Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Feb;11(2):139-148.
doi: 10.1080/17474124.2017.1269601. Epub 2016 Dec 14.

The possible role of gastrointestinal endocrine cells in the pathophysiology of irritable bowel syndrome

Affiliations
Review

The possible role of gastrointestinal endocrine cells in the pathophysiology of irritable bowel syndrome

Magdy El-Salhy et al. Expert Rev Gastroenterol Hepatol. 2017 Feb.

Abstract

The etiology of irritable bowel syndrome (IBS) is unknown, but several factors appear to play a role in its pathophysiology, including abnormalities of the gastrointestinal endocrine cells. The present review illuminates the possible role of gastrointestinal hormones in the pathophysiology of IBS and the possibility of utilizing the current knowledge in treating the disease. Areas covered: Research into the intestinal endocrine cells and their possible role in the pathophysiology of IBS is discussed. Furthermore, the mechanisms underlying the abnormalities in the gastrointestinal endocrine cells in IBS patients are revealed. Expert commentary: The abnormalities observed in the gastrointestinal endocrine cells in IBS patients explains their visceral hypersensitivity, gastrointestinal dysmotility, and abnormal intestinal secretion, as well as the interchangeability of symptoms over time. Clarifying the role of the intestinal stem cells in the pathophysiology of IBS may lead to new treatment methods for IBS.

Keywords: Diet; Musashi-1; genes; low-grade inflammation; microbiota; neurogenin 3; stem cells.

PubMed Disclaimer

MeSH terms

Substances

LinkOut - more resources