Alterations in intestinal permeability

Arrieta, Marie‐Claire

doi:10.1136/gut.2005.085373

Cited by 539 publications

(511 citation statements)

References 95 publications

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“…In another study investigating plasma endotoxin (LPS) levels in the bloodstream, it was discovered that a high-fat meal promotes the absorption of LPS across the intestinal barrier, leading to plasma levels characteristic of ME [50]. Previous studies also support these findings, demonstrating that meals high in fatty acids were linked with increased intestinal barrier permeability [52,53]. Further investigation elevated endotoxin levels in the bloodstream found that merely 10 pg endotoxin/mL caused a significant increase in endothelial cell expression of Eselectin for 6 hours [50].…”

Section: Copyrightsupporting

confidence: 61%

Broad-Spectrum Antibiotic Abuse and its Connection to Obesity

Czaja¹

2017

JNHFS

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The purpose of this review was to assess patterns of antibiotic prescriptions across the United States and evaluate their relationship with associated conditions. A focus on national antibiotic prescriptions and proposed side effects was studied from 1993-2008. State-to-state differences in antibiotic prescribing and associated patterns of obesity were studied from 2011-2014. Data for these study periods was extracted from the CDC and affiliated institutions. Correlation assessments between antibiotic prescription patterns and a set of variables related to the proposed mechanism of antibiotic effects were made. From 2011-2014, cephalosporin prescriptions demonstrated the strongest relationship with associated obesity rates, while beta-lactams (cephalosporins and penicillins) showed weaker relationships when taken as a holistic class. To make light of these results, drug use of Ceftriaxone, a broad-spectrum, third-generation cephalosporin and Amoxicillin, a narrow-spectrum penicillin, was compared from 1993 to 2008 in relation to the prevalence of various health conditions: obesity; diabetes mellitus; sleep disorders; endocrine, nutritional, metabolic diseases and immunity disorders; and infectious and parasitic diseases. Ceftriaxone demonstrated a strong, significant, and positive relationship with all of the above variables, except for parasitic and infectious diseases. By comparison, Amoxicillin showed weak and non-significant relationships with all of the above variables. Despite their correlational limitations, these results suggest that broad-spectrum antibiotics play a significant role in the development and persistence of many chronic conditions in the United States. A mechanism providing a hypothesized explanation for these results was proposed based on extensive literature review.

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Section: Copyrightsupporting

confidence: 61%

Broad-Spectrum Antibiotic Abuse and its Connection to Obesity

Czaja¹

2017

JNHFS

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“…Changes observed in endotoxaemia levels under the ASO SAA treatment may be due to the effects of SAA on gut permeability or on LPS clearance. SAA is produced by colonic epithelium in response to the gut microbiota [11] and it is expected that inflammatory mediators cause an increase in gut permeability [43], and therefore, endotoxaemia. After reaching the blood stream, virtually all LPS molecules are rapidly complexed with circulating proteins and lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice

et al. 2016

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Aims/hypothesis Pre-adipocytes and adipocytes are responsive to the acute phase protein serum amyloid A (SAA). The combined effects triggered by SAA encompass an increase in preadipocyte proliferation, an induction of TNF-α and IL-6 release and a decrease in glucose uptake in mature adipocytes, strongly supporting a role for SAA in obesity and related comorbidities. This study addressed whether SAA depletion modulates weight gain and insulin resistance induced by a high-fat diet (HFD). Methods Male Swiss Webster mice were fed an HFD for 10 weeks under an SAA-targeted antisense oligonucleotide (ASO SAA ) treatment in order to evaluate the role of SAA in weight gain. Results With ASO SAA treatment, mice receiving an HFD did not differ in energy intake when compared with their controls, but were prevented from gaining weight and developing insulin resistance. The phenotype was characterised by a lack of adipose tissue expansion, with low accumulation of epididymal, retroperitoneal and subcutaneous fat content and decreased inflammatory markers, such as SAA3 and toll-like receptor (TLR)-4 expression, as well as macrophage infiltration into the adipose tissue. Furthermore, a metabolic status similar to chow-fed mice counterparts could be observed, with equivalent levels of leptin, adiponectin, IGF-I, SAA, fasting glucose and insulin, and remarkable improvement in glucose and insulin tolerance test profiles. Surprisingly, the expected HFD-induced metabolic endotoxaemia was also prevented by the ASO SAA treatment. Conclusions/interpretationThis study provides further evidence of the role of SAA in weight gain and insulin resistance. Moreover, we also suggest that beyond its proliferative and inflammatory effects, SAA is part of the lipopolysaccharide signalling pathway that links inflammation to obesity and insulin resistance.

