deoxycholic-acid and Intestinal-Diseases

Topics: Bile Acids and Salts; Biliary Tract Diseases; Celiac Disease; Chenodeoxycholic Acid; Cholelithiasis; Cholestasis; Cholic Acids; Colonic Neoplasms; Deoxycholic Acid; Diarrhea; Humans; Intestinal Diseases; Intestine, Small; Lipid Metabolism; Lithocholic Acid; Liver; Liver Circulation; Malabsorption Syndromes; Portal System

The crosstalk between macrophages and gastric epithelial cells has emerged as a player in chronic inflammation during intestinal metaplasia. However, the role of bile acid on this modulation remains to be studied. We hypothesized that deoxycholic acid-induced macrophages secreted exosomes to mediate intercellular communication and promoted intestinal metaplasia in human gastric epithelial cells (GES-1 cells). Macrophage-derived exosomes (M-Exos) and deoxycholic acid-induced macrophage-derived exosomes (D-Exos) were isolated by ultracentrifugation. EdU staining and CCK-8 assay were utilized to evaluate the effects of exosomes on the proliferation of GES-1 cells. Intestinal metaplasia was assessed by the expression of caudal-related homeobox transcription factor 2 (CDX2) at both mRNA and protein level. MicroRNA sequencing revealed the microRNA (miRNA) expression profiles of M-Exos and D-Exos. The role of a specific miRNA and mRNA was analyzed by using miRNA mimics, miRNA inhibitors and siRNAs. D-Exos promoted the expression of CDX2 and suppressed the proliferation of GES-1 cells, compared to M-Exos. The miRNA profiles and quantitative real-time PCR examination showed D-Exos enriched a higher level of hsa-miR-30a-5p than M-Exos. Overexpressed has-miR-30a-5p increased CDX2 expression and inhibited the proliferation in GES-1 cells via targeted Forkhead Box D1 (FOXD1), a potential regulatory factor in the process of intestinal metaplasia. D-Exos may promote intestinal metaplasia and suppress proliferation of GES-1 cells via hsa-miR-30a-5p targeting FOXD1, which may be involved in the action mechanism of bile acid on gastric mucosa.

Topics: CDX2 Transcription Factor; Cell Line; Cell Proliferation; Deoxycholic Acid; Epithelial Cells; Exosomes; Forkhead Transcription Factors; Gastric Mucosa; Humans; Intestinal Diseases; Macrophages; Metaplasia; MicroRNAs; Stomach

Metabolic syndrome is characterized by low-grade chronic systemic inflammation, which is associated with intestinal hyperpermeability. This study examined the effects of 3 high-fat diets (HFDs) composed of different fat sources (soybean oil and lard) on the intestinal permeability, tight junction (TJ) protein expression, and cecal bile acid (BA) concentrations in mice, and then analyzed their interrelations. C57/BL6 mice were fed the control diet, HFD (soybean oil), HFD (lard), and HFD (mix; containing equal concentrations of soybean oil and lard) for 8 wk. Glucose tolerance, intestinal permeability, TJ protein expression, and cecal BA concentration were evaluated. Feeding with the 3 HDFs similarly increased body weight, liver weight, and fat pad weight, and induced glucose intolerance and intestinal hyperpermeability. The expression of TJ proteins, zonula occludens-2 and junctional adhesion molecule-A, were lower in the colons of the 3 HFD groups than in the control group (P < 0.05), and these changes appeared to be related to intestinal hyperpermeability. Feeding with HFDs increased total secondary BA (SBA) and total BA concentrations along with increases in some individual BAs in the cecum. Significant positive correlations between intestinal permeability and the concentrations of most SBAs, such as deoxycholic acid and ω-muricholic acids, were detected (P < 0.05). These results suggest that the HFD-induced intestinal hyperpermeability is associated with increased BA secretion. The abundance of SBAs in the large intestine may be responsible for the hyperpermeability.

Topics: Adipose Tissue; Animals; Bile Acids and Salts; Cecum; Cholic Acids; Colon; Deoxycholic Acid; Diet, High-Fat; Dietary Fats; Inflammation; Intestinal Diseases; Intestine, Large; Junctional Adhesion Molecules; Liver; Male; Metabolic Syndrome; Mice, Inbred C57BL; Soybean Oil; Tight Junctions; Weight Gain; Zonula Occludens-2 Protein

Repair of superficial damage to gastrointestinal mucosa occurs by a process called restitution, with epithelial integrity and continuity reestablished before cell proliferation occurs. The aim of the present study was to investigate the diversity of restitution in rat jejunum exposed to different concentrations of deoxycholic acid (DOC; 1.5-100 mmol/liter). Following a 30-min exposure, the intestine was allowed to recover for 15-330 minutes. DOC caused dose-dependent tissue destruction. Exfoliating epithelial cells were already observed after 5 min of exposure (1.5 mmol/liter), with simple sloughing off and resealing of the tips. Moderately affected epithelium (20 mmol/liter) demonstrated denudation of villous tips and then became covered with goblet cells. Severely affected epithelium (100 mmol/liter) also appeared to be replaced with goblet cells. These data suggest that the reversibility of mucosal damage induced by DOC is due to a variety of processes, which depend on the severity of the mucosal insult.

