Relevant bibliographies by topics / Permeabilità intestinale

Academic literature on the topic 'Permeabilità intestinale'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Permeabilità intestinale"

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Bottaccioli, Anna Giulia. "La malattia infiammatoria cronica intestinale: cure integrate in ottica Pnei." PNEI REVIEW, no. 2 (November 2020): 30–40. http://dx.doi.org/10.3280/pnei2020-002004.

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La malattia infiammatoria cronica intestinale (MICI) è una malattia idiopatica autoimmune che colpisce l'apparato digerente a causa dalla risposta immunitaria disregolata contro la microflora intestinale. I due principali tipi di MICI sono la rettocolite ulcerosa (RCU) e il morbo di Crohn (MC). Lo studio dell'asse intestino-cervello applicato alle MICI ha correlato lo stress con il peggioramento dell'attività di malattia. Durante lo stress, il cortisolo incrementa la permeabilità della barriera intestinale, favorendo la disbiosi intestinale e l'attivazione immunitaria in senso pro-infiammatorio. Un altro elemento osservato nelle MICI è l'alterazione del sistema neurovegetativo e in particolare la riduzione delle fibre efferenti vagali nel tratto digerente con conseguente fallimento del riflesso anti-infiammatorio vagale ed aumento dell'infiammazione. Vengono illustrate le evidenze scientifiche di approcci terapeutici non farmacologici integrati alla terapia standard delle MICI, come dieta anti-infiammatoria, pre- e probiotici, trapianto di microbiota fecale, fitoterapia, stimolazione nervosa vagale, agopuntura, terapie mente-corpo (meditazione, yoga e rilassamento) e psicoterapia.
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Bianchi, Alfio Ernesto, Antonio Maggi, and Riccardo Raddino. "Il microbiota intestinale, tra salute e malattia: un vero attore a due facce." CARDIOLOGIA AMBULATORIALE 30, no. 2 (October 14, 2021): 85–91. http://dx.doi.org/10.17473/1971-6818-2021-2-1.

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Il microbiota intestinale è un ecosistema batterico cha ha proprietà difensive per l’ospite ma che in particolari condizioni può produrre metaboliti tossici e dannosi per l’organismo. Metaboliti benefici sono gli acidi grassi a catena corta (SCAF), i metaboliti biliari ed i probiotici. Metaboliti dannosi sono la trimetilamina-N-ossidata (TMAO), i lipopolisaccaridi (LPS) e le tossine uremiche. La permeabilità della mucosa intestinale è la causa principale del passaggio in circolo di metaboliti dannosi. Il microbiota può intervenire in modo difensivo o dannoso in molte patologie cardiovascolari come la cardiopatia ischemica e lo scompenso ed in situazioni cliniche come il diabete, l’obesità, la malattia renale, la colite ulcerosa, il morbo di Chron e le malattie neurodegenerative. La dieta corretta è il cardine per mantenere una una favorevole funzionalità del microbiota.
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Bertossi, Francesca. "Il ruolo del microbiota nell'aumento ponderale associato alla terapia antipsicotica." PNEI REVIEW, no. 2 (November 2022): 108–22. http://dx.doi.org/10.3280/pnei2022-002010.

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Per il trattamento di un disturbo mentale severo e la prevenzione delle ricadute sono indicate delle terapie a lungo termine con farmaci antipsi- cotici. Gli antipsicotici di seconda generazione sono associati ad un minor numero di sintomi extrapiramidali, tuttavia sono gravati da importanti effetti collaterali di tipo metabolico e dal rischio di aumento ponderale, effetti mediati sia dai recettori centrali e periferici, sia a modifiche della composizione del microbiota. Numerose sono le evidenze del ruolo del microbiota intestinale nell'indur- re l'aumento ponderale ed i disturbi metabolici indotti dagli antipsicotici di seconda generazione attraverso un alterato segnale dello stimolo della fame e della sazietà, una riduzione della spesa energetica, la modulazione del metabolismo lipidico e glucidico, le modifiche dell'infiammazione e del- la permeabilità della barriera intestinale. Nella prevenzione e nel trattamento integrato dell'aumento ponderale as- sociato alla terapia antipsicotica, oltre alle terapie di tipo farmacologico, i programmi nutrizionali e l'attività fisica trova impiego un approccio volto a modulare il microbiota intestinale per correggere la disbiosi. Tra i diversi probiotici impiegati quello più promettente sembra essere l'Akkermansia muchiniphila.
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Pabla, D., F. Akhlaghi, H. Zia, Marco Centanni, and Nunzia Brusca. "Incremento della permeabilità intestinale alla levotiroxina sodica mediante acidi grassi a catena lineare studiata in linee di cellule epiteliali MDCK." L'Endocrinologo 12, no. 5 (October 2011): 259–60. http://dx.doi.org/10.1007/bf03344845.

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Cavin, Jean-Baptiste, Hailey Cuddihey, Wallace K. MacNaughton, and Keith A. Sharkey. "Acute regulation of intestinal ion transport and permeability in response to luminal nutrients: the role of the enteric nervous system." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 2 (February 1, 2020): G254—G264. http://dx.doi.org/10.1152/ajpgi.00186.2019.