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“…34 In several associations, this has also been demonstrated in CD and other autoimmune diseases. 4,35 Here, we aimed to assess whether differences in intestinal permeability, characterized by TJP1 mRNA expression, and intestinal regulatory T cells, measured by Foxp3 mRNA expression, as well as different serum antibodies levels exist between CD patients with and without accompanying T1D. Our task was also to evaluate differences in the effect of transamidating activity of serum tTG antibodies on tTG between patients with CD and controls.…”

Section: Introductionmentioning

confidence: 99%

Celiac disease in patients with type 1 diabetes: a condition with distinct changes in intestinal immunity?

et al. 2011

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Two common chronic childhood diseases-celiac disease (CD) and type 1 diabetes (T1D)-result from complex pathological mechanisms where genetic susceptibility, environmental exposure, alterations in intestinal permeability and immune responses play central roles. In this study, we investigated whether these characteristics were universal for CD independently of T1D association. For this purpose, we studied 36 children with normal small-bowel mucosa and 26 children with active CD, including 12 patients with T1D. In samples from the small-bowel mucosa, we detected the lowest expression of tight junction protein 1 (TJP1) mRNA in CD patients with T1D, indicating an increase in intestinal permeability. Furthermore, these samples displayed the highest expression of forkhead box P3 (FoxP3) mRNA, a marker for regulatory T cells, as compared with other patient groups. At the same time, serum levels of IgA antibodies specific for the CD-related antigens deamidated gliadin and tissue transglutaminase (tTG) were the highest in CD patients with T1D. In contrast, no significant differences were found in IgA or IgG antibodies specific for bovine beta-lactoglobulin or Bifidobacterium adolescentis DSM 20083-derived proteins. There were also no differences in the transamidating activity of serum autoantibodies between patients and control individuals. Our results show that patients with T1D and newly detected CD exhibit severely altered intestinal permeability, strong local immune activation and increased immunoregulatory mechanisms in the small bowel. Further study is required to determine whether these extreme changes in this CD subgroup are due to some specific environmental factors (virus infections), unknown genetic effects or autoimmune reactions to antigenic targets in intracellular tight junctions. INTRODUCTIONWith an approximate prevalence of 1.0% in Western countries, celiac disease (CD) is one of the most common lifelong chronic disorders. 1 CD and type 1 diabetes (T1D) form a significant sector of childhood diseases with high rate of co-occurrence. 2 Both diseases are autoimmune in origin and develop as a result of complex pathological mechanisms, involving several common genetic, environmental and immunological factors. Among these, the common susceptibility loci of HLA and other immune system-related genes, 3 permeability changes in the small-bowel mucosa, 4 and association with wheat consumption 4,5 are prominent. Both diseases are increasing in most regions of the world, 6,7 as are several other autoimmune diseases, but the actual cause of the disease remains unknown. However, several recent studies have highlighted the role of environmental and social changes that have taken place over the last several decades. 8,9 The central event in the pathogenesis of CD is damage to the small intestinal mucosa that occurs after ingestion of gluten or related prolamins in genetically susceptible individuals. During this process, several morphological and immunological alterations have been demonstrated in the small-bowel mucos...

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Alterations in intestinal permeability

Cited by 539 publications

References 95 publications

Broad-Spectrum Antibiotic Abuse and its Connection to Obesity

Broad-Spectrum Antibiotic Abuse and its Connection to Obesity

Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice

Celiac disease in patients with type 1 diabetes: a condition with distinct changes in intestinal immunity?

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