Circulating levels of glucagon-like peptide-2 in human subjects with inflammatory bowel disease

2000 ◽  
Vol 278 (4) ◽  
pp. R1057-R1063 ◽  
Author(s):  
Qiang Xiao ◽  
Robin P. Boushey ◽  
Maria Cino ◽  
Daniel J. Drucker ◽  
Patricia L. Brubaker
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Human Subjects ◽  
Normal Subjects ◽  
Relative Activity ◽  
Human Inflammatory Bowel Disease ◽  
Inflammatory Bowel ◽  
Glucagon Like Peptide ◽  
Circulating Levels

Glucagon-like peptide-2 (GLP-2) is a recently characterized intestine-derived peptide that exerts trophic activity in the small and large intestine. Whether circulating levels of GLP-2 are perturbed in the setting of human inflammatory bowel disease (IBD) remains unknown. The circulating levels of bioactive GLP-2-(1—33) compared with its degradation product GLP-2-(3—33) were assessed using a combination of RIA and HPLC in normal and immunocompromised control human subjects and patients hospitalized for IBD. The activity of the enzyme dipeptidyl peptidase IV (DP IV), a key determinant of GLP-2-(1—33) degradation was also assessed in the plasma of normal controls and subjects with IBD. The circulating levels of bioactive GLP-2-(1—33) were increased in patients with either ulcerative colitis (UC) or Crohn's Disease (CD; to 229 ± 65 and 317 ± 89%, P < 0.05, of normal, respectively). Furthermore, the proportion of total immunoreactivity represented by intact GLP-2-(1—33), compared with GLP-2-(3—33), was increased from 43 ± 3% in normal healthy controls to 61 ± 6% ( P < 0.01) and 59 ± 2% ( P < 0.01) in patients with UC and CD, respectively. The relative activity of plasma DP IV was significantly reduced in subjects with IBD compared with normal subjects (1.4 ± 0.3 vs. 5.0 ± 1.1 mU/ml, respectively; P< 0.05). These results suggest that patients with active IBD may undergo an adaptive response to intestinal injury by increasing the circulating levels of bioactive GLP-2-(1—33), facilitating enhanced repair of the intestinal mucosal epithelium in vivo.

scholarly journals Zebrafish modeling of intestinal injury, bacterial exposures and medications defines epithelial in vivo responses relevant to human inflammatory bowel disease

2019 ◽  
Vol 12 (8) ◽  
pp. dmm037432 ◽  
Author(s):  
Ling-shiang Chuang ◽  
Joshua Morrison ◽  
Nai-yun Hsu ◽  
Philippe Ronel Labrias ◽  
Shikha Nayar ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Injury ◽  
Human Inflammatory Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Resveratrol and inflammatory bowel disease: the evidence so far

2017 ◽  
Vol 31 (1) ◽  
pp. 85-97 ◽  
Author(s):  
Sandra Nunes ◽  
Francesca Danesi ◽  
Daniele Del Rio ◽  
Paula Silva
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Mucosa ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Human Subjects ◽  
Intestinal Immunity ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

AbstractDespite the fact that inflammatory bowel disease (IBD) has still no recognised therapy, treatments which have proven at least mildly successful in improving IBD symptoms include anti-inflammatory drugs and monoclonal antibodies targeting pro-inflammatory cytokines. Resveratrol, a natural (poly)phenol found in grapes, red wine, grape juice and several species of berries, has been shown to prevent and ameliorate intestinal inflammation. Here, we discuss the role of resveratrol in the improvement of inflammatory disorders involving the intestinal mucosa. The present review covers three specific aspects of resveratrol in the framework of inflammation: (i) its content in food; (ii) its intestinal absorption and metabolism; and (iii) its anti-inflammatory effects in the intestinal mucosa in vitro and in the very few in vivo studies present to date. Actually, if several studies have shown that resveratrol may down-regulate mediators of intestinal immunity in rodent models, only two groups have performed intervention studies in human subjects using resveratrol as an agent to improve IBD conditions. The effects of resveratrol should be further investigated by conducting well-designed clinical trials, also taking into account different formulations for the delivery of the bioactive compound.