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The small intestine regulates barrier function to absorb nutrients while avoiding the entry of potentially harmful substances or bacteria. Barrier function is dynamically regulated in part by the enteric nervous system (ENS). The role of the ENS in regulating barrier function in response to luminal nutrients is not well understood. We hypothesize that the ENS regulates intestinal permeability and ion flux in the small intestine in response to luminal nutrients. Segments of jejunum and ileum from mice were mounted in Ussing chambers. Transepithelial electrical resistance (TER), short-circuit current ( Isc), and permeability to 4-kDa FITC-dextran (FD4) were recorded after mucosal stimulation with either glucose, fructose, glutamine (10 mM), or 5% Intralipid. Mucosal lipopolysaccharide (1 mg/mL) was also studied. Enteric neurons were inhibited with tetrodotoxin (TTX; 0.5 μM) or activated with veratridine (10 μM). Enteric glia were inhibited with the connexin‐43 blocker Gap26 (20 μM). Glucose, glutamine, Intralipid, and veratridine acutely modified Isc in the jejunum and ileum, but the effect of nutrients on Isc was insensitive to TTX. TTX, Gap26, and veratridine treatment did not affect baseline TER or permeability. Intralipid acutely decreased permeability to FD4, while LPS increased it. TTX pretreatment abolished the effect of Intralipid and exacerbated the LPS‐induced increase in permeability. Luminal nutrients and enteric nerve activity both affect ion flux in the mouse small intestine acutely but independently of each other. Neither neuronal nor glial activity is required for the maintenance of baseline intestinal permeability; however, neuronal activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. NEW & NOTEWORTHY Luminal nutrients and enteric nerve activity both affect ion transport in the mouse small intestine acutely, but independently of each other. Activation or inhibition of the enteric neurons does not affect intestinal permeability, but enteric neural activity is essential for the acute regulation of intestinal permeability in response to luminal lipids and lipopolysaccharide. The enteric nervous system regulates epithelial homeostasis in the small intestine in a time-dependent, region- and stimulus-specific manner.
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Dahlgren, David, Maria-Jose Cano-Cebrián, Tobias Olander, Mikael Hedeland, Markus Sjöblom, and Hans Lennernäs. "Regional Intestinal Drug Permeability and Effects of Permeation Enhancers in Rat." Pharmaceutics 12, no. 3 (March 8, 2020): 242. http://dx.doi.org/10.3390/pharmaceutics12030242.

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Sufficient colonic absorption is necessary for all systemically acting drugs in dosage forms that release the drug in the large intestine. Preclinically, colonic absorption is often investigated using the rat single-pass intestinal perfusion model. This model can determine intestinal permeability based on luminal drug disappearance, as well as the effect of permeation enhancers on drug permeability. However, it is uncertain how accurate the rat single-pass intestinal perfusion model predicts regional intestinal permeability and absorption in human. There is also a shortage of systematic in vivo investigations of the direct effect of permeation enhancers in the small and large intestine. In this rat single-pass intestinal perfusion study, the jejunal and colonic permeability of two low permeability drugs (atenolol and enalaprilat) and two high-permeability ones (ketoprofen and metoprolol) was determined based on plasma appearance. These values were compared to already available corresponding human data from a study conducted in our lab. The colonic effect of four permeation enhancers—sodium dodecyl sulfate, chitosan, ethylenediaminetetraacetic acid (EDTA), and caprate—on drug permeability and transport of chromium EDTA (an established clinical marker for intestinal barrier integrity) was determined. There was no difference in jejunal and colonic permeability determined from plasma appearance data of any of the four model drugs. This questions the validity of the rat single-pass intestinal perfusion model for predicting human regional intestinal permeability. It was also shown that the effect of permeation enhancers on drug permeability in the colon was similar to previously reported data from the rat jejunum, whereas the transport of chromium EDTA was significantly higher (p < 0.05) in the colon than in jejunum. Therefore, the use of permeation enhancers for increasing colonic drug permeability has greater risks than potential medical rewards, as indicated by the higher permeation of chromium EDTA compared to the drugs.
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Pijls, Kirsten E., Ger H. Koek, Elhaseen E. Elamin, Hanne de Vries, Ad A. M. Masclee, and Daisy M. A. E. Jonkers. "Large intestine permeability is increased in patients with compensated liver cirrhosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 306, no. 2 (January 15, 2014): G147—G153. http://dx.doi.org/10.1152/ajpgi.00330.2013.

