Diet in Irritable Bowel Syndrome (IBS): Interaction with Gut Microbiota and Gut Hormones

Abstract

Diet plays an important role not only in the pathophysiology of irritable bowel syndrome (IBS), but also as a tool that improves symptoms and quality of life. The effects of diet seem to be a result of an interaction with the gut bacteria and the gut endocrine cells. The density of gut endocrine cells is low in IBS patients, and it is believed that this abnormality is the direct cause of the symptoms seen in IBS patients. The low density of gut endocrine cells is probably caused by a low number of stem cells and low differentiation progeny toward endocrine cells. A low fermentable oligo-, di-, monosaccharide, and polyol (FODMAP) diet and fecal microbiota transplantation (FMT) restore the gut endocrine cells to the level of healthy subjects. It has been suggested that our diet acts as a prebiotic that favors the growth of a certain types of bacteria. Diet also acts as a substrate for gut bacteria fermentation, which results in several by-products. These by-products might act on the stem cells in such a way that the gut stem cells decrease, and consequently, endocrine cell numbers decrease. Changing to a low-FODMAP diet or changing the gut bacteria through FMT improves IBS symptoms and restores the density of endocrine cells.

Keywords: IBS; diet; fecal microbiota transplantation; gut endocrine cells; gut microbiota.

Figure 1

Schematic illustration of the gut endocrine cells. The endocrine cells are scattered among the epithelial cells of the mucosa facing the gut lumen. These cells secret at least 14 different hormones that regulate gut motility, secretion, absorption, visceral sensitivity, local immune defense, cell proliferation, and appetite. These hormones also interact and integrate with the enteric, autonomic, and central nervous systems.

Figure 2

The gut endocrine cells have specialized microvilli that project into the gut lumen and act as sensors for the gut contents (mostly for nutrients). They respond to luminal content by releasing their hormones into the lamina propria. These hormones act locally on nearby structures (paracrine mode of action) or enter the blood stream and act on more distant structures (endocrine mode of action).

Figure 3

Duodenal cholecystokinin (CCK) cells of a healthy subject (A) and of a patient with irritable bowel syndrome (IBS) (B). Patients with IBS have a low density of CCK cells.

Figure 4

Musashi 1 cells in the duodenum of a healthy subject (A) and in the duodenum of a patient with IBS (B). Musashi 1 is a marker for stem cells and their early progenitors.

Figure 5

Schematic illustration of the possible role of the interaction of diet, gut microbiota, and gut endocrine cells in the pathophysiology of IBS. The foods we ingest act as prebiotics that favor the growth of a certain type of bacteria. These bacteria in turn ferment the diet, resulting in by-products. These by-products may act on the stem cells in a way that reduces their number. This in turn would result in a low density of gut endocrine cells. The low density of gut endocrine cells gives rise to the gut dysmotility, visceral hypersensitivity, and abnormal gut secretion that are seen in IBS patients.