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The following LinkOut resources are supplied by external providers. These providers are responsible for maintaining the links. National Center for Biotechnology Information , U. Gene Genes and mapped phenotypes. Add to Clipboard. Add to Collections. Summary Go to the top of the page Help. The absence of this enzyme results in classic galactosemia in humans and can be fatal in the newborn period if lactose is not removed from the diet. The pathophysiology of galactosemia has not been clearly defined. Two transcript variants encoding different isoforms have been found for this gene. Genomic context Go to the top of the page Help.
Annotation release Status Assembly Chr Location Genomic regions, transcripts, and products Go to the top of the page Help. Go to reference sequence details. Expression Go to the top of the page Help. See details. Bibliography Go to the top of the page Help. Related articles in PubMed Molecular basis and clinical presentation of classic galactosemia in a Croatian population. J Pediatr Endocrinol Metab, Jan PMID Association of presenile cataract with galactosephosphate uridyl transferase gene mutations. Nema N, et al. Schulpis KH, et al.
De Lucca M, et al. Clin Chim Acta, Jul. PMID Genetic and functional studies reveal a novel noncoding variant in GALT associated with a false positive newborn screening result for galactosemia. Liu Y, et al. Clin Chim Acta, Jun Study found no statistically significant difference in the occurrence of the GALT gene mutation between Indian patients with idiopathic presenile cataract and controls.
Puzder had to withdraw his nomination after allegations that his restaurant companies mistreated workers and promulgated sexist advertising. The Whole Foods founder and chief executive John Mackey, an ardent libertarian and admirer of Rand, last month had to cede control of the troubled upscale grocery company to Amazon and Jeff Bezos who, while often likened to a fictional Rand hero, has not mentioned her books when asked about his favorites.
Though people close to Mr. But Mr. Kalanick remains on the board. She can be very inspirational, especially to entrepreneurs. But she was by no means an economist. Brook said that while Mr. He emphasized that Rand would never have tolerated sexual harassment or any kind of mistreatment of employees. Of course, some people had to be fired. But she makes a big deal out of the virtue of justice, which applies in business as well as politics.
Activated neutrophils infiltrate the mucosa and their products can be detected in feces. Numerous neutrophil derived proteins present in stool have been studied, including calprotectin, lactoferrin, and elastase. The most promising marker is calprotectin, because of its remarkable resistance to proteolytic degradation and its stability in stool kept at room temperature for at least seven days [ ].
It is released during cell activation or cell death and has antiproliferative, antimicrobial, and immunomodulating functions [ ],[ ]. Fecal calprotectin is nowadays used in clinical practice to evaluate disease activity in the follow-up of patients treated for active IBD and can be easily performed [ ]. Apart from calprotectin, other markers of intestinal immunity such as secretory IgA [ ] and defensins have been proposed as markers of intestinal permeability.
Whereas secretory IgA has been examined in patients with celiac disease, defensins have been analyzed mostly in patients with IBD [ ]. Since many years, the macromolecules ovalbumin , which is measured in the serum, and FITC-labeled dextran that is uptaken in the ileum and transported further to the mesenteric lymph nodes, have been used as markers for small intestinal permeability. Likely, such high-MW markers indicate different qualities of the intestinal barrier than oligosaccharides, but direct comparisons of the different tracers are lacking.
On the other hand, their value remains unclear, because in vivo data in humans are scare. Most experiments using ovalbumin or FITC-labeled dextran have been made either in rodents or in Ussing chambers. Altered tight junction composition can lead to changes in epithelial permeability. Recently this technique was used to measure changes in tight junction staining in human duodenal tissue and in vitro epithelial cell monolayers following administration of a probiotic [ ].
Tight junctions in the intestine. This figure is based on previously published data [ ] and shows fluorescent staining of occludin in a tissue section perpendicular to the cell surface of the epithelium A. The fluorescence intensities of 3 different uniform areas per section were plotted as a function of cell location using the peak fluorescence signal from the tight junction region to align each intensity profile B.
Administration of live L. Among these, IBD and IBS, critical illness, and — more recently — obesity and metabolic diseases have experienced increasing attention and therefore they will be discuss in this chapter in more detail. Other diseases such as celiac disease need to be mentioned as an example of a disease related to intestinal permeability [ ],[ ].