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Intestinal barrier dysfunction, facilitating translocation of bacteria and bacterial products, plays an important role in the pathophysiology of liver cirrhosis and its complications. Increased intestinal permeability has been found in patients with liver cirrhosis, but data on small and large intestine permeability and tight junctions (TJs) in patients with compensated cirrhosis are scarce. We aimed to investigate both small and large intestine permeability in patients with stable compensated cirrhosis compared with healthy controls and evaluated the expression of TJ proteins in mucosal biopsies at duodenal and sigmoid level. Intestinal permeability was assessed in 26 patients with compensated cirrhosis and 27 matched controls using a multisugar test. Duodenal and sigmoid biopsies were available from a subgroup for analyses of gene transcription and expression of key TJ proteins by qRT-PCR and ELISA, respectively. Median 0–5-h urinary sucrose excretion and lactulose/rhamnose ratio were comparable between patients with compensated cirrhosis and controls, whereas 5–24-h urinary sucralose/erythritol ratio was increased in these patients. Downregulation of gene transcription was found for claudin-3 in duodenal biopsies and claudin-4 in sigmoid biopsies, and at the protein level occludin expression was significantly increased in both duodenal and sigmoid biopsies. This study shows that gastroduodenal and small intestine permeability are not altered, whereas large intestine permeability is increased in patients with stable compensated cirrhosis. Only limited alterations were found regarding the expression of TJ proteins in both the small and large intestine.
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Markovic, Milica, Moran Zur, Sapir Garsiani, Daniel Porat, Sandra Cvijić, Gordon L. Amidon, and Arik Dahan. "The Role of Paracellular Transport in the Intestinal Absorption and Biopharmaceutical Characterization of Minoxidil." Pharmaceutics 14, no. 7 (June 27, 2022): 1360. http://dx.doi.org/10.3390/pharmaceutics14071360.

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The purpose of this study was to evaluate mechanisms behind the intestinal permeability of minoxidil, with special emphasis on paracellular transport, and elucidate the suitability of minoxidil to be a reference drug for Biopharmaceutics Classification System (BCS). The permeability of minoxidil (vs. metoprolol) was evaluated in-silico, in-vitro using both the PAMPA assay and across Caco-2 cell monolayers, as well as in-vivo in rats throughout the entire intestine. The permeability was studied in conditions that represent the different segments of the small intestine: upper jejunum (pH 6.5), mid small intestine (pH 7.0), distal ileum (pH 7.5), and colon (pH 6.5). Since we aimed to investigate the paracellular transport of minoxidil, we have also examined its permeability in the presence of quercetin (250 µM), which closes the tight junctions, and sodium decanoate (10 mM), which opens the tight junctions. While metoprolol demonstrated segmental-dependent rat and PAMPA permeability, with higher permeability in higher pH regions, the permeability of minoxidil was pH-independent. Minoxidil PAMPA permeability was significantly lower than its rat permeability, indicating a potential significant role of the paracellular route. In rat intestinal perfusion studies, and across Caco-2 monolayers, tight junction modifiers significantly affected minoxidil permeability; while the presence of quercetin caused decreased permeability, the presence of sodium decanoate caused an increase in minoxidil permeability. In accordance with these in-vitro and in-vivo results, in-silico simulations indicated that approximatelly 15% of minoxidil dose is absorbed paracellularly, mainly in the proximal parts of the intestine. The results of this study indicate that paracellular transport plays a significant role in the intestinal permeability of minoxidil following oral administration. Since this permeation route may lead to higher variability in comparison to transcellular, these findings diminish the suitability of minoxidil to serve as the low/high BSC permeability class benchmark.
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Willems, D., S. Cadranel, and W. Jacobs. "Measurement of urinary sugars by HPLC in the estimation of intestinal permeability: evaluation in pediatric clinical practice." Clinical Chemistry 39, no. 5 (May 1, 1993): 888–90. http://dx.doi.org/10.1093/clinchem/39.5.888.

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Abstract Determinations of the permeability of the intestine to various sugars have been used to assess intestinal mucosal abnormalities, but the widespread application of such tests has been prohibited by the complexity of most classically used techniques. In this study, we evaluated the sensitivity and practicability of using HPLC to estimate intestinal permeability, with mannitol and lactulose as mono- and disaccharides, respectively. The results of the permeability tests were compared with those of intestinal biopsy in 20 children. All patients with an abnormal intestinal biopsy showed a low mannitol recovery, and the patients with allergic symptoms showed a high lactulose recovery. Our preliminary data suggest that HPLC is reliable, gives results comparable with those of other methods, and is a practical way to determine intestinal permeability noninvasively.
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Oscarsson, Elin, Tim Lindberg, Kathrin S. Zeller, Malin Lindstedt, Daniel Agardh, Åsa Håkansson, and Karolina Östbring. "Changes in Intestinal Permeability Ex Vivo and Immune Cell Activation by Three Commonly Used Emulsifiers." Molecules 25, no. 24 (December 15, 2020): 5943. http://dx.doi.org/10.3390/molecules25245943.

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Food additives such as emulsifiers are used in increasing quantities in the food industry. The aim of this study was to compare three different emulsifiers (polysorbate 80 (P80), carboxymethyl cellulose (CMC), and β-lactoglobulin (β-lac) with regards to their effect on the stimulation of immune cells and intestinal permeability. The immune stimulatory effects were studied in the myeloid cell line MUTZ-3-cells, while the change in intestinal permeability was studied in the Caco-2 cell line and ex vivo in the Ussing chamber system using small intestinal fragments from rats. The tested concentrations of the emulsifiers ranged from 0.02% up to 1%, which are concentrations commonly used in the food industry. The results showed that P80 affected both the myeloid cells and the intestinal permeability more than CMC (p < 0.05) and β-lac (p < 0.05) at the highest concentration. CMC was found to neither affect the permeability in the intestine nor the MUTZ-3 cells, while β-lac changed the permeability in the total part of the small intestine in rats. These findings indicate that P80 might be more cytotoxic compared to the other two emulsifiers.
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Dissertations / Theses on the topic "Permeabilità intestinale"

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Ponce, de Leon Rodriguez Maria del Carmen. "Développement d’un modèle in vitro d’inflammation intestinale par l’utilisation de lignées cellulaires humaines en co-culture pour l’étude des interactionsavec les micro-constituants alimentaires." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTG009/document.