Preparation, characterization, and in vivo evaluation of anti-inflammatory activities of selenium nanoparticles synthesized by Kluyveromyces lactis GG799

2021 ◽  
Author(s):  
Xiao fan Song ◽  
Lei Qiao ◽  
Shuqi Yan ◽  
Yue Chen ◽  
Xina Dou ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Kluyveromyces Lactis ◽  
Selenium Nanoparticles ◽  
Human Diseases ◽  
In Vivo Evaluation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Selenium (Se) as an essential micronutrient that has implications in human diseases, including inflammatory bowel disease (IBD), especially with respect to Se deficiencies. Recently, selenium nanoparticles (SeNPs) have attracted significant...

scholarly journals The food additive EDTA aggravates colitis and colon carcinogenesis in mouse models

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rayko Evstatiev ◽  
Adam Cervenka ◽  
Tina Austerlitz ◽  
Gunther Deim ◽  
Maximilian Baumgartner ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Models ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Food Additives ◽  
Colorectal Carcinogenesis ◽  
Testing Procedures ◽  
Inflammatory Models ◽  
Inflammatory Bowel

AbstractInflammatory bowel disease is a group of conditions with rising incidence caused by genetic and environmental factors including diet. The chelator ethylenediaminetetraacetate (EDTA) is widely used by the food and pharmaceutical industry among numerous other applications, leading to a considerable environmental exposure. Numerous safety studies in healthy animals have revealed no relevant toxicity by EDTA. Here we show that, in the presence of intestinal inflammation, EDTA is surprisingly capable of massively exacerbating inflammation and even inducing colorectal carcinogenesis at doses that are presumed to be safe. This toxicity is evident in two biologically different mouse models of inflammatory bowel disease, the AOM/DSS and the IL10−/− model. The mechanism of this effect may be attributed to disruption of intercellular contacts as demonstrated by in vivo confocal endomicroscopy, electron microscopy and cell culture studies. Our findings add EDTA to the list of food additives that might be detrimental in the presence of intestinal inflammation, but the toxicity of which may have been missed by regulatory safety testing procedures that utilize only healthy models. We conclude that the current use of EDTA especially in food and pharmaceuticals should be reconsidered. Moreover, we suggest that intestinal inflammatory models should be implemented in the testing of food additives to account for the exposure of this primary organ to environmental and dietary stress.

scholarly journals An objective in vivo diagnostic method for inflammatory bowel disease

2018 ◽  
Vol 5 (3) ◽  
pp. 180107 ◽  
Author(s):  
Sophie C. Payne ◽  
Robert K. Shepherd ◽  
Alicia Sedo ◽  
James B. Fallon ◽  
John B. Furness
Keyword(s):  
Inflammatory Bowel Disease ◽  
Real Time ◽  
Bowel Disease ◽  
Experimental Models ◽  
Mucosal Barrier ◽  
Trinitrobenzene Sulfonic Acid ◽  
Inflammatory Damage ◽  
Mucosal Barrier Function ◽  
Inflammatory Bowel

Inflammatory damage to the bowel, as occurs in inflammatory bowel disease (IBD), is debilitating to patients. In both patients and animal experimental models, histological analyses of biopsies and endoscopic examinations are used to evaluate the disease state. However, such measurements often have delays and are invasive, while endoscopy is not quantitatively objective. Therefore, a real-time quantitative method to assess compromised mucosal barrier function is advantageous. We investigated the correlation of in vivo changes in electrical transmural impedance with histological measures of inflammation. Four platinum (Pt) ball electrodes were placed in the lumen of the rat small intestine, with a return electrode under the skin. Electrodes placed within the non-inflamed intestine generated stable impedances during the 3 h testing period. Following an intraluminal injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS), an established animal model of IBD, impedances in the inflamed region significantly decreased relative to a region not exposed to TNBS ( p  < 0.05). Changes in intestinal transmural impedance were correlated ( p  < 0.05) with histologically assessed damage to the mucosa and increases in neutrophil, eosinophil and T-cell populations at 3 h compared with tissue from control regions. This quantitative, real-time assay may have application in the diagnosis and clinical management of IBD.

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