The Relationship between Intestinal Motility and Interstitial Cells of Cajal in Nonalcoholic Fatty Liver Mice

Abstract

BackgroundNonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in western world. However, NAFLD shows an increasing trend in China every year, which has attracted the attention of national health authorities. The previous studies have shown that NAFLD caused severe gastrointestinal motor disorders, but little is known about the interstitial cells of Cajal (ICC) role in gastrointestinal motor disorders.ObjectivesThe aim of this study was to observe the ICC in jejunum of nonalcoholic fatty liver mice by immunohistochemistry and assessed the relationship between intestinal motility and ICC.Materials and MethodsThirty five Sprague-Dawley (SD) rats were randomly divided into nonalcoholic fatty liver (n = 25) and control groups (n = 10), rats were housed individually in cages and had free access to food and water, nonalcoholic fatty liver group was duplicated by high-fat diet (consisted of ordinary food, 20 g/kg cholesterol and 100 g/kg fat) feeding. Dextran blue-2000 was used to monitor the intestinal motility. The proximal small intestine was harvested to investigate the C-kit positive ICC. The hepatic tissue slices were used for pathological observation.ResultsNonalcoholic fatty liver disease was successfully established. The intestinal motility in nonalcoholic fatty liver group (49.5 ± 10.9) was weaker compared to the control group (57.3 ± 8.9), P < 0.05. The rate of ICC also have shown statistically significant differences between nonalcoholic fatty liver (4.87 ± 2.97/mm 2) and control groups (6.54 ± 3.13/mm 2), P < 0.05.ConclusionsICC may be related to the intestinal motility in nonalcoholic fatty liver mice.

Small intestinal bacterial overgrowth and orocecal transit time in patients of nonalcoholic fatty liver disease

“…The excessive growth and reproduction of bacteria in the intestine leads to an increase in the number of metabolites, wherein endotoxin is one of the metabolites closely related to NAFLD. Endotoxin is an important component of the cell wall of Gram-negative bacteria, which will be released when bacteria in the intestine grow rapidly or are dissolved after death [7] Under normal circumstances, the barrier function of the intestinal mucosa can effectively prevent intestinal bacterial translocation and endotoxin invasion [8]. When NAFLD occurs, the endotoxin released by intestinal bacteria increases, the permeability of intestinal mucosa increases, and the barrier function is impaired, which cannot effectively prevent endotoxin from entering the portal system [9].…”