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L’épithélium intestinal, siège de l’absorption des (micro)-nutriments est aussi le premier système de défense de l’organisme. Un déséquilibre dans l’homéostasie peut être à l’origine d’une réaction inflammatoire associée à des défauts de la barrière intestinale et de la fonction immunitaire, ainsi qu’une malabsorption des nutriments, comme rencontré dans les MICI (Maladies Inflammatoires Chroniques de l’Intestin), dans les stratégies de fortification en micronutriments et les pathologies non transmissibles (obésité). Il est donc important de trouver des moyens d’action, via l’alimentation par exemple, pour prévenir ou au minima réduire, les conséquences nutritionnelles et pathologiques de l’inflammation intestinale, et de comprendre les mécanismes impliqués. Parmi les modèles d’études de l’intestin, les modèles in vitro de culture cellulaire sont de plus en plus utilisés et permettent d'évaluer les mécanismes moléculaires d'une manière simple et reproductible et de réduire l'expérimentation animale.Dans ce contexte et dans le but d’étudier l’interaction de composés bioactifs de l’alimentation avec l’intestin en état d’inflammation, le premier objectif de ce travail de thèse a été la mise au point d’un modèle in vitro d’intestin enflammé associant en co-culture deux lignées intestinales humaines : les Caco-2 TC7 (entérocytes) et HT29-MTX (cellules caliciformes) et une lignée immunitaire de macrophages (THP1). Plusieurs marqueurs d’inflammation ont été évalués et nous avons pu montrer que le modèle de tri-culture répondait à un stimulus inflammatoire (LPS/IFNγ), par une augmentation de la production de cytokines pro-inflammatoires (TNF-α, IL6 et IL8) et d’enzymes (INOS et COX2) ainsi que l’expression de leurs gènes. Par ailleurs, une augmentation de la perméabilité épithéliale via une altération des jonctions serrées (TJs) a également pu être mise en évidence ainsi qu’une surproduction de mucus, lesquels sont des caractéristiques reconnus d’inflammation.Le deuxième objectif était d’étudier l’interaction de la β-cryptoxanthine (BCX), caroténoïde des agrumes, lipophile et anti-oxydant, avec le modèle enflammé. Nous avons utilisé pour solubiliser la BCX deux types de micelles (artificielles et physiologiques) et étudié les marqueurs d’inflammation. Bien qu’il semble d’après les résultats préliminaires que les micelles de BCX montrent une tendance à diminuer la production de certaines cytokines (IL6 et IL8), le rôle des constituants des micelles (Tween 40 ou sels biliaires/phospholipides) dans ce phénomène observé et dans la perméabilité épithéliale reste à clarifier par la suite
The intestinal epithelium, main place of the absorption of (micro)-nutrients is also the first body's defense system. An imbalance in homeostasis can lead to an inflammatory reaction associated with defects in the intestinal barrier and immune function as well as malabsorption of nutrients, as seen in IBD (Inflammatory Bowel Diseases), in micronutrient fortification strategies and noncommunicable diseases (obesity). It is therefore important to find ways of action, for example through diet, to prevent or at least reduce the nutritional and pathological consequences of intestinal inflammation, and to understand the mechanisms involved. Among intestinal models, in vitro cell culture models are increasingly used and allow to evaluate the molecular mechanisms in a simple and reproducible way and to reduce animal experimentation.In this context and in order to study the interaction of dietary bioactive compounds with the intestine in state of inflammation, the first objective of this work was the development of an in vitro model of inflamed intestine combining in co-culture two human intestinal cell lines: Caco-2 TC7 (enterocytes) and HT29-MTX (goblet cells) and an immune cell line of macrophages (THP1). Several inflammation markers were evaluated and we were able to show that the tri-culture model responded to an inflammatory stimulus (LPS / IFNγ), by increasing the production of pro-inflammatory cytokines (TNF-α, IL6 and IL8) and enzymes (INOS and COX2) as well as the expression of their genes. In addition, an increase of epithelial permeability via tight junctions (TJs) alteration has also been demonstrated, as well as overproduction of mucus, which are recognized inflammation characteristics.The second objective was to study the interaction of β-cryptoxanthin (BCX), a lipophilic and antioxidant carotenoid of citrus, with the inflamed model. To solubilize BCX, we used two types of micelles (artificial and physiological) and studied markers of inflammation. Although it appears from the preliminary results that BCX micelles show a tendency to decrease the production of some cytokines (IL6 and IL8), the role of micelle constituents (Tween 40 or bile salts / phospholipids) in the phenomenon observed and in the epithelial permeability remains to be therefore clarified
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Weaver, Laurence Trevelyan. "The intestinal permeability of infants." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289788.

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Smethurst, Paul R. "Small intestinal permeability in man." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315531.

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Lundin, Pål. "Intestinal permeability a parameter of mucosal dysfunction /." Lund : Dept. of Animal Physiology, Lund University, 1997. http://books.google.com/books?id=wuNqAAAAMAAJ.

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Lang, Mia E. "Intestinal permeability in the irradiated ferret." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7772.