The realization that the barrier is so important, raises the question of what can disrupt the barrier. Intestinal barrier dysfunction is a main feature of CD and UC [ 1 ],[ 16 ],[ ]. Already 20 years ago it was found that increased intestinal permeability precedes clinical manifestations of CD, but is insufficient to cause disease suggesting other factors being involved [ ],[ ]. Leak flux diarrhea and a facilitated uptake of noxious antigens are the two consequences resulting from an impaired epithelial barrier.
Recently, prion protein, a ubiquitous cellular glycoprotein being involved in cell adhesion, was found to be dislocated in IBD supporting the concept that disrupted barrier function contributes to this disorder [ ]. Moreover, increased incidence of apoptotic events, epithelial cell shedding, as well as erosions and ulcerations can add to that leakiness [ ]. They can be detected in vivo in humans by fluorescein leakage analysis and confocal laser endomicroscopy.
Crucially, increased cell shedding causing microerosions and barrier loss as assessed by confocal laser endomicroscopy predicts relapse in CD over a 12 month period [ 35 ]. Although the etiology of IBD is far from being clear, chronic inflammation is believed to result from an inadequate immune response as a consequence of genetic predisposition as well as changes in, and altered responses to the intestinal microbiota.
On the other hand, an insufficient mucosal response to bacterial stimuli results in an insufficient immune response towards intestinal pathogens. The detailed characterization of barrier defects offers the opportunity to consider and test therapeutic interventions. Beside cytokine antagonists, different plant compounds and probiotics have been shown to stabilize the barrier function by affecting TJ protein expression and distribution [ 16 ].
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Among the plant compounds, Kiwifruit extracts as well as different polyphenols have been found to exert anti-inflammatory effects in models of IBD and in human disease [ ]-[ ]. The first reports on beneficial effects of probiotics in IBD was on E. The next important finding was that the probiotic mixture VSL 3 reduces and protects against pouchitis in patients with UC [ ],[ ].
Since then, more than 80 RCT have been published showing beneficial effects of probiotics in adults and children with UC, but hardly in CD. For example, VSL 3 seems to be effective not only in pouchitis, but also in mild to moderate UC not responding to conventional therapy [ ]. More recently, the positive findings could be extended to children with active UC, who improved after treatment with the probiotic L.
The mechanisms of probiotic effects in IBD is unclear at present, but might involve direct anti-inflammatory effects, e. Most importantly, there is evidence now that increased intestinal permeability is related to low-grade inflammation, visceral hypersensitivity and pain in IBS [ ].
In diarrhea-predominant IBS IBS-D , electron microscopy studies showed cytoskeleton condensation and enlarged intercellular spaces between epithelial cells, providing the morphological basis for increased intestinal permeability in IBS. These structural changes were found to correlate both with mast cell activation and symptoms including diarrhea and pain severity [ ]. These data confirm and extent earlier observations derived from Ussing chamber experiments showing increased paracellular permeability in colon tissue of IBS patients [ ].
The primary cause of the described morpho-functional changes in intestinal permeability remains to be determined.
Potential factors include intestinal food allergies, genetic and epigenetic factors, changes in intestinal microbiota. Regardless the cause, mucosal barrier defects determine an increased flow of antigenic substances that challenge the mucosal immune system. Interestingly, several studies have provided evidence of low-grade immune activation and release of inflammatory molecules in IBS which in turn maintain the increase in intestinal permeability [ ].
Possibly, the loss of particular TJ proteins such as occludin is a result of increased proteasome-mediated degradation observed in IBS triggered by low-grade inflammation and resulting in increased intestinal permeability [ ]. Such data point out the importance of the intestinal barrier in the pathophysiology of IBS and provide evidence for the organic nature of such so-called functional gastrointestinal disorders.
Food, microbiota and bile acids have been discussed as possible inducers of low-grade inflammation and impaired permeability in IBS. In a subgroup of patients, IBS is probably related to food allergy [ ],[ ]. Apart from external inducers, endogenous triggers such as mast cell-derived histamine, proteases and eicosanoids can increase intestinal permeability, either directly or via stimulation of neurons of the enteric nervous system [ ],[ ],[ ].
Serotonin, another biogenic amine besides histamine, produced by enterochromaffin cells in the gut, is another endogenous trigger of pain, inflammation and increased permeability in IBS [ ]. Consequently, LX, an oral inhibitor of tryptophan hydroxylase, the key enzyme for mucosal serotonin synthesis has been successful for treatment of patients with non-constipating IBS [ ].
