Gershon · Current opinion in endocrinology, diabetes, and obesity 2013 · narrative review · n=?

5-Hydroxytryptamine (serotonin) in the gastrointestinal tract.

Cited 620 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review summarizing animal and mechanistic research

PubMed 23222853 · doi:10.1097/MED.0b013e32835bc703 · record verified 2026-08-27

What was done

This narrative review summarizes findings regarding the biological functions of gut 5-hydroxytryptamine (serotonin, 5-HT). The discussed evidence focuses on mechanistic insights from transgenic mouse models, specifically tryptophan hydroxylase 1 knockout (TPH1KO, lacking enterochromaffin cell 5-HT), tryptophan hydroxylase 2 knockout (TPH2KO, lacking neuronal 5-HT), and serotonin transporter knockout models.

What was found

The abstract reports no quantitative data. It notes that neuronal 5-HT appears more important for constitutive gastrointestinal transit than enteroendocrine 5-HT, though TPH2KO mice also exhibit an incomplete complement of enteric neurons, obscuring whether slowed transit results from missing serotonergic transmission or broader neuronal deficiency. Neuronal 5-HT promotes mucosal growth, maintenance, and neurogenesis. Enteroendocrine-derived 5-HT is involved in intestinal inflammation, with inflammation severity decreasing in TPH1KO mice and increasing with serotonin transporter deletion. Enteroendocrine 5-HT also acts hormonally to inhibit osteoblast proliferation and promote liver regeneration.

Why it matters

The review outlines how gut serotonin functions beyond simple peristaltic initiation, acting as a neurotransmitter, paracrine factor, growth factor, and endocrine hormone affecting intestinal motility, mucosal integrity, inflammation, and extra-intestinal organ physiology.

Limits

As a narrative review, it provides no systematic search methodology, meta-analytic synthesis, or quantitative effect sizes. The reported mechanisms rely on rodent genetic knockout models, and structural neurodevelopmental defects in TPH2KO models confound the distinction between signaling and developmental effects. Human clinical data were not reported in the abstract.

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