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Ferrets received whole-body irradiation (5 Gy, gamma). At different times post-irradiation (PIRR, 2, 24, and 48 hours), measurements of fluid and electrolyte fluxes, and of the blood-to-lumen clearance of $\sp{51}$Cr-EDTA, were compared between in situ perfused loops of jejunum and ileum. Intestinal permeation of $\sp{51}$Cr-EDTA was increased (4x control) in both the jejunum and ileum at 2 hours PIRR. At 24 hours PIRR, $\sp{51}$Cr-EDTA permeation was the same as control. At 48 hours PIRR, jejunal permeation of $\sp{51}$Cr-EDTA was not statistically different from control animals, whereas in the ileum, $\sp{51}$Cr-EDTA permeation was increased 10x control. Absorption of luminal fluid was abolished 2 hours PIRR in the ileum. Sodium and chloride fluxes were unaffected by radiation exposure, but at 48 hours PIRR there was a significant secretion of potassium in the ileum. Diarrhea rarely occurred after the first hour post-irradiation. Serotonin, acting via 5-HT$\sb3$ receptors, was investigated as a possible mediator of radiation-induced alterations in intestinal permeability. Pretreatment with the 5-HT$\sb3$ antagonist and anti-emetic BRL 43694 significantly reduced the severity of radiation-induced vomiting. It offered some therapeutic benefit to radiation-induced diarrhea. However BRL 43694 pretreatment had no effect on intestinal permeability. (Abstract shortened by UMI.)
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Anderson, Alexander Douglas Gray. "Measurement of intestinal permeability in surgical patients." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24575.

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Aim: The aim of this study was to investigate the use of a triple sugar test of intestinal permeability as a surrogate marker of gut barrier function in surgical patients. Methods: Original laboratory work included the development of a technique for the quantification of urinary sucralose using high performance liquid chromatography (HPLC) with refractive index detection. Other techniques used included HPLC analysis of urinary lactulose and rhamnose, quantification of urinary 51Cr-EDTA by gamma counting, and a lactulose-hydrogen breath test. The triple sugar test involved ingestion of a test drink containing sucralose (5g), lactulose (5g) and rhamnose (1g). Urine was collected for 24 hours in 2 aliquots (first 5 and last 19 hours) and sugar concentrations determined by HPLC. A 51Cr-EDTA test was administered separately as an independent measure of “whole-gut” permeability. Healthy volunteers (n=21) and ileostomists (n=18) were studied in order to investigate the sites of absorption of sugar probes. A number of patient groups were then studied; these included subjects with Crohn’s disease (n=16),acute colitis (n=18), IBS (n=11), acute pancreatitis (n=9) and patients undergoing chemotherapy (n=7). Results: Assays for urinary sugars were both accurate and precise (coefficient of variation approximately 5%). Studies in ileostomists and controls indicated that 24-hr sucralose excretion represented “whole-gut” permeability, whereas the 5-hr lactulose/rhamnose excretion ratio represented small intestinal permeability. Small intestinal permeability was increased in subjects with Crohn’s disease (p=0.007) and acute pancreatitis (p=0.004), versus controls. “Whole gut” permeability was significantly increased in patients with Crohn’s (p=0.001) and pancreatitis (p<0.001), and significantly reduced in patients undergoing chemotherapy (p=0.012). The proportion of sucralose excreted in the last 19 hours of collection was significantly increased in patients with Crohn’s (p=0.026), acute colitis (0.023) and acute pancreatitis (p=0.049), implying an increase in colonic permeability.
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Salameh, Emmeline. "Développement d'un modèle murin de dénutrition avec entéropathie et évaluation de molécules d'intérêt permettant de contribuer au rétablissement de la fonction de barrière intestinale." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR064.

