Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis.

By P. Brun, I. Castagliuolo, V. di Leo, A. Buda, M. Pinzani, G. Palù, D. Martines. American Journal of Physiology - Gastrointestinal and Liver Physiology, 2007

858 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/c5a08257f855680b58c0ab352acbfaa5d44f8d3f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Patrice D Cani
2. N. Delzenne
3. F. Bäckhed
4. A. Neyrinck
5. A. Chait
6. W. D. de Vos
7. Laura J. den Hartigh

In Molecular Biology

1. Patrice D Cani
2. N. Delzenne
3. W. D. de Vos
4. F. Bäckhed
5. A. Everard
6. A. Neyrinck
7. M. Derrien
8. G. Muccioli

In Neurology

1. Patrice D Cani

Citations in the corpus

• Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation. (2010, background): “Alteration in occludin distribution had been reported in ob/ob mice (9), and in vitro on epithelial cells stimulated with proinflammatory cytokines (8), occludin was chosen as a marker of tight junction disruption.”
• Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic Obese and Diet-Induced Leptin-Resistant Mice (2011, background): “For instance, recent evidence suggests that changes in gut microbiota composition may play a critical role in the development of obesity-associated inflammation (7,8,13,14).”
• Negative Effects of a High-Fat Diet on Intestinal Permeability: A Review. (2019, background): “Interestingly, because FAS is an insulin-sensitive enzyme, FAS downregulation in the setting of HFD-induced insulin resistance (diabetes or metabolic syndrome) may provide additional insight into the pathophysiology of enhanced intestinal permeability and associated endotoxemia seen in these patient”
• Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity (2012, background): “Given that genetic models of obesity fed with a normal chow diet still develop metabolic endotoxemia, we cannot exclude the involvement of factors other than fat absorption.(10,25,36,37) Therefore, we hypothesized that metabolic endotoxemia could be linked to the gut microbiota.”
• Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability (2009, background): “a disruption of the key tight-junction proteins, ZO-1 and occludin.(26) Here we confirm that obese mice exhibit an altered”
• Linking Gut Microbiota and Inflammation to Obesity and Insulin Resistance. (2016, background): “The breakdown of tightjunction function leads to LPS translocation, which may be an early factor in the development of inflammation and insulin resistance in humans and mice (4, 12, 13, 17, 18) (FIGURE 2).”
• Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia (2007, background): “have recently demonstrated that obese and diabetic mice (ob/ob and db/db) exhibited significantly higher plasma endotoxin levels, which correlated to higher plasma inflammatory markers [30].”
• The endocannabinoid system links gut microbiota to adipogenesis (2010, methodology): “In the first experiment, we blocked the CB1 receptor with a specific, selective antagonist (SR141716A) in obese ob/ob mice with disrupted gut barrier and metabolic endotoxaemia (Brun et al, 2007; Cani et al, 2009) (Figure 2C and F; Ob-CT versus CT, Po0.”
• Energy intake is associated with endotoxemia in apparently healthy men. (2008, background): “In this respect, an increased intestinal permeability, a higher circulating concentration of endotoxins, and an increased expression of membrane CD14 mRNA concentrations (the main receptor of LPS) were found in genetically obese (leptin-deficient) mice (28).”
• Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitis. (2007, background): “[34] demonstrated that feeding MCDD impaired the expression of junctional complex proteins between adjacent enterocytes, and significantly impaired gut barrier function.”
• Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice (2008, background): “These animals are characterized by different gut microbiota (8,12), higher inflammatory tone, and endotoxemia when compared with wild-type mice (23).”
• The role of the gut microbiota in energy metabolism and metabolic disease. (2009, result): “In the same line of our results, recent studies report that plasma LPS is increased in ob/ob and db/db mice [45].”
• Effects of Gut Microbes on Nutrient Absorption and Energy Regulation (2012, background): “It has been suggested that the increases in systemic endotoxin levels may result from increased intestinal permeability caused by the compositional changes in the microbiota.(103) Endotoxemia may then contribute to the low-grade inflammation, insulin resistance, adipocyte hyperplasia, and decreased ”
• Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease (2020, background): “Such ectopic WAT areas are mostly located within the visceral cavity, and include intrahepatic (discussed in the section on Ectopic Abbreviations: ALT, Alanine transaminase; M2, Alternatively activated macrophages; AMPK, AMP-activated protein kinase; ARG1, arginase-1; AST, aspartate transaminase; β-”