Role of Gut Serotonin

in GI Motility & Intestinal Crosstalk with Microbia

This article is from the I-ACT 2024 Winter Quarterly Magazine By Wendy Sebastian | I-ACT Board Member & Instructor

Serotonin, also known as 5-hydroxytryptamine (5-HT), is mainly synthesized in the gastrointestinal (GI) tract. It has been studied for decades as it plays a crucial role in regulating the different neurogenic motor patterns in the GI tract. Recently, two separate studies by Keating, Damien J., and Ge, Xiaolong, have shed some light on the connection between gut serotonin and microbiota, and their impact on GI motility. In this blog post, we will dive deeper into these studies, and explore the scientific evidence behind the claims.

One of the primary studies we will discuss is Keating, Damien J.’s article, “Gut Serotonin in the Control of Gastrointestinal Motility.” The study highlights the essential role that serotonin plays in the control of gastrointestinal motility. It found that serotonin is synthesized in the enterochromaffin cells of the intestinal mucosa, via the enzyme tryptophan hydroxylase-1 (TPH1). Additionally, about 1% of nerve cell bodies found in the enteric nervous system, synthesize serotonin via a different enzyme called tryptophan hydroxylase-2 (TPH2). The study concluded that the high quantity of serotonin that is synthesized within the gut wall explains why it plays a vital role in the different neurogenic motor patterns in the gastrointestinal tract.

The second study we will discuss is Xiaolong Ge’s “Intestinal Crosstalk between Microbiota and Serotonin and its Impact on Gut Motility.” The study found that there is a connection between the gut microbiota and serotonin. The microbiota in the gut produces a vast array of compounds that interact with the different cells in the gastrointestinal tract, including those involved in serotonin synthesis. It is speculated that this microbiota-serotonin interaction may play a role in the control of GI motility. Therefore, the study concluded that intestinal crosstalk between microbiota and serotonin could affect gut motility.

Another study by Gershon, Michael D. et al., “Serotonin and Its Receptors in the GI Tract: Regulation, Function, and Therapeutic Targets,” explored the scientific evidence on the various serotonin receptors and their role in modulating GI motility. The study highlights the role of 5-HT receptors on the various types of cells located in the GI tract that are involved in the regulation of motility. The authors found that pharmacological manipulation of these receptors could affect GI motility, a discovery that still drives the development of new potential therapies.

In contrast, studies by Mayer, Emeran A., and Tillisch, Kirsten, et al., “The Brain-Gut Axis in Abdominal Pain Syndromes,” examined the connection between gut serotonin and brain- function in people experiencing abdominal pain syndromes. Mayer found that the brain-gut axis played a significant role in the development and maintenance of different abdominal pain syndromes by modulating the neurogenic motor patterns in the GI tract. These studies highlight the importance of serotonin in the brain-gut axis in modulating GI motility in stress-associated diseases of the GI tract.

In conclusion, serotonin plays a crucial role in the GI motility and the connection between the gut microbiota and serotonin is becoming apparent in contemporary scientific research. The studies by Keating, Damien J., Ge, Xiaolong, Gershon, Michael D., as well as Mayer, Emeran A. and Tillisch, Kirsten, provide evidence of the importance of gut serotonin in GI motility and its modulation by microbiota, stress and brain-gut axis. Moving forward, understanding the complex nature of the gut serotonin and its interaction with the microbiota and other factors will pave the way for the development of novel therapeutic targets and treatment of GI-related gut disorders.

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Wu, T., Rayner, C. K., Young, R. L., & Horowitz, M. (2013). Gut Motility and enteroendocrine secretion. Current Opinion in Pharmacology, 13(6), 928–934. https://doi.org/10.1016/j.coph.2013.09.002