Increased intestinal permeability in inflammatory bowel diseases assessed by iohexol test

Gerova, V.; Stoynov, Simeon G; Katsarov, D.; Svinarov, Dobrin

doi:10.3748/wjg.v17.i17.

Cited by 42 publications

(35 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Their results indicate a potential association between TGR5 exon 1 polymorphisms and the overall transit time in a subgroup of patients [81]. As previously noted, the TGR5-knockout mouse exhibits microscopic changes in colonic epithelial structure and alteration of epithelial tight junctions, inducing an abnormal increase in epithelial permeability, reported as a contributing mechanism in the pathophysiology of both IBD [62] and IBS [82,83]. …”

Section: Tgr5: Relevance In Diseasesmentioning

confidence: 82%

The bile acid TGR5 membrane receptor: From basic research to clinical application

Duboc

Taché

Hofmann

2014

Digestive and Liver Disease

376

335

View full text Add to dashboard Cite

The TGR5 receptor (or GP-BAR1, or M-BAR) was characterized ten years ago as the first identified G-coupled protein receptor specific for bile acids. TGR5 gene expression is widely distributed, including endocrine glands, adipocytes, muscles, immune organs, spinal cord, and the enteric nervous system. The effect of TGR5 activation depends on the tissue where it is expressed and the signalling cascade that it induces. Animal studies suggest that TGR5 activation influences energy production and thereby may be involved in obesity and diabetes. TGR5 activation also influences intestinal motility. This review provides an overview of TGR5-bile acid interactions in health as well as the possible involvement of TGR5 in human disease.

show abstract

Section: Tgr5: Relevance In Diseasesmentioning

confidence: 82%

The bile acid TGR5 membrane receptor: From basic research to clinical application

Duboc

Taché

Hofmann

2014

Digestive and Liver Disease

376

335

View full text Add to dashboard Cite

show abstract

“…An intact barrier is a prerequisite for normal health, and rapid resealing after injury is essential for prevention of disease [6, 7]. The epithelial barrier has the unenviable task of confining the microbiome and any potentially harmful substances to the lumen while regulating the flow of solutes, nutrients, and ions into the underlying mucosa [8, 9].…”

Section: The Intestinal Barriermentioning

confidence: 99%

Diet, Microbiome, and the Intestinal Epithelium: An Essential Triumvirate?

Guzman

Conlin

Jobin

2013

BioMed Research International

View full text Add to dashboard Cite

The intestinal epithelium represents a critical barrier protecting the host against diverse luminal noxious agents, as well as preventing the uncontrolled uptake of bacteria that could activate an immune response in a susceptible host. The epithelial monolayer that constitutes this barrier is regulated by a meshwork of proteins that orchestrate complex biological function such as permeability, transepithelial electrical resistance, and movement of various macromolecules. Because of its key role in maintaining host homeostasis, factors regulating barrier function have attracted sustained attention from the research community. This paper will address the role of bacteria, bacterial-derived metabolism, and the interplay of dietary factors in controlling intestinal barrier function.

show abstract

“…Microbiota‐related low‐grade inflammation is characterized by elevated pro‐inflammatory gene expression and is a common consequence of an altered host–microbiota relationship caused by instigator bacteria or dietary components that influence intestinal permeability (Chassaing & Gewirtz, ). There is accumulating evidence that asserts the importance of intestinal permeability, a barrier aspect closely associated with the intestinal commensal microbiota as well as with the mucosal immune system, in intestinal and systemic health (Brun et al , ; Manco et al , ; Gerova et al , ; Neves et al , ; Bischoff et al , ). Heightened intestinal permeability can allow for an increased translocation of bacterial products such as LPS and other pathogen‐associated molecular pattern molecules (PAMPs) (Cani et al , ; Cerf‐Bensussan & Gaboriau‐Routhiau, ; Mehal, ).…”

Section: Introductionmentioning

confidence: 99%

Gut microbiota influences pathological angiogenesis in obesity‐driven choroidal neovascularization

et al. 2016

View full text Add to dashboard Cite

Age‐related macular degeneration in its neovascular form (NV AMD) is the leading cause of vision loss among adults above the age of 60. Epidemiological data suggest that in men, overall abdominal obesity is the second most important environmental risk factor after smoking for progression to late‐stage NV AMD. To date, the mechanisms that underscore this observation remain ill‐defined. Given the impact of high‐fat diets on gut microbiota, we investigated whether commensal microbes influence the evolution of AMD. Using mouse models of NV AMD, microbiotal transplants, and other paradigms that modify the gut microbiome, we uncoupled weight gain from confounding factors and demonstrate that high‐fat diets exacerbate choroidal neovascularization (CNV) by altering gut microbiota. Gut dysbiosis leads to heightened intestinal permeability and chronic low‐grade inflammation characteristic of inflammaging with elevated production of IL‐6, IL‐1β, TNF‐α, and VEGF‐A that ultimately aggravate pathological angiogenesis.

show abstract

Increased intestinal permeability in inflammatory bowel diseases assessed by iohexol test

Abstract: Serum levels of iohexol at 3 h and 6 h after its ingestion reflect increased IP, which is related to the disease activity in patients with IBD.

Cited by 42 publications

References 22 publications

The bile acid TGR5 membrane receptor: From basic research to clinical application

The bile acid TGR5 membrane receptor: From basic research to clinical application

Diet, Microbiome, and the Intestinal Epithelium: An Essential Triumvirate?

Gut microbiota influences pathological angiogenesis in obesity‐driven choroidal neovascularization

Contact Info

Product

Resources

About