In conclusion, there is now substantial evidence that increased intestinal permeability is associated with immune activation and symptoms like pain and diarrhea in IBS. Such knowledge paves the way for the identification of new disease biomarkers and novel therapeutic targets in IBS. Apart from mast cell stabilizers [ ] and serotonin antagonists [ ], also dietetic approaches [ ] and probiotics have been found to be effective to some extent. The value of probiotics for treatment in IBS was debated for long time; however, several recent systematic reviews, guidelines and meta-analyses confirmed, despite all gaps and methodological limitations, that selected probiotics are effective in selected subpopulations of patients with IBS [ ]-[ ].
In particular, bloating and distension, for with other therapeutic approaches are limited, may improve by probiotic treatment [ ],[ ]. Most interestingly, some of the probiotic trials demonstrated that the effects are correlated with an improvement of the intestinal permeability [ ]. The new concepts on the pathophysiology of obesity and associated metabolic diseases such as NAFLD and NASH, type 2 diabetes mellitus or cardiovascular diseases, stating that such pathologies are related to the intestinal barrier and the intestinal microbiota, derived predominantly from mouse studies.
It could be clearly shown that metabolic diseases are linked to increased intestinal permeability and translocation of bacteria or bacterial products like endotoxin from the intestine to the liver and to other tissues [ 96 ],[ ],[ ],[ ]. Moreover, it became clear that the microbiota of obese [ ],[ ] and diabetic [ ] individuals differs from that of the healthy, lean population.
In the meantime, evidence is growing suggesting that these alterations are of functional relevance. The altered microbiota in obesity and metabolic diseases contributes to an enhanced harvest of energy from nutrients. In particular, energy harvest from food carbohydrates depends on the microbiota, because specific bacteria found to be increased in obese individuals provide enzymes not expressed by host cells and allowing the digestion of otherwise more or less indigestible carbohydrates [ ]-[ ]. In type 2 diabetes, the microbiota looses its capacity to generate SCFA from prebiotics [ ], which might be a genuine defect or an adaptation to low fiber intake, which has been revealed by several epidemiologic studies [ ],[ ].
The altered intestinal barrier and the subsequent translocation of small amounts of bacteria or bacterial products is now regarded as one important mechanism causing the low-grade inflammation characteristic for metabolic diseases possibly linked to the subsequent infiltration of organs such as liver, muscle and heart muscle with fat [ ]-[ ]. Western style diet rich in fat and sugars alters the intestinal barrier in a way resulting in enhanced permeability and elevated endotoxin levels in the portal vein [ ],[ ],[ ].
The result of such alterations is enhanced infiltration of tissues with bacteria and bacterial products and subsequent tissue inflammation and fat accumulation, which can be observed first in the liver and later on in other tissues such as muscle or heart muscle [ ],[ ],[ ]. Also in peripheral blood and in adipose tissue bacteria or bacterial products can be observed following feeding with energy-rich Western style diet, an observation that might enable to define new bacterial biomarkers of intestinal barrier dysfunction in metabolic diseases [ 89 ],[ ].
However, the two alterations, barrier dysfunction and microbiota alteration, are not necessarily linked, but can occur independently [ ]. Current concepts on the pathophysiology of obesity and metabolic diseases related to the gut. Considering these mechanisms it is tempting to speculate that probiotics and prebiotics might have beneficial effects in chronic metabolic disorders.
First data derived from experimental studies in mice or from preliminary, human pilot studies indeed point in this direction. For example, possible effects of probiotic bacteria or particular diets on the gut barrier can be studied using organ culture models [ ] or feeding models [ 13 ],[ ]. In humans, overfeeding alters the bacterial composition of the commensal microbiota in healthy individuals in a way that results in increased energy harvest from food [ ].
The composition of the commensal microbiota might allow the prediction of weight gain in human individuals at risk like pregnant women [ ]. In addition, administration of selected prebiotics or probiotics can improve metabolic alterations in animal models of metabolic liver disease [ ],[ ] and in obese human individuals [ ],[ ]. Such data suggest that new therapeutic concepts could be developed in the future to support treatment or prevention of obesity and associated diseases. Not only chronic diseases such as IBD, IBS and metabolic diseases, but also acute intestinal failure and gram-negative sepsis typically observed in the critically ill patient are associated with an impaired intestinal barrier and marked enhancement of intestinal permeability.
For that reason, gram-negative sepsis and subsequent MOF is a common cause of death in the intensive care unit ICU [ ]. Such complications are seen in patients undergoing major abdominal surgery, but also in trauma patients, burn patients and other ICU patients [ ]-[ ]. Hypo-perfusion of the intestinal tract is regarded as the culprit of such complications. Therefore, such events occur also in patients suffering from acute CVD, acute intestinal ischemia of any cause, and acute enterocyte toxicity, e.
