# New research for constipation



## eric (Jul 8, 1999)

FYI: A new study in progress.Neurotrophic Factors Stimulate GutMotility in Humans WESTPORT, Aug 16 (Reuters Health) - Recombinant humanneurotrophic factors accelerate colonic transit and relieveconstipation, according to a report published in the July issueof Gastroenterology. Patients treated with recombinant human brain-derivedneurotrophic factor (r-metHuBDNF) for variousneurodegenerative disorders commonly reported altered bowelfunction, suggesting that r-metHuBDNF may havegastrointestinal actions that parallel its central nervous systemeffects, the authors explain. Dr. Michael Camilleri, of the Mayo Clinic, in Rochester,Minnesota, and colleagues measured gastrointestinal transit andcollected bowel movement diaries from 40 healthy subjectsand 10 patients with constipation treated with subcutaneousr-metHuBDNF or sc recombinant human neurotrophic factor 3(r-metHuNT-3). Compared with placebo treatment, r-metHuBDNF significantlyaccelerated colonic transit at 24 hours and 48 hours, the authorsreport. Gastric emptying and small intestine transit were notsignificantly affected. Stool frequency increased by 2.5 the first week and by 3.5 thesecond week of r-metHuBDNF treatment, the investigatorsnote, compared with 0.75 and 0.77, respectively, for placebotreatment. Stool consistency and ease of passage did not changesignificantly with treatment. Injection-site reactions, arthralgia, and myalgia were reportedmore commonly among r-metHuBDNF-treated patients thanamong placebo-treated patients, the report indicates, but noserious adverse events were encountered and no participantwithdrew from the study. Similar results were obtained with r-metHuNT-3, theresearchers report. In addition, r-metHuNT-3 acceleratedgastric emptying and small intestine transit. It also increasedthe ease of stool passage, but only in constipated patients. "The present studies are the first to show that exogenousneurotrophic factors, r-metHuBDNF and r-metHuNT-3,accelerate colonic transit and increase stool frequency inhumans," the authors write. They conclude "that recombinanthuman neurotrophins are promising agents capable ofmodifying transit in the entire gastrointestinal tract." In a related commentary, Drs. Jan Tack and Pieter VandenBerghe from University of Leuven, Belgium, agree. "Treatmentwith neurotrophins might be of particular interest in patientswith intestinal neurodegenerative disorders," they write. "It is conceivable," they add, "that several of the so-calledfunctional bowel disorders may be the symptomatic outcome ofmalfunction of the neurologic organization with the entericnervous system." ------------------ http://www.ibshealth.com/


----------



## JeanG (Oct 20, 1999)

Thanks for posting this, ERic!







More and more progress is being made in this field. It really is exciting.







JeanG


----------



## JeanG (Oct 20, 1999)

Bump


----------



## moldie (Sep 25, 1999)

Interesting. This might be a future drug that could help me, being a slow transit, but I am already "myalgic." I wonder if it would make that condition worse. There is always some drawback with these medications it seems.


----------



## Guest (Sep 14, 2000)

Just wanted to say thank you eric for the post. Recent thoughts seem to be that all ibs is just a malfunctioning enteric nervous system. I am looking into a study for people with motility problems. This stuff is actually supposed to regrow nerves which means maybe no more drug bandaids someday. I was going to have my colon removed, but if I can hang in there to try this study I will. ------------------------------GASTROENTEROLOGY 1999;116:5 COMMENT FROM THE EDITORSAdvances in understanding of the developmental biology of enteric neurons bring insights on the mechanisms that accomplish "homing" of enteric neurons from the embryonic neural crest to the gut. "Knock-out" of key proteins or transcription factors such as endothelin- receptors, MASH-1, or laminin provides an understanding of rare congenital forms of localized or generalized intrinsic denervations, e.g., Hirschsprung's disease, pyloric stenosis, or congenital pseudo-obstruction. This work has also brought a greater understanding of the plasticity of enteric neurons and the role of neurotrophic factors in their maintenance and possibly their repair, e.g., glial-derived and brain-derived (BDNF) neurotrophic factors and neurotrophins 3 and 4. Interestingly, BDNF may also play a role in mechanosensation and influences survival of specific subsets of sensory neurons during development. Transgenic introduction of endothelin- receptors to deficient rats results in restoration of the myenteric plexus, normal intestinal morphology, and normal growth. Michael Camilleri, M.D.Associate Editor ----------------------------------------------------------------------------------------------------------------------------------------------------------------


----------