Topics: Animals; Bromodeoxyuridine; Collagen Type IV; Deoxycholic Acid; Detergents; DNA; DNA Fragmentation; Female; Goblet Cells; Immunohistochemistry; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Microscopy, Electron, Scanning; Rats; Rats, Wistar; Wound Healing

Reports conflict regarding the effect of nitric oxide (NO) on intestinal epithelium. In chronic injury, NO appears detrimental by combining with reactive oxygen to form potent-free radicals. In contrast, inhibition of NO synthesis after acute injury exacerbates damage and inflammation. Recent studies have disclosed constitutive expression of inducible NO synthase (iNOS) by normal intestinal epithelia, yet little attention has been given to the role of iNOS in acute epithelial repair. We studied the local effects of iNOS on early epithelial repair of porcine ileal mucosa injured by deoxycholate within Ussing chambers. iNOS was constitutively expressed by the villous epithelium, and after deoxycholate injury, iNOS was expressed by injured and detaching enterocytes. Selective inhibition of iNOS abolished increases in NO synthesis and villous reepithelialization after injury. Exogenous L-arginine rescued baseline reepithelialization from NOS inhibitors but was only capable of stimulating additional repair in the presence of serum. These results demonstrate that iNOS-derived NO is a key mediator of early villous reepithelialization following acute mucosal injury.

Topics: Animals; Arginine; Deoxycholic Acid; Detergents; Enterocytes; Female; Ileum; Intestinal Diseases; Intestinal Mucosa; Microvilli; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Swine; Wound Healing

(1) To evaluate the performance of in-house and pre-poured commercially available enteric agar by challenge with a large number of positive clinical specimens. (2) To set the standard (critical independent evaluation) which new products should reach. (3) To publish this information, so that others can make informed decisions about enteric media.. Thirteen media of anonymous source were challenged with "known" positive stool samples.. In-house desoxycholate citrate agar performed best for overall pathogen isolation rates, for shigella isolation rates, and for most pathogens available on primary culture.. Desoxycholate citrate agar made by our own laboratory yielded the most pathogens and proved the most effective.

Topics: Agar; Citrates; Culture Media; Deoxycholic Acid; Feces; Humans; Intestinal Diseases; Microbiological Techniques; Quality Control; Reference Standards

Serial measurement of serum bile acid levels was carried out in patients with digestive diseases before and after oral loading with 500 mg of ursodeoxycholic acid. In control cases, serum bile acid reached the maximum level 30 min after loading. Elevation also, of cholic, chenodeoxycholic and deoxycholic acid levels was noted in addition to marked enhancement of the ursodeoxycholic acid level. In patients with chronic aggressive hepatitis and cirrhosis, the serum bile acid level was higher than the controls in fasting state, and increased more significantly after loading. On the other hand, in patients with small intestinal disorders, the serum bile acid level in fasting state tended to be lower than the controls, and became significantly lower after loading. Thus, oral ursodeoxycholic acid tolerance test is found to be useful as a diagnostic test for digestive diseases.

Topics: Adult; Bile Acids and Salts; Deoxycholic Acid; Digestive System Diseases; Female; Hepatitis; Humans; Intestinal Diseases; Liver Cirrhosis; Male; Ursodeoxycholic Acid

Topics: Animals; Calcium; Deoxycholic Acid; Diet; Hydrogen-Ion Concentration; In Vitro Techniques; Intestinal Absorption; Intestinal Diseases; Intestine, Small; Lead; Male; Rats

In an experimental jejunal perfusion study, distress in healthy subjects occurred during eight out of 16 perfusions in which intestinal secretion was provoked. Calculation demonstrates the volumetric consequences of inadequate recovery of secretory perfusates, and analysis of the perfusion studies shows that distress was significantly associated with poor recovery of the perfusate. These observations are pertinent to increasing interest in the phenomenon of intestinal fluid secretion.

Topics: Carbon Radioisotopes; Chenodeoxycholic Acid; Deoxycholic Acid; Diarrhea; Glycocholic Acid; Humans; Intestinal Absorption; Intestinal Diseases; Intestinal Mucosa; Jejunum; Perfusion; Vomiting

Topics: Bile Acids and Salts; Deoxycholic Acid; Hydrogen-Ion Concentration; Ileum; Intestinal Absorption; Intestinal Diseases