Also under physiological conditions, a hypo-perfusion of the gut can happen resulting in gut dysfunction, e. This can be assessed by gastric tonometry and by using appropriate biomarkers of enterocyte damage such as intestinal fatty acid binding protein I-FABP and ileal bile acid binding protein I-BABP. In particular, I-FABP, a cytosolic protein in differentiated enterocytes, which can be measured in urine and plasma, has been confirmed as valuable marker for the early diagnosis of intestinal ischemia [ ]. A 15 min ischemia causes the appearance of small subepithelial spaces thought to be morphological correlates of an impaired gut barrier [ ].
Multiple consequences of enteral ischemia have to be anticipated including mucus barrier loss, bacterial translocation, and enhanced Paneth cell apoptosis causing breakdown of the defensing shield in the intestine [ ],[ ]. Fortunately, such alterations are rapidly counteracted, e. Even the structural defects such as the subepithelial spaces are quickly restored by lamina propria retraction and zipper-like constriction of the epithelium [ ].
Such repair mechanisms have been identified in both rodents and man [ ]. The classical treatment of loss of barrier functions in the ICU patient is usage of antibiotics directed against gram-negative bacteria and improvement of intestinal perfusion by catecholamines and volume. If pre- or probiotics can support prevention or treatment of sepsis and MOF is unclear at present.
Some studies suggested a beneficial effect of selected probiotics and synbiotics on sepsis complications in patients with major abdominal surgery and in immunocompromised patients who underwent liver transplantation; however, the trials were rather small and limited in number [ ]-[ ].
Other studies performed in patients with severe acute pancreatitis yielded conflicting results.
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Whereas a few initial studies suggested beneficial effects by treatment with synbiotics [ ],[ ], one trial reported increased mortality in the verum group [ ]. Although this report hat several methodological limitations, the results underline that otherwise harmless probiotics have to be selected and assessed very carefully in severely ill patients similar to pharmaceutical evaluations. Provided that caution is considered, clinical trials are warranted to support the potential use of probiotics in ICU, namely for prevention of antibiotic-associated and Clostridium difficile -associated diarrhea, ventilator-associated pneumonia and sepsis [ ].
A recent meta-analysis drew the conclusion that the administration of probiotics does not significantly reduce ICU or hospital mortality rates but does reduce the incidence of ICU-acquired pneumonia and ICU length of stay [ ]. Apart from IBD, IBS, metabolic diseases and intestinal failure in critically ill patients, other diseases might be related to the gut microbiota and the intestinal barrier such as celiac disease [ ],[ ], colon carcinoma [ ] or inflammatory joint diseases [ ].
Therefore, alteration of the gut barrier seems to have multiple consequences facilitating the onset of a variety of diseases depending on other hits and on genetic or epigenetic constellations, respectively. The growing significance of the gut barrier and bacterial translocation raises the questions of how we can improve gut barrier functions and gut microbiota. The research on modulation of gut permeability is just starting. On the other hand, a few approaches have been identified among which are dietetic concepts including prebiotics, as well as probiotics, and possibly also fecal transplantation that can be regarded as an unspecific and global probiotic treatment.
Indeed, fecal transplantation now enters clinical medicine, after beneficial effects in patients with therapy-refractory Clostridium difficile infection have been reported [ ],[ ]. Among the diets, some sound promising such as dietary restriction of fat and sugars, or possibly also of poorly absorbed short-chain carbohydrates FODMAPs [ ]-[ ]. Clearly, more intervention trials are urgently needed now to asses the effects of such substances as preventive or therapeutic agents in different populations and diseases, respectively.
To conduct such trials in a scientifically sound way, we need a clear definition and validation of the tools needed to assess gut barrier functions and intestinal permeability. New approaches such as mucus analysis, quantification of translocated bacteria and bacterial products in blood or tissue, and host responses to such alterations, e. Even though European authorities strictly differ between nutrients and drugs, the new tools to modulate intestinal permeability, such as probiotics, prebiotics or other possibly enriched dietetic components, need clear scientific evaluation independent of their legal classification, which can be questioned from a scientific point of view [ ],[ ].
The fact that such substances can be used both for prevention of disease in the general population and for prophylaxis or treatment of disease in defined subpopulations and thus touch both legal categories of substances, a third category should be considered placed between the two existing ones. Despite many open questions, intestinal permeability becomes an area of growing interest both in basic science and for clinicians, because it might by a valuable new target for disease prevention and therapy.