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Contexte : La malnutrition aiguë sévère (MAS) est un problème majeur de santé publique dans lemonde et affecte 17 millions d’enfants âgés de moins de 5 ans. La MAS induit une perte de poidsrapide, souvent associée à une dysfonction entérique environnementale (DEE). La DEE se caractérisepar une augmentation de l’inflammation, de la perméabilité intestinale, une diminution de la taille des villosités et de l’absorption des nutriments. La DEE peut ainsi limiter l’efficacité des protocolesde stabilisation et de re-nutrition chez l’enfant dénutri.L’objectif de cette thèse a été de développer un modèle de dénutrition avec entéropathie pour évaluer des laits thérapeutiques enrichis en nutriments ciblant la fonction de barrière intestinale.Résultats : Lors de la phase de développement du modèle, plusieurs approches ont été testées comme la restriction calorique, le régime hypoprotéiné, l’utilisation de lipopolysaccharides et de l’indométacine. Seule la combinaison d’un gavage quotidien d’indométacine pendant une semaine chez des souris dénutries par un régime pauvre en protéines a permis de développer un retard de croissance associé à une entéropathie. Suite à la validation de ce modèle, nous avons évalué la supplémentation du lait thérapeutique F-75 avec de la glutamine, de la leucine, de la gomme arabique et des levures séléniées. La glutamine et la leucine améliorent la fonction de barrière intestinale. Dans nos conditions expérimentales, l’enrichissement du lait thérapeutique avec la glutamine et la leucine combinés a eu des effets limités sur la fonction de barrière. La gomme arabique et les levures séléniées ont des propriétés prébiotiques et probiotiques et exercent des effets bénéfiques sur la barrière intestinale. L’enrichissement du lait thérapeutique avec l’association de ces deux composés permet d’inhiber l’inflammation intestinale et d’augmenter l’abondance de bactéries bénéfiques comme Faecalibacterium prausnitzii.Conclusion : Les travaux réalisés au cours de cette thèse ont permis de développer un nouveau modèle de dénutrition avec entéropathie. Le lait thérapeutique enrichi en gomme arabique et levures séléniées exerce des effets bénéfiques sur la fonction de barrière intestinale dans notre modèle
Background : Severe acute malnutrition (SAM) is a global health issue affecting 17 million children under the age of 5. SAM induces rapid weight loss and is often associated with environmental enteric dysfunction (EED). EED is characterized by intestinal hyperpermeability and inflammation, villus blunting and nutrient malabsorption. EED might, therefore, limit stabilization and re-nutrition protocol efficacy. Objectives : This thesis aimed to develop an undernutrition model with enteropathy to evaluate the effect of a therapeutic milk enriched with nutrients on gut barrier function. Results : During preclinical model development, several approaches were tested: calorie restriction, low-protein diet, use of lipopolysaccharides and indomethacin. Only daily indomethacin gavage during one week in protein-energy undernourished mice induced growth faltering associated with enteropathy. After preclinical model validation, we evaluated the effect of therapeutic milk supplemented with glutamine, leucine, gum arabic and/or selenium-enriched yeast on gut barrier function. Glutamine and leucine induce beneficial effects on gut barrier function. In ourexperimental conditions, therapeutic milk enriched with a combination of glutamine and leucine had a limited impact on this parameter. Gum arabic and selenium-enriched yeasts have prebiotic and probiotic properties on gut barrier function. Therapeutic milk supplemented with gum arabic and selenium-enriched yeast inhibited intestinal inflammation and enhanced specific bacteria abundance such as Faecalibacterium prausnitzii.Conclusion : The studies conducted during this thesis permitted to develop a new model of undernutrition with enteropathy. Therapeutic milk enriched with arabic gum and selenium-enriched yeast triggered beneficial effects on gut barrier function in our preclinical model
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Yao, Shengtao. "The effect of denervation on intestinal permeability and function following small intestinal transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq22692.pdf.

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Wang, Chuan. "Pathologically and experimentally induced intestinal barrier changes evaluated by permeability measurements." Lund : Dept. of Animal Physiology, Lund University, 1995. http://books.google.com/books?id=ddlqAAAAMAAJ.

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Bahlouli, Wafa. "Régulation de la perméabilité intestinale au cours du syndrome de l'intestin irritable : role du système ubiquitine-protéasome et impact de l'obésité." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR047.

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Le syndrome de l’intestin irritable (SII) est un trouble fonctionnel d’origine multifactorielle, impliquant des facteurs environnementaux tels que le stress, l’alimentation et met en jeu un dysfonctionnement de l’axe intestin-cerveau, une micro-inflammation, une dysbiose et une hyperperméabilité intestinale. Le rôle du protéasome dans la régulation de la barrière intestinale au cours du SII a été étudié. De plus, ces troubles fonctionnels intestinaux (TFI) ont également été décrits comme exacerbés chez des patients souffrant d’obésité, dont la physiopathologie est complexe. Néanmoins, les mécanismes impliqués dans cette association restent mal compris et ont donc été recherchés. Dans ce travail, des modèles murins « SII-like » comme le modèle de stress « water avoidance stress » ou WAS et le modèle post-inflammatoire « post-TNBS » ont été utilisés afin d’étudier l’impact d’une inhibition du protéasome sur la régulation de la perméabilité intestinale. L’inhibition pharmacologique du protéasome par le PR-957 ou l’utilisation de souris invalidées pour une sous unité β2i du protéasome limite l’hyperperméabilité intestinale. Une supplémentation orale en glutamine permet également de diminuer la perméabilité intestinale. Une étude protéomique au niveau colique des souris WAS et une étude de l’ubiquitome colique de patients souffrant de SII à profil diarrhéique confirment l’implication du protéasome dans la physiopathologie du SII. Nous avons ensuite cherché à comprendre le lien entre l’obésité et le SII en combinant des modèles d’obésité (génétique et induite par une alimentation riche en graisses ou HFD) et le modèle WAS. Seules les souris HFD présentent une exacerbation de l’hyperperméabilité intestinale et une corticostéronémie plasmatique élevée en réponse au modèle WAS. Des études complémentaires suggèrent que ces résultats sont indépendants de la leptine, de la glycémie et du microbiote intestinal. Nos travaux proposent donc de nouvelles pistes de prise en charge des patients souffrant de SII, par intervention nutritionnelle via la glutamine ou en utilisant le protéasome comme cible thérapeutique. Nous suggérons également un rôle de l’alimentation (riche en graisse) dans le développement des TFI au cours de l’obésité
Irritable bowel syndrome (IBS) is a multifactorial functional disorder, involving environmental factors (stress and diet for instance), gut-brain-axis dysfunction, micro-inflammation, dysbiosis and an alteration of intestinal permeability. The role of the proteasome in the regulation of the intestinal barrier during IBS has been studied. In addition, these intestinal functional disorders have also been described in patients with obesity. Nevertheless, the mechanisms underlying an association of intestinal functional disorders in the obesity context, remain poorly understood and have therefore been investigated in this thesis. In this study, "IBS-like" mouse models such as water avoidance stress (WAS) and the post-inflammatory (post-TNBS) models, were used to study the impact of proteasome inhibition on the regulation of intestinal permeability. We found that the pharmacological inhibition of the proteasome (with PR-957) or the use of knock-out mice for a subunit of the proteasome (β2i -/-) limit intestinal hyperpermeability occured in IBS-Like models. Moreover, we found that oral supplementation with glutamine also reduces intestinal hyperpermeability, wich, thus, can be considered as a putative nutritional treatment for IBS. A colonic proteomic study of WAS mice and a study of colonic ubiquitoma in IBS patients with diarrheal profiles confirmed the involvement of proteasome in the pathophysiology of IBS. Therefore, the link between obesity and IBS was examined by combining models of obesity (ob/ob genetic and high-fat diet [HFD] models) with WAS model. Only HFD mice displayed enhanced intestinal hyperpermeability and higher plasma corticosterone levels in response to WAS. Further studies suggest that these results, themselve, are independent of leptin, glycaemia and gut microbiota. This study paves new ways of treating patients suffering from IBS, by nutritional intervention via glutamine or by using the proteasome as a therapeutic target. We also suggest a role of diet (high fat) in the development of intestinal functional disorders during obesity
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Books on the topic "Permeabilità intestinale"

