestinal peristalsis. We also reported that TRPM8 agonist suppressed colonic peristalsis and abdominal pain. However, how the menthol, TRPM8 agonist, works on the gastrointestinal peristalsis and visceral hypersensitivity was poorly documented. We are studying the involvement of TRPM8 in regulating colonic peristalsis using TRPM8 deficient mice. In the lower gastrointestinal tract, TRPA1 activation results in PGE2 release and consequently promotes colorectal contraction.
In the future, elucidation of this multimodal sensing function of the digestive tract may lead to the development of new diagnosis and new drug discovery of FGIDs.
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