The expert panel agreed on several conclusions:. Given the importance of the physiological and thus the clinical role of the intestinal permeability there is a need for biomarkers that not only reflect lost functionality of the intestine, but also permeability per se and permeability-related functions such as mucus quality. More research is needed to develop reliable non-invasive, rapid diagnostic means. The role of microbiota in the regulation of intestinal permeability also requires additional research.
Food intake is of importance for the intestinal microbiota composition as well as for intestinal permeability, but to which extent? Apart from dietetic approaches, what else can attenuate negative effects of nutrients? What is the preventive capacity of pre- and probiotics? The question of how to define a healthy microbiota needs to be addressed.
Can an "unhealthy microbiota" affect intestinal permeability in a negative way? Can an "unhealthy" intestinal microbiota impair the mucosal immune system through an excessively permeable mucosal barrier, and thus perturb bowel physiology and sensory perception? Can we look at the intestinal microbiota as a novel therapeutic tool to improve intestinal permeability and gut health?
All authors participated in the round table discussion on which the article is based. The manuscript was written by SCB and revised and extended by all co-authors. All authors read and approved the final paper. We acknowledge the support by Dr. Apart form the financial support by Yakult Europe B. The funding body had no role in the writing of the manuscript and in the decision to submit the manuscript for publication. Competing interests. The round table was financially supported by Yakult Europe B. The supporting company was not involved in the preparation of the manuscript neither influenced the content of the manuscript in any respect.
Apart from this support, the authors declare that they have no competing interests. Stephan C Bischoff, Email: ed. Giovanni Barbara, Email: ti. Wim Buurman, Email: ln. Theo Ockhuizen, Email: ln. Matteo Serino, Email: rf. Herbert Tilg, Email: ta. Alastair Watson, Email: ku. Jerry M Wells, Email: ln. National Center for Biotechnology Information , U. BMC Gastroenterol. Published online Nov Author information Article notes Copyright and License information Disclaimer. Corresponding author.
Received Dec 27; Accepted Oct This article is published under license to BioMed Central Ltd. This article has been cited by other articles in PMC. Abstract Data are accumulating that emphasize the important role of the intestinal barrier and intestinal permeability for health and disease. Electronic supplementary material The online version of this article doi Introduction Why do we need a gut barrier? Open in a separate window. Figure 1. Review Definition of intestinal permeability Definition of intestinal permeability and intestinal barrier The term "mucosal barrier" was adopted by Cummings in to describe the complex structure that separates the internal milieu from the luminal environment [ 14 ].
Table 1 Definitions. Intestinal barrier is a functional entity separating the gut lumen from the inner host, and consisting of mechanical elements mucus, epithelial layer , humoral elements defensins, IgA , immununological elements lymphocytes, innate immune cells , muscular and neurological elements Intestinal permeability is defined as a functional feature of the intestinal barrier at given sites, measurable by analyzing flux rates across the intestinal wall as a whole or across wall components of defined molecules that are largely inert during the process and that can be adequately measured in these settings Normal intestinal permeability is defined as a stable permeability found in healthy individuals with no signs of intoxication, inflammation or impaired intestinal functions Impaired intestinal permeability is defined as a disturbed permeability being non-transiently changed compared to the normal permeability leading to a loss of intestinal homeostasis, functional impairments and disease.
Figure 2. Figure 3. Endogenous cannabinoid system The plant Cannabis sativa has bee used to treat various disorders of the gastrointestinal tract such as vomiting, anorexia, diarrhea, and intestinal inflammation [ 52 ]. Regulation of intestinal permeability by diet and bacteria Intestinal barrier and the microbiota The intestinal tract harbors the largest bacterial community associated with the human body, reaching densities of about 10 12 bacteria per gram of luminal content in the distal colon. Table 2 Proposed functions of the human intestinal microbiota. I Host defense against pathogens and toxins II Development and maintenance of the intestinal immune system III Support of digestion by supply of enzymatic capacity.
The intestinal barrier and bacterial pathogens Many pathogens specifically interact with defined element of the intestinal barrier underlining the importance of bacterial-host interactions in both health and disease. Table 3 Pathogen interactions with epithelial tight junctions. Regulation of gut permeability by diet, prebiotics and probiotics Since we now know about the clinical implications, interest in understanding the regulation of this barrier is growing. Vitamins Vitamin A and its derivatives have been shown to regulate the growth and differentiation of intestinal cells, whereas vitamin A deficiency is associated with increased susceptibility to infection in both human and animal models [ 1 ].