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Ford, Jayne. Non-steroidal anti-inflammatory drugs and intestinal permeability. Manchester: Universityof Manchester, 1994.

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Sinclair, David Graeme. Changes in pulmonary endothelial and intestinal permeability following cardiopulmonary bypass and in the critically ill. Birmingham: University of Birmingham, 1995.

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Intestinal Permeability [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.82968.

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Naturopath, Case Adams. The Science of Leaky Gut Syndrome: Intestinal Permeability and Digestive Health. Logical Books, 2014.

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Singh, Marvin M., and Gerard E. Mullin. Diet, Environmental Chemicals, and the Gut Microbiome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0006.

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This chapter reviews the latest research on gut health and addresses the nutritional and environmental effects on the gut microbiome, a key player in pathogenesis of diseases such as inflammation, intestinal permeability, obesity, metabolic syndrome, diabetes, cardiovascular disease, and neurologic conditions. The 100 trillion microorganisms that cohabit within each of us play a critical role in maintaining health and preventing disease. Many factors can alter and interact with the microbiome, including nutrition, genetics, and environmental exposures. Clinicians need to understand these relationships to help patients make the informed decisions that can impact their daily lives and the health of subsequent generations.
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Bazzan, Anthony J., and Daniel A. Monti. Diet, Gut, and Brain: A New Horizon. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0001.

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There is growing data that dietary factors have profound effects on inflammation, the gut microbiome, intestinal permeability, and the blood–brain barrier; all of which impact brain health and psychological well-being. The Western diet in particular is deleterious for both physical and cognitive/emotional health. This occurs primarily by causing inflammation in the gut and an activation of the immune system along with causing impairment in the integrity of the gut lining. This allows many reactive molecules to enter the general circulation and even cross the blood–brain barrier. Recent research advances elucidate that understanding the harmful physiological effects of certain dietary behaviors is as important as knowing the role of critical nutrients for optimal brain health. This chapter reviews current knowledge regarding diet and nutrition in the context of psychiatric disorders and brain health. Information is reviewed regarding the most appropriate dietary and nutrition approaches to support optimum brain health.
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Book chapters on the topic "Permeabilità intestinale"

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First, Michael B., Elizabeth Spencer, Elizabeth Spencer, Sander Begeer, Brynn Thomas, Danielle Geno Kent, Maria Fusaro, et al. "Intestinal Permeability Studies." In Encyclopedia of Autism Spectrum Disorders, 1650–52. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_28.

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Reynolds, Ann. "Intestinal Permeability Studies." In Encyclopedia of Autism Spectrum Disorders, 2549–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_28.

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Bjarnason, I., A. Macpherson, and I. S. Menzies. "Intestinal permeability: the basics." In Inflammatory Bowel Disease, 53–70. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_6.

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Westerbeek, E. A. M., B. Stahl, and R. M. van Elburg. "Human milk and intestinal permeability." In Handbook of dietary and nutritional aspects of human breast milk, 99–116. The Netherlands: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-764-6_5.

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Wells, C. L., and S. L. Erlandsen. "Bacterial Translocation: Intestinal Epithelial Permeability." In Update in Intensive Care and Emergency Medicine, 131–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80224-9_9.

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Pecoraro, C., M. T. Saravo, P. Stanziale, M. M. Balletta, G. Parrilli, and G. Budillon. "Abnormal Intestinal Permeability in IgA Nephropathy." In Current Therapy in Nephrology, 65–67. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0865-2_17.

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Oami, Takehiko, and Craig M. Coopersmith. "Measurement of Intestinal Permeability During Sepsis." In Methods in Molecular Biology, 169–75. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1488-4_15.