Short chain fatty acids SCFA These organic acids comprising acetate, propionate, butyrate and valerate are produced by intestinal microbial fermentation of undigested dietary carbohydrates in the colon. Prebiotics Apart from the effects of fermentation products of prebiotics such as SCFA, prebiotics by itself might have stabilizing effects on the intestinal barrier.
Western style diet A number of animal studies investigated effects of high-fat diets on the composition of gut microbiota and on intestinal permeability [ 9 ],[ 13 ]. Probiotics Several studies report the use of commensal bacteria and probiotics to promote intestinal barrier integrity in vivo [ ]-[ ] although some studies have been negative or inconclusive. Measurement of intestinal permeability Intestinal permeability and integrity can be measured in many ways. Figure 4. Table 4 Means for the assessment of intestinal permeability functional tests, bacteria-related tests.
Table 5 Means for the assessment of intestinal permeability biomarkers, histology. Means Hu An Test molecules Test site Material needed Disadvantages In vivo — biomarkers of epithelial cell damage Citrulline x x endogenous ep product small intestine plasma FABP x x endogenous ep marker site- specific plasma only in acute phase? Claudin-3 x x ep tight junction protein n. The Ussing chamber The Ussing chamber allows the measurement of short-circuit current as an indicator of active ion transport taking place across the intestinal epithelium.
Figure 5. Permeability assays Permeability assays usually use oligosaccharides of large size, e. Bacteria-related markers LPS measurement Despite well-known technical limitations of the assay, resulting from the low levels detectable in peripheral blood, several studies have successfully used LPS assays to show endotoxemia, mostly in patients with sepsis [ ].
Circulating endotoxin core antibodies EndoCAb Alternatively to the measurement of endotoxin, which yields best results if measured in portal vein plasma, measurement of circulating EndoCAb allowing the quantification of immunoglobulins IgG, IgM and IgA against the inner core of endotoxin have been proposed for the acute phase of intestinal barrier damage. Fecal butyrate concentrations Generation of SCFA such as butyrate depends on prebiotic and other dietetic factors as well as on the composition and activity oft he intestinal microbiota.
Assessment of fatty liver disease Translocation of bacterial or bacterial products such as LPS from the intestine to the liver has been proposed as trigger for liver inflammation and fatty liver disease [ ]. Analysis of intestinal mucus for bacterial content Most recently, it has been shown that under conditions characterized by an impaired intestinal barrier, luminal bacteria enter the inner colon mucus normally impenetrable for the commensals [ 28 ]. Biomarkers of epithelial cell integrity Plasma levels of citrulline, an amino acid not incorporated into proteins, but produced by small intestinal enterocytes from glutamine have been proposed as a marker of functional enterocyte mass.
Biomarkers of intestinal inflammation and intestinal immunity Fecal calprotectin A broad range of pathologies can lead to intestinal inflammation such as neoplasia, IBD, IBS, infections, autoimmune diseases, allergies, intestinal hypoperfusion, and selected drugs like non-steroidal anti-inflammatory drugs. Histological approaches Altered tight junction composition can lead to changes in epithelial permeability.
Figure 6. Intestinal permeability — a new target in health and disease?
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Table 6 Diseases related to intestinal permeability. Table 7 Possible causes of impairment of the intestinal barrier. Role of intestinal permeability and probiotics in obesity and fatty liver disease The new concepts on the pathophysiology of obesity and associated metabolic diseases such as NAFLD and NASH, type 2 diabetes mellitus or cardiovascular diseases, stating that such pathologies are related to the intestinal barrier and the intestinal microbiota, derived predominantly from mouse studies.
Figure 7. Role of intestinal permeability and probiotics in the critically ill patient Not only chronic diseases such as IBD, IBS and metabolic diseases, but also acute intestinal failure and gram-negative sepsis typically observed in the critically ill patient are associated with an impaired intestinal barrier and marked enhancement of intestinal permeability.
Conclusion Apart from IBD, IBS, metabolic diseases and intestinal failure in critically ill patients, other diseases might be related to the gut microbiota and the intestinal barrier such as celiac disease [ ],[ ], colon carcinoma [ ] or inflammatory joint diseases [ ]. Table 8 Factors proposed to support the gut barrier. Acknowledgments We acknowledge the support by Dr.
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