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Caspary, W. F. "Wirkung nichtsteroidaler Antirheumatika auf die intestinale Permeabilität." In Ökosystem Darm VI, 92–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85187-2_10.

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Fu, Linglin, Bobby J. Cherayil, Haining Shi, Yanbo Wang, and Yang Zhu. "Intestinal Permeability and Transport of Food Allergens." In Food Allergy, 41–67. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6928-5_3.

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Mielants, H., E. M. Veys, S. Goemaere, M. De Vos, C. Cuvelier, M. Maertens, and C. Ackerman. "Intestinal mucosal permeability in inflammatory rheumatic diseases." In Side-Effects of Anti-Inflammatory Drugs 3, 80–88. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2982-4_12.

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Conference papers on the topic "Permeabilità intestinale"

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Guliaev, Sergei, Leonid Strizhakov, Sergey Moiseev, Ivan Gmoshinskii, and Vladimir Mazo. "SAT0229 INTESTINAL PERMEABILITY IN IGA-VASCULITIS IN ADULTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3722.

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Sprooten, Roy T. M., I. Grimbergen, D. Braeken, K. Lenaerts, E. Rutten, E. F. M. Wouters, and G. G. U. Rohde. "Increased small intestinal permeability during severe acute exacerbations of COPD." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa3525.

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Aubert, P., J. Chevalier, T. Durand, A. Bessard, O. Kelber, H. Abdel-Aziz, and M. Neunlist. "Intestinal permeability induced by psychological stress: Action of STW 5." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608493.

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Singhvi, D. G., B. Methe, K. Li, A. Fitch, Y. Zhang, F. C. Sciurba, S. M. Nouraie, A. Morris, and J. M. Bon. "Influence of Smoking on Intestinal Microbiota Composition and Permeability in COPD." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6283.

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Seethaler, B., S. Beetz, M. Basrai, A. Schweinlin, J. Walter, M. Laville, NM Delzenne, and SC Bischoff. "Auswirkungen einer Lebensstilveränderung auf die intestinale Permeabilität bei adipösen TeilnehmerInnen eines Gewichtsreduktionsprogramms." In Kongress Ernährung 2020 – Medizin fürs Leben. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710245.

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Aubert, P., J. Chevalier, T. Durand, A. Bessard, O. Kelber, H. Aziz-Kalbhenn, and M. Neunlist. "Stress-induced changes in intestinal permeability in mice: Influence of STW 5." In Phytotherapiekongress 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1697324.

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Barreto, Mario, Maurizio Simmaco, Luigi Principessa, Alfonso Lostia, Rosanna Zambardi, Susanna Bonafoni, Valentina Negro, Carla Olita, and Maria P. Villa. "Asthma And Intestinal Permeability In Children: Role Of Age, Symptoms And Allergen Sensitization." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6250.

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Aubert, P., J. Chevalier, T. Durand, A. Bessard, O. Kelber, H. Abdel-Aziz, and M. Neunlist. "STW 5 prevents stress-induced changes in intestinal permeability in mice in-vivo." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608490.

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Luneva, O. E. "Food supplement “carrageenan” and its effect on the organism." In VIII Information school of a young scientist. Central Scientific Library of the Urals Branch of the Russian Academy of Sciences, 2020. http://dx.doi.org/10.32460/ishmu-2020-8-0014.

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Food additives are positioned as harmless, although, their components affectthe physiological processes associated with the permeability of the wall of the gastrointestinal tract (GIT) and intestinal microbiota. This article describes thecarrageenan supplement and its effects on the body in in vitro and in vivo experiments. The experimental part is devoted to analysis of the intestinalmicrobiota of laboratory rats with the consumption of the carrageenan dietary supplement in the amount of about 4,4 % of the standard feed.
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Nogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira, and Leiz Maria Costa Véras. "The autistic spectrum disorder and its relation to intestinal dysbiosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.283.

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Introduction: Autistic Spectrum Disorder (ASD) is characterized by a neurodevelopmental disorder, in which the child has persistent deficits in verbal and / or non-verbal communication, social interaction and behavior. One of the factors related to the cause of ASD are nutritional aspects, such as intestinal dysbiosis. Objective: To analyze the relationship between imbalance in the intestinal microbiota and the pathophysiological characteristics of ASD. Methodology: This is a systematic review, carried out in the Pubmed, SciELO databases, in order to answer the question: what is the relationship between intestinal microbiota imbalance and ASD? 139 articles were found, of which 12 were selected, through the simultaneous crossing between the descriptors “Autistic Disorder”, “Dysbiosis”. Articles written in Portuguese and English published from 2016 to 2021 were inserted. Results/Discussion: Most children with ASD exhibit gastrointestinal symptoms, such as constipation and diarrhea, and greater intestinal permeability, with major differences in the composition of microorganisms in the gastrointestinal tract (GIT). Patients with ASD have a lower microbiota diversity in the GIT. However, it is not possible to identify the origin of this change, since children with ASD often have changes in diet and eating behavior, which could alter the microbiota. Conclusion: It is still complex to understand what are the main causes of ASD. The gut-brain axis is an important associated factor both in the etiology and in the clinical manifestations of ASD. The use of diets, together with the modulation of the microbiota, by the use of probiotics and specific antibiotics, are possibilities for promising